The New Evolutionary Timetable
timot...@my-deja.com
PE but that's all I was able to find. When I searhed for it all I got
was creationists garbage "geologic record supports a young earth" etc.
Hardly usefull!
Sent via Deja.com http://www.deja.com/
Share what you know. Learn what you don't.
Will Pratt
timot...@my-deja.com wrote in message <7o7q87$7ue$1...@nnrp1.deja.com>...
>Anyone ever hear of this? I know it's a book written by and advokate of
>PE but that's all I was able to find. When I searhed for it all I got
>was creationists garbage "geologic record supports a young earth" etc.
>Hardly usefull!
Results of an OCLC search:
AUTHOR: Stanley, Steven M.
TITLE: The new evolutionary timetable : fossils, genes and the origin of
the species
PLACE: New York : London :
PUBLISHER: Basic Books ; Harper & Row,
YEAR: 1981
PUB TYPE: Book
FORMAT: xvi, 222 p. : ill. ; 24 cm.
NOTES: Includes index.
ISBN: 0063370220 :
SUBJECT: Evolution. Organisms -- Evolution
Any help?
Will
--
William L. Pratt, Ph.D., Curator of Invertebrates, Barrick Museum
Mail Stop 4012, Univ. Nevada, Las Vegas 89154-4012
(702) 895-1403; Fax (702) 895-3094; pra...@nevada.edu
Richard Harter
>Anyone ever hear of this? I know it's a book written by and advokate of
>PE but that's all I was able to find. When I searhed for it all I got
>was creationists garbage "geologic record supports a young earth" etc.
>Hardly usefull!
_The New Evolutionary Time Table, Fossils, Genes, and the Origin of
Species_, Steven M. Stanley, Harper Colophon Books, 1981,
ISBN 0-465-05014-X, pbk, 222pg.
Chapter Headings:
Introduction
The Voyage Toward Evolution
The Origin and Its Very Slow Progress
Darwinism Challenged, Darwinism Affirmed
The Fossil Record: Our Window on the Past
On the Rapid Origin of Species
Human Origins
Continuity or Creation?
Macroevolution and the Direction of Change
Punctuationalism and Society
What do you want to know?
Richard Harter, c...@tiac.net, The Concord Research Institute
URL = http://www.tiac.net/users/cri, phone = 1-978-369-3911
The mere fact that my assumptions are wrong and my conclusions
are erroneous does not mean that I am not right in principle.
david ford
Level" _Proceedings of the National Academy of Sciences USA_ 72: 646-50.
Stanley was with the Dept of Earth and Planetary Sciences, The Johns
Hopkins University, and coauthored _Principles of Paleontology_ (1971,
1978) with David Raup. On 646:
Phylogenies have traditionally been characterized as having
tree-like patterns. In plots depicting morphologic change on a
horizontal scale and time on a vertical scale, continuous phyletic
change is typically represented by diagonal branches and twigs.
Being based on fragmentary fossil evidence, such plots are
interpretive. They represent the concept of evolution that has
been called _phyletic gradualism_ (2). In reality, gradual
phyletic change is recognized for only a few fossil lineages, and
in these it is of minor morphologic consequence.
On 648 of the same article, Stanley observes,
_A Disclaimer_. It must be emphasized that the above tests do not
demonstrate that no gradual change occurs within established
species, but only that such change is generally slow and of minor
consequence relative to changes that frequently occur in speciation
events.
Woodruff, David S. 1980. Book review "Evolution: The Paleobiological
View" _Science_ 208: 716-17. Woodruff is with the University of
California at San Diego's department of biology, and is reviewing
Stanley's _Macroevolution: Pattern and Process_ (1979). On 716, 717:
Darwin and most subsequent authors including G. G. Simpson have
held that most evolutionary transitions occur within established
lineages by phyletic gradualism guided by natural selection. But
fossil species remain unchanged throughout most of their history
and the record fails to contain a single example of a significant
transition. Similarly, it is difficult to account for the greatly
accelerated pace of evolution during periods of adaptive radiation.
An alternative model of evolution, that of punctuated equilibria,
introduced by Niles Eldredge and Stephen Jay Gould in the early
1970's, more fully accounts for these same observations.[the
preceding probably was Woodruff describing Stanley's positions]
.... Stanley concludes that microevolutionary agents are
inadequate to account for macroevolution. He sees the two
processes as being decoupled, one involving primarily phyletic
gradualism and the other quantum speciation.
Martin, R.D. 1982. Book review "A new paradigm for evolutionary
change?" _Nature_ 296: 509-510. Martin is a reader in physical
anthropology at University College London, and is reviewing Stanley's
_The New Evolutionary Timetable: Fossils, Genes and the Origin of
Species_ (1982). The last paragraph:
In the absence of a clear model of the mechanism of "quantum
speciation", the case for a radically new paradigm remains somewhat
unconvincing, as was the case with continental drift prior to the
recognition of sea-floor spreading. Stanley devotes a whole
chapter to demonstrating that his doubts about conventional theory
do not open the door to creationism; but without a clear concept of
the mechanism involved in "punctuated evolution" he is unlikely to
convince any creationist! Stanley is right to alert the general
reader to the surprising new findings of paleontologists, but he
really goes much farther than the present evidence permits.
"New findings of paleontologists" nothing-- the fossil record's pattern
of stasis and sudden appearance was known from the get-go. Darwin and
T.H. Huxley, for example, knew of it.
david ford
Scientist_, 320. This is a review of Steven Stanley's _The New
Evolutionary Timetable_. What follows is probably Kemp summarizing
Stanley's claims. Three paragraphs, which amounts to over half of the
review:
Steven Stanley's new book describes in non-technical terms the
essential features of the revolution that has overtaken
paleontology during the past decade or so. Until very recently,
fossil evidence played almost no role in the formulation of ideas
about the mechanism of evolution because of its manifest
incompleteness. Rather, the causes of evolution have been deduced
from studies of the properties of living organisms, such as their
genetics, ecology, distribution, adaptations and so on, leading to
the view that evolution occurs by gradual, continuous changes in
the genetic structure of an interbreeding population. This
gradualistic model was generally accepted to apply to the origin of
new species and even major new kinds of organisms, and it predicts
that a complete fossil record would consist of lineages of
organisms showing gradual change continuously over long periods of
time.
Unfortunately, the fossil record does not meet this expectation,
for individual species of fossils are rarely connected to one other
by known intermediate forms. Thus, as Stanley makes clear in his
earlier chapters describing the rise and development of the theory
of evolution, the fossil record was believed to be too incomplete
to be helpful, except to illustrate rather crudely the course of
evolution in the past.
However, the question of why the fossil record should be so
incomplete led to the thought that perhaps the accepted model of
the mechanism was inadequate. Thus an alternative model has
arisen, based on the concept of "punctuated equilibria". This
claims that most evolutionary change occurs rapidly in small,
isolated populations, resulting in the relatively sudden formation
of new species. The main populations of species undergo relatively
little, if any evolutionary change. Such a theory actually
predicts that the fossil record will lack intermediate forms,
because these existed for a brief period only in a very limited
area, and are simply unlikely to be found as fossils.
Futumaya, Douglas J. 1983. _Science on Trial: The Case for Evolution_
(NY: Pantheon Books), 251pp. On 224-5, in response to the creationist
argument that Futumaya summarizes as "Despite a rich fossil record,
transitional intermediates between ancestors and descendants are not
found in the fossil record," Futumaya replies in part,
The modern genetic theory of evolution holds that adaptation to new
conditions proceeds rapidly, so that few intermediates are likely
to be found.
ReMine, Walter James. 1993. _The Biotic Message: Evolution Versus
Message Theory_ (Saint Paul, MN: Saint Paul Science), 538pp. On 334,
335:
Punctuated equilibria is not a prediction of genetics or any other
well-understood biological processes. Rather, it is specially
constructed to adapt evolutionary theory to explain the observed
fossil record. .... With punctuated equilibria, evolutionists try
to steal the creationists' prediction. "So the creationist
prediction of systematic gaps in the fossil record has no value in
validating the creationist model, since evolution theory makes
precisely the same prediction."
The quote is from S. Weinberg, review of _Fossils: Key to the Present_,
in _Reviews of Thirty-one Creationist Books_, S. Weinberg, ed. (NY:
National Center for Science Education, Inc., 1984), 7-9, 8.
more on Stanley
http://www.deja.com/=dnc/getdoc.xp?AN=511300184
Schindel
http://www.deja.com/=dnc/getdoc.xp?AN=493994218
david ford
Looks at Life Today_ (NY: The New American Library), 191pp. In the
chapter "Darwinism Today," on 166, 175:
Later, it was discovered that the majority of gene mutations are of
small extent, often quite difficult of detection save by the most
refined techniques. And the accumulation of such small mutations,
constantly buffered by new recombinations, will give precisely the
type of change that Darwin had in mind. Evolution does go by
jumps, but in most cases the jumps are so small that they hardly
ever take the new type outside the range of variation already
existing in the species, and the visible result is a gradual one.
Discontinuity of variation is thus translated by selection into
continuity of evolutionary change: life marches up a ramp, not a
staircase. So much for the mechanism of evolution. .... To-day
we are able to reject these subsidiary [Lamarckian] hypotheses, and
can demonstrate that natural selection is omnipresent and virtually
the only guiding agency in evolution.
Lewin, Roger. 1986. "Punctuated Equilibrium Is Now Old Hat" _Science_
231: 672-3. On 672:
There was no reason to expect-- and Darwin and the Neo-Darwinians
were explicit about this-- that change would for the most part be
other than a steady accumulation of small modifications. In other
words, the pattern of change would be gradual. The fact that the
fossil record does not show this-- instead, it typically reveals
long periods of stasis and bursts of change-- has long been
explained as the result of the record's woeful incompleteness.
about Lewin
http://www.deja.com/=dnc/getdoc.xp?AN=258072920
Kemp, Tom. 5 December 1985. "A fresh look at the fossil record" _New
Scientist_, 66-67. Kemp is curator of the University Museum, Oxford.
On 66, three and a half paragraphs:
Before the early 1970s, most paleontologists interpreted the fossil
record in the light of the prevailing view of how evolution works,
the NeoDarwinian, or synthetic theory. Thus, they attributed
differences in the fossils found at different points in geological
time to natural selection acting on individual organisms, causing a
gradual evolutionary change in a more or less continuous fashion.
Species became extinct, they said, because of competition from
other, better adapted species. Even whole taxonomic groups
competed with one another, to the advantage of some and the demise
of others. New species arose by gradual transformation of a
species, largely in response to environmental changes. Even mass
extinctions resulted from a simple loss of fitness following a
change in the environment.
The fact that the fossil data did not, on the whole, seem to fit
this prevailing model of the process of evolution-- for example, in
the absence of intermediate forms and of gradually changing
lineages over millions of years-- was really explained by the
notorious incompleteness of the fossil record. In other words,
when the assumed evolutionary processes did not match the pattern
of fossils that they were supposed to have generated, the pattern
was judged to be "wrong". A circular argument arises: interpret
the fossil record in terms of a particular theory of evolution,
inspect the interpretation, and note that it confirms the theory.
Well, it would, wouldn't it?
Spearheaded by this extraordinary journal [_Paleobiology_],
paleontology is now looking at what it actually finds, not what it
is told that it is supposed to find. As is now well known, most
fossil species appear instantaneously in the record, persist for
some millions of years virtually unchanged, only to disappear
abruptly-- the "punctuated equilibrium" pattern of Eldredge and
Gould. ....
Kemp's review of a Stanley book; Futuyma; ReMine
http://www.deja.com/=dnc/getdoc.xp?AN=513978648
Lewontin, R.C. Autumn 1991. "Facts and the Factitious in Natural
Sciences" _Critical Inquiry_, 140-53. Lewontin is Alexander Agassiz
professor at Harvard University, a theoretical and experimental
evolutionary geneticist, and a Marxist. On 143:
Natural selection is certainly not the only mechanism for
evolutionary change, and there is at present a major struggle in
evolutionary biology about how commonly natural selection operates.
Huxley in 1944: "To-day we... can demonstrate that natural selection is
omnipresent and virtually the only guiding agency in evolution."
wf...@ptd.net
>ReMine, Walter James. 1993. _The Biotic Message: Evolution Versus
>Message Theory_ (Saint Paul, MN: Saint Paul Science), 538pp. On 334,
>335:
> Punctuated equilibria is not a prediction of genetics or any other
> well-understood biological processes. Rather, it is specially
> constructed to adapt evolutionary theory to explain the observed
> fossil record.
HORRORS!!! imagine....scientists trying to adapt theories to
observations....
something creationists would do well to imitate. of course that would
mean the death of creationism
dave, why, when one does a literature search, does one find NO
research being done on creationism ANYWHERE by ANY scientists in the
world?
could it be it's not science??
.
wf...@ptd.net
wf...@ptd.net
>Huxley, Julian. 1944. _Man in the Modern World: An Eminent Scientist
>Looks at Life Today_ (NY: The New American Library), 191pp. In the
>chapter "Darwinism Today," on 166, 175:
dave, of course, living in the 18th century, tries to re-create
science as it was then, through his disinformation
dave cant...and wont..answer a basic question:
if evolution is wrong, and creationism right, why is there NO research
being done on creationism by any scientists ANYWHERE in the world. why
is research being done ONLY on evolution?
i appreciate dave's efforts to make american christianity a world
science...but it aint gonna happen.
by the by dave, try TRY to post references that are younger than i
am...and im 45 yrs old!! quotes 1/2 century old dont help your case.
>
>Lewin, Roger. 1986. "Punctuated Equilibrium Is Now Old Hat" _Science_
>231: 672-3. On 672:
> There was no reason to expect-- and Darwin and the Neo-Darwinians
> were explicit about this-- that change would for the most part be
> other than a steady accumulation of small modifications. In other
> words, the pattern of change would be gradual. The fact that the
> fossil record does not show this-- instead, it typically reveals
> long periods of stasis and bursts of change-- has long been
> explained as the result of the record's woeful incompleteness.
>about Lewin
> http://www.deja.com/=dnc/getdoc.xp?AN=258072920\
\
except, of course, creationism has a problem: how DID diversity
happen? science has a mechanism...evolution thru natural selection
(inter alia). creationism's mechanism?
magic.
>
>Kemp, Tom. 5 December 1985. "A fresh look at the fossil record" _New
>Scientist_, 66-67. Kemp is curator of the University Museum, Oxford.
>On 66, three and a half paragraphs:
.. In other words,
> when the assumed evolutionary processes did not match the pattern
> of fossils that they were supposed to have generated, the pattern
> was judged to be "wrong". A circular argument arises: interpret
> the fossil record in terms of a particular theory of evolution,
> inspect the interpretation, and note that it confirms the theory.
> Well, it would, wouldn't it?
>
if this were the case punctuated equilibrium would never have been
born. dave kinda forgets how science works. you test a theory against
accumulated evidence. a practice creationists have never tried.
tell us dave, how does creationism work?
> Spearheaded by this extraordinary journal [_Paleobiology_],
> paleontology is now looking at what it actually finds, not what it
> is told that it is supposed to find. As is now well known, most
> fossil species appear instantaneously in the record, persist for
> some millions of years virtually unchanged, only to disappear
> abruptly-- the "punctuated equilibrium" pattern of Eldredge and
> Gould. ....
>
except, of course, this quote mining confuses your view of evolution:
it confirms in rather an elegant manner that evolutionary biology IS
science; science adapts its theories to observations.
creationism tries to adapt observations to theory. thats why science
CHANGED and creationism DIDNT.
.
Elroy Willis
>david ford <dfo...@gl.umbc.edu> wrote:
>>ReMine, Walter James. 1993. _The Biotic Message: Evolution Versus
>>Message Theory_ (Saint Paul, MN: Saint Paul Science), 538pp. On 334,
>>335:
>> Punctuated equilibria is not a prediction of genetics or any other
>> well-understood biological processes. Rather, it is specially
>> constructed to adapt evolutionary theory to explain the observed
>> fossil record.
>HORRORS!!! imagine....scientists trying to adapt theories to
>observations....
Unheard of. It's a bloody crime, let me tell you!!
>something creationists would do well to imitate. of course that would
>mean the death of creationism
>dave, why, when one does a literature search, does one find NO
>research being done on creationism ANYWHERE by ANY scientists in the
>world?
What sort of research needs to be done? "Goddidit" answers everything
in one swoop. Who cares how he did it, he just did it.
>could it be it's not science??
Hmm... I think you're on to something here.
--
Elroy Willis
BAAWA (Undercover News Division)
http://www.cyberramp.net/~elo/news
G & G
Note to wf3h. I think you are missing the point. Dave Ford is not a
creationist. I don't know what you are trying to say, but it appears that
you think Dave is trying to support creationism when, in fact, he is doing
pretty much the opposite.
wf...@ptd.net wrote in message <37cda041....@news.ptd.net>...
>On 1 Sep 1999 16:08:43 -0400, david ford <dfo...@gl.umbc.edu> wrote:
>
>>Huxley, Julian. 1944. _Man in the Modern World: An Eminent Scientist
>>Looks at Life Today_ (NY: The New American Library), 191pp. In the
>>chapter "Darwinism Today," on 166, 175:
>
>
>dave, of course, living in the 18th century, tries to re-create
>science as it was then, through his disinformation
>
>dave cant...and wont..answer a basic question:
>
>if evolution is wrong, and creationism right, why is there NO research
>being done on creationism by any scientists ANYWHERE in the world. why
>is research being done ONLY on evolution?
>
>i appreciate dave's efforts to make american christianity a world
>science...but it aint gonna happen.
>
>by the by dave, try TRY to post references that are younger than i
>am...and im 45 yrs old!! quotes 1/2 century old dont help your case.
>
>
>>
>>Lewin, Roger. 1986. "Punctuated Equilibrium Is Now Old Hat" _Science_
>>231: 672-3. On 672:
>> There was no reason to expect-- and Darwin and the Neo-Darwinians
>> were explicit about this-- that change would for the most part be
>> other than a steady accumulation of small modifications. In other
>> words, the pattern of change would be gradual. The fact that the
>> fossil record does not show this-- instead, it typically reveals
>> long periods of stasis and bursts of change-- has long been
>> explained as the result of the record's woeful incompleteness.
>>about Lewin
>> http://www.deja.com/=dnc/getdoc.xp?AN=258072920\
>\
>
>except, of course, creationism has a problem: how DID diversity
>happen? science has a mechanism...evolution thru natural selection
>(inter alia). creationism's mechanism?
>
>magic.
>
>>
>>Kemp, Tom. 5 December 1985. "A fresh look at the fossil record" _New
>>Scientist_, 66-67. Kemp is curator of the University Museum, Oxford.
>>On 66, three and a half paragraphs:
>
>
>.. In other words,
>> when the assumed evolutionary processes did not match the pattern
>> of fossils that they were supposed to have generated, the pattern
>> was judged to be "wrong". A circular argument arises: interpret
>> the fossil record in terms of a particular theory of evolution,
>> inspect the interpretation, and note that it confirms the theory.
>> Well, it would, wouldn't it?
>>
>
>if this were the case punctuated equilibrium would never have been
>born. dave kinda forgets how science works. you test a theory against
>accumulated evidence. a practice creationists have never tried.
>
>tell us dave, how does creationism work?
>
>> Spearheaded by this extraordinary journal [_Paleobiology_],
>> paleontology is now looking at what it actually finds, not what it
>> is told that it is supposed to find. As is now well known, most
>> fossil species appear instantaneously in the record, persist for
>> some millions of years virtually unchanged, only to disappear
>> abruptly-- the "punctuated equilibrium" pattern of Eldredge and
>> Gould. ....
>>
>
Gregory Gyetko
On 17 Aug 1999 18:31:29 -0400, david ford <dfo...@gl.umbc.edu> wrote:>ReMine, Walter James. 1993. _The Biotic Message: Evolution Versus
>Message Theory_ (Saint Paul, MN: Saint Paul Science), 538pp. On 334,
>335:
> Punctuated equilibria is not a prediction of genetics or any other
> well-understood biological processes. Rather, it is specially
> constructed to adapt evolutionary theory to explain the observed
> fossil record.
Charles Darwin even expected evolution to occur this way:
"One other consideration is worth notice: with animals and plants that
can
propagate rapidly and are not highly locomotive, there is reason to
suspect,
as we have formerly seen, that their varieties are generally at first
local;
and that such local varieties do not spread widely and supplant their
parent-forms until they have been modified and perfected in some considerable
degree. According to this view, the chance of discovering in
a formation in
any one country all the early stages of transition between any two
forms, is
small, for the successive changes are supposed to have been local or
confined
to some one spot." - Charles Darwin on P.E.
HORRORS!!! imagine....scientists trying to adapt theories to
observations....
something creationists would do well to imitate. of course that would
mean the death of creationism
dave, why, when one does a literature search, does one find NO
research being done on creationism ANYWHERE by ANY scientists in the
world?
could it be it's not science??
.
Greg.
-- alt.atheism atheist #911, BAAWA Knight "I'd worship Satan, but I'm going to hell anyway, so why bother?." EAC Homepage: http://eac.home.dhs.org
Adam Noel Harris
:Note to wf3h. I think you are missing the point. Dave Ford is not a
:creationist.
When did this happen? Perhaps you are confusing him with Dave Greene, who
is a troll.
-Adam
--
Opinions expressed are not necessarily those of Stanford University.
PGP Fingerprint = C0 65 A2 BD 8A 67 B3 19 F9 8B C1 4C 8E F2 EA 0E
cz...@ecn.ab.ca
: >> Punctuated equilibria is not a prediction of genetics or any other
: >> well-understood biological processes. Rather, it is specially
: >> constructed to adapt evolutionary theory to explain the observed
: >> fossil record.
: >HORRORS!!! imagine....scientists trying to adapt theories to
: >observations....
: Unheard of. It's a bloody crime, let me tell you!!
Truly, these maniacs must be stopped.
--
*************************************************************
In science, "fact" can only mean "confirmed to such a
degree that it would be perverse to withold provisional
assent." I suppose that apples might start to rise
tomorrow, but the possibility does not merit equal time
in physics classrooms.
-Stephen Jay Gould
*************************************************************
Eriksongs
> degree that it would be perverse to withold provisional
> assent." I suppose that apples might start to rise
> tomorrow, but the possibility does not merit equal time
> in physics classrooms.
> -Stephen Jay Gould
I don't agree with Mr. Gould's assessment of 'facts' in science. It rules out
completely the concept of Universals, the principle one being existance.
raven1
How?
david ford
Publishing Company), 176pp. James (1842-1910) was an American
philosopher adhering to a joke of a philosophy called
"pragmatism." On 134:
Humbug is humbug, even though it bear the scientific
name....
John Wilkins
<Pine.SGI.4.10A.B3.99090...@umbc9.umbc.edu>, david
ford <dfo...@gl.umbc.edu> wrote:
David - at last you touch on something I am interested in. Do please tell
me why you think pragmatism is a joke, epistemologicaly. As a
card-carrying fellow traveller of a pragmatist, I'm keen to see the error
of my ways.
--
John Wilkins, Head, Graphic Production
The Walter and Eliza Hall Institute of Medical Research, Melbourne,
Australia <mailto:wil...@WEHI.EDU.AU><http://www.wehi.edu.au/~wilkins>
Homo homini aut deus aut lupus - Erasmus of Rotterdam
wf...@ptd.net
>James, William. 1948. _Essays in Pragmatism_ (NY: Hafner
>Publishing Company), 176pp. James (1842-1910) was an American
>philosopher adhering to a joke of a philosophy called
>"pragmatism." On 134:
> Humbug is humbug, even though it bear the scientific
> name....
>
then what is left to call creationism which is humbug and ISNT
scientific?
david ford
david ford:
df James, William. 1948. _Essays in Pragmatism_ (NY: Hafner
df Publishing Company), 176pp. James (1842-1910) was an American
df philosopher adhering to a joke of a philosophy called
df "pragmatism." On 134:
df Humbug is humbug, even though it bear the scientific name....
JW David - at last you touch on something I am interested in. Do please
JW tell me why you think pragmatism is a joke, epistemologicaly. As a
JW card-carrying fellow traveller of a pragmatist, I'm keen to see the
JW error of my ways.
If the pragmatists presented some arguments on behalf of their point of
view, maybe I could critique those arguments. But as it is, I'm unaware
of any such arguments.
Rorty, Richard. 1995. "Is Truth a Goal of Enquiry? Davidson _VS._
Wright" _The Philosophical Quarterly_ 45: 281-300. The last paragraph:
In the end, we pragmatists have no real arguments against the
intuitions [that 'truth is some sort of correspondence to, or
accurate representation of, reality'-281] to which books like
Wright's _Truth and Objectivity_ appeal. All we have are
rhetorical questions like:
Are all those epicycles really worth the trouble?
What good do the intuitions you painstakingly salvage do us?
What practical difference do they make?
But such rhetorical questions have been instruments of
socio-cultural change in the past, and may be again.
After answering Rorty's questions as if I were a flippant physicist,
I'll be on my way.
1) Epicycles went out years ago. Go read a book on Kepler.
2) Using our realist approach to the physical world, we physicists have
figured out that one gets big explosions by splitting atoms. What
good does this do us? Well, now we can easily blow each other up.
3) Microwaves. Airplanes. Medicine. We live longer. We can now enjoy
frying our brains on television.
John Wilkins
<Pine.LNX.4.10A.B3.9909...@jabba.gl.umbc.edu>, david
ford <dfo...@gl.umbc.edu> wrote:
|John Wilkins <wil...@wehi.edu.au> on 9 Sep 1999:
|david ford:
|
|df James, William. 1948. _Essays in Pragmatism_ (NY: Hafner
|df Publishing Company), 176pp. James (1842-1910) was an American
|df philosopher adhering to a joke of a philosophy called
|df "pragmatism." On 134:
|df Humbug is humbug, even though it bear the scientific name....
|
|JW David - at last you touch on something I am interested in. Do please
|JW tell me why you think pragmatism is a joke, epistemologicaly. As a
|JW card-carrying fellow traveller of a pragmatist, I'm keen to see the
|JW error of my ways.
|
|If the pragmatists presented some arguments on behalf of their point of
|view, maybe I could critique those arguments. But as it is, I'm unaware
|of any such arguments.
Then perhaps you should go read up on the extensive literature on the
topic. Nicholas Rescher provides a relatively good introduction into it.
Here's a Q&D search result on the topic:
Rescher, Nicholas. Methodological pragmatism : a systems-theoretic
approach to the theory of knowledge. Oxford: Blackwell, 1977.
Goodman, Russell B. Pragmatism : a contemporary reader. New York:
Routledge, 1995.
Margolis, Joseph. Pragmatism without foundations : reconciling realism and
relativism. Oxford ; New York: Blackwell, 1986.
Putnam, Hilary. Pragmatism : an open question. Oxford, England: Blackwell, 1995.
|
|Rorty, Richard. 1995. "Is Truth a Goal of Enquiry? Davidson _VS._
|Wright" _The Philosophical Quarterly_ 45: 281-300. The last paragraph:
| In the end, we pragmatists have no real arguments against the
| intuitions [that 'truth is some sort of correspondence to, or
| accurate representation of, reality'-281] to which books like
| Wright's _Truth and Objectivity_ appeal. All we have are
| rhetorical questions like:
| Are all those epicycles really worth the trouble?
| What good do the intuitions you painstakingly salvage do us?
| What practical difference do they make?
| But such rhetorical questions have been instruments of
| socio-cultural change in the past, and may be again.
|
|After answering Rorty's questions as if I were a flippant physicist,
|I'll be on my way.
|1) Epicycles went out years ago. Go read a book on Kepler.
|2) Using our realist approach to the physical world, we physicists have
| figured out that one gets big explosions by splitting atoms. What
| good does this do us? Well, now we can easily blow each other up.
|3) Microwaves. Airplanes. Medicine. We live longer. We can now enjoy
| frying our brains on television.
Rorty is not my choice of source for these things. But the epicycles point
would be made from the standpoint of a Ptolemaic astronomer asking whether
that or the new Copernican heliocentric theory ought to be preferred. The
rest needs more context to be sure what Rorty is saying.
Note: pragmatism is not an alternative view to realism WRT scientific
entities. It is an alternative to Correspondence theories of truth in
epistemology.
maff91
wrote:
[...]
>
>Then perhaps you should go read up on the extensive literature on the
>topic. Nicholas Rescher provides a relatively good introduction into it.
>
>Here's a Q&D search result on the topic:
>
>Rescher, Nicholas. Methodological pragmatism : a systems-theoretic
>approach to the theory of knowledge. Oxford: Blackwell, 1977.
http://www.amazon.com/exec/obidos/ASIN/0631170308/
>
>Goodman, Russell B. Pragmatism : a contemporary reader. New York:
>Routledge, 1995.
http://www.amazon.com/exec/obidos/ASIN/0415909104/
>
>Margolis, Joseph. Pragmatism without foundations : reconciling realism and
>relativism. Oxford ; New York: Blackwell, 1986.
http://www.amazon.com/exec/obidos/ASIN/063115034X/
>
>Putnam, Hilary. Pragmatism : an open question. Oxford, England: Blackwell, 1995.
http://www.amazon.com/exec/obidos/ASIN/063119343X/
[...]
--
L.P.#0000000001
david ford
[snips throughout]
r dave, why, when one does a literature search, does one find NO
r research being done on creationism ANYWHERE by ANY scientists in
r the world? could it be it's not science??
Science is about *describing* (_not_ explaining) the physical and
biological world. Intelligent design theory is about _explaining_ the
physical world. Hence, intelligent design theory is not science.
Evolution theory is similarly not science because it's all about
_explaining_ the biological world. The question then becomes, Does
evolution theory or intelligent design theory more simply/ compactly/
economically explain what we see in the realm of biology? In short,
both intelligent design theory and evolution theory are not science.
===============begin inserted text===============
Isham, C.J. 1996. "Quantum Theories of the Creation of the Universe"
in _Quantum Cosmology and the Laws of Nature: Scientific Perspectives on
Divine Action_, Russell, Murphy, and Isham, ed., 53:
The distinction between _explaining_ and _describing_ opens up a
Pandora's box of questions concerning the status and role of
mathematical theories of physics. Nevertheless, the distinction
is one with which most practicing physicists are familiar, even if
it _is_ somewhat ambiguous.
Penzias, Arno. In a 4 May 1994 interview with Fred Heeren, in Heeren's
_Show Me God: What the Message From Space is Telling Us About God_
(1995), 129:
And since science can't _explain_ anything--it can only _describe_
things--that's perfectly sensible. If every time you wanted to
describe a new phenomenon and you found an explanation for it,
you'd be in a lot of trouble. Because you'd say the tree gets
green because it _wants_ to. Or it gets green because nature
wanted it that way. Or a fairy comes there every March, or
something like that. Each one of those are explanations.
If you don't see the distinction between "description" and "explanation"
there's not much I can do. Supposing you do see the distinction, can
you think of anything in science where we have explanation but no
description?
> So, how does your "God" explanation work? Does it explain why bat
> wings have one structure and bird wings have another and pteranodon
> wings had yet a third?
Same concept of flight, 3 different implementations. The same thing
happens when an engineer conceives of attaching wings to a container and
proceeds to design an F-16 fighter, a commercial jet, and a helicopter.
> Does it explain why there are no native snakes
> in Hawaii? Does it help us understand under what circumstances
> antibiotic resistance or pesticide resistance develop? What, exactly,
> is "God" supposed to explain about the history of life on earth?
For the "history of life" question, after creating Adam and Eve, God
ceased from His creative activity. Thus we do not see new organisms
appearing today, unlike was the case in the past, when God at various
intervals of time created different sets of creatures, whose appearance
was recorded by the fossil record. For the Hawaii question, perhaps God
put snakes there and they became extinct, resulting in there being "no
native snakes in Hawaii." Another possible explanation, which would
depend on how old Hawaii is and when snakes last appear in the fossil
record, is saying that Hawaii came into existence after God did the last
round of snake creations; hence, no snakes on Hawaii.
Your question "Does it [the God explanation] help us understand under
what circumstances antibiotic resistance or pesticide resistance
develop?" requires a description, a description of the inner workings of
bacteria and insects at the molecular level and their relations with
differing environments, not an explanation. Your question is best
answered in asking "_how_ is it that resistance develops."
If you want a "for what reason?" of resistance development, my
explanation would be that the master Programmer's programs were designed
to allow for a limited degree of change; this change occasionally
expresses itself when the environment changes. E.g., a mutation
conferring on a plant the ability to live in an area with high levels of
heavy metals may occur, and when the environment becomes one of high
heavy metal levels, then that resistance is revealed, and plants with
such ability flourish. Having variability such as this is good for the
organism, for it helps the organism survive amidst changing
environments. However, there are limits to the amount of variability,
and the DNA program can only change so much before the thing crashes.
Though a say pea plant may become friends with heavy metals, it'll never
become an oak tree.
I'd like to emphasize that these are very minor explanations flowing
from the Designer hypothesis. The biggie is the hypothesis's superb
explanation of the huge degree of design in the biological world.
Dawkins, Richard. _The Blind Watchmaker_ (1987), 15:
Meanwhile I want to follow Paley in emphasizing the magnitude of
the problem that our explanation [i.e, natural selection] faces,
the sheer hugeness of biological complexity and the beauty and
elegance of biological design.
The design is there for all to see. How best to explain it? A brief
reflection on the immensity of the design present, from the biochemical
pathway of photosynthesis to the supposed evolution of eyes 40-60+
times, plus some consideration of genetics make it apparent that
Dawkins's defunct blind watchmaker, natural selection, is no match for a
seeing Watchmaker.
================end inserted text================
r if evolution is wrong, and creationism right, why is there NO
r research being done on creationism by any scientists ANYWHERE
r in the world. why is research being done ONLY on evolution?
Julie T. is a scientist and has conducted research using intelligent
design thought.
links to Julie T. posts
http://www.deja.com/=dnc/getdoc.xp?AN=506979684
r except, of course, creationism has a problem: how DID diversity
r happen? science has a mechanism...evolution thru natural selection
r (inter alia). creationism's mechanism? magic.
See this sequence of letters? What's the mechanism behind this sequence
of letters' appearance? Look now at your computer. What's the
mechanism behind its appearance? magic? intelligence? what?
Please list the mechanisms you have in mind by [r]"inter alia."
Andrew Dalton
david ford <dfo...@gl.umbc.edu> wrote in message
news:Pine.SGI.4.10A.B3.99091...@umbc8.umbc.edu...
> robert <wf...@ptd.net> on 1 Sep 1999, and on 1 Sep 1999:
>
> [snips throughout]
>
> r dave, why, when one does a literature search, does one find NO
> r research being done on creationism ANYWHERE by ANY scientists in
> r the world? could it be it's not science??
>
> Science is about *describing* (_not_ explaining) the physical and
> biological world. Intelligent design theory is about _explaining_ the
> physical world. Hence, intelligent design theory is not science.
> Evolution theory is similarly not science because it's all about
> _explaining_ the biological world. The question then becomes, Does
> evolution theory or intelligent design theory more simply/ compactly/
> economically explain what we see in the realm of biology? In short,
> both intelligent design theory and evolution theory are not science.
Unless you are prepared to give definite criteria which distinguish
"description" from "explanation" (as these terms are used by you), this is
nothing but smoke and mirrors.
[snip]
>
> If you don't see the distinction between "description" and "explanation"
> there's not much I can do. Supposing you do see the distinction, can
> you think of anything in science where we have explanation but no
> description?
Is this a new variation on "Credo ut intellegam"? Your argument is
completely fallacious, but if you can't see why, then there's not much I can
do.
Andrew Dalton
David Johnston
>
> robert <wf...@ptd.net> on 1 Sep 1999, and on 1 Sep 1999:
>
> [snips throughout]
>
> r dave, why, when one does a literature search, does one find NO
> r research being done on creationism ANYWHERE by ANY scientists in
> r the world? could it be it's not science??
>
> Science is about *describing* (_not_ explaining) the physical and
> biological world.
Geez. Where did you get that definition from? The 16th century?
Orac
<Pine.SGI.4.10A.B3.99091...@umbc8.umbc.edu>, david
ford <dfo...@gl.umbc.edu> wrote:
>Science is about *describing* (_not_ explaining) the physical and
>biological world.
Jeez, where did you get THIS definition of science, out of a cereal box?
>Intelligent design theory is about _explaining_ the
>physical world. Hence, intelligent design theory is not science.
>Evolution theory is similarly not science because it's all about
>_explaining_ the biological world. The question then becomes, Does
>evolution theory or intelligent design theory more simply/ compactly/
>economically explain what we see in the realm of biology? In short,
>both intelligent design theory and evolution theory are not science.
You really need to crack open a few basic science textbooks.
--
Orac |"A statement of fact cannot be insolent."--Orac
a.k.a. |
David Gorski|"If you cannot listen to the answers, why do you
| inconvenience me with questions?"--Orac again
Wesley R. Elsberry
DF>[snips throughout]
r> dave, why, when one does a literature search, does one find NO
r> research being done on creationism ANYWHERE by ANY scientists in
r> the world? could it be it's not science??
DF>Science is about *describing* (_not_ explaining) the physical
DF>and biological world. Intelligent design theory is about
DF>_explaining_ the physical world. Hence, intelligent design
DF>theory is not science. Evolution theory is similarly not
DF>science because it's all about _explaining_ the biological
DF>world. The question then becomes, Does evolution theory or
DF>intelligent design theory more simply/ compactly/
DF>economically explain what we see in the realm of biology? In
DF>short, both intelligent design theory and evolution theory
DF>are not science.
[...]
In short, David Ford is only a few decades and a few
philosophies out of date. Robert Pennock thoroughly explodes
this "describing" versus "explaining" view of science in his
book, "Tower of Babel". Adherence to a "description only"
view of science is a tell-tale sign of positivism. Pennock
notes that Hempel's work beginning in 1948 changed the view
concerning explanation, since he put it on an empirical
rather than necessarily metaphysical basis.
--
Wesley R. Elsberry, Student in Wildlife & Fisheries Sciences, Tx A&M U.
Visit the Online Zoologists page (http://www.rtis.com/nat/user/elsberry)
Email to this account is dumped to /dev/null, whose Spam appetite is capacious.
"Between the horror of space\And the terror of time" - BOC
Thomas Scharle
|> david ford wrote:
|> >
|> > robert <wf...@ptd.net> on 1 Sep 1999, and on 1 Sep 1999:
|> >
|> > [snips throughout]
|> >
|> > r dave, why, when one does a literature search, does one find NO
|> > r research being done on creationism ANYWHERE by ANY scientists in
|> > r the world? could it be it's not science??
|> >
|> > Science is about *describing* (_not_ explaining) the physical and
|> > biological world.
|>
|> Geez. Where did you get that definition from? The 16th century?
There is a well known explanation of "fundamentalism" that it
started in the 19th century as an emulation of science, as
described by Francis Bacon, as passed through the Scottish "common
sense philosophers", in the realm of religion.
I think that a lot of the "creationist" objections to
evolution as science can be understood as a kind of Baconian
critique. That is, if science is just a collection of regularities,
if its hypotheses are of the sort "all crows are black", then
much of science since Bacon, including evolutionary biology, does
not fit that model.
Perhaps we can understand this model of the world ... there is
"science", which contains descriptions of natural events, and there
are "gods" which function as explanations for the events. Benjamin
Franklin encroached on the realm of Thor when Ben Franklin explained
lightning as electricity, rather than confining himself to saying
"there is a phenomenon of lightning."
--
Tom Scharle scha...@nd.edu "standard disclaimer"
hrgr...@my-deja.com
100...@umbc8.umbc.edu>,
david ford <dfo...@gl.umbc.edu> wrote:
> robert <wf...@ptd.net> on 1 Sep 1999, and on 1 Sep 1999:
>
> [snips throughout]
>
> r happen? science has a mechanism...evolution thru natural selection
> r (inter alia). creationism's mechanism? magic.
>
> See this sequence of letters? What's the mechanism behind this
sequence
> of letters' appearance? Look now at your computer. What's the
> mechanism behind its appearance? magic? intelligence? what?
>
The mechanism is well-known physics and chemistry: neurons firing in
the brain - motoric nerve fibers - muscle fibers contracting - keys
struck - various unspeakable things done by a confused operating system
(i.e. solid state physics) - various things done to electrons coming
from the monitor cathode - photons emitted from the screen.
Which mechanisms did the supposed creator use for implementation of his
design ?
Morale: Intelligent design (a volitional activity) is only the first
part of the story; it must be implemented by *mechanisms*. This second
part is usually neglected by the I.D. crowd.
HRG.
> Please list the mechanisms you have in mind by [r]"inter alia."
>
>
Sent via Deja.com http://www.deja.com/
Share what you know. Learn what you don't.
Matt
> Science is about *describing* (_not_ explaining) the physical and
> biological world. Intelligent design theory is about _explaining_ the
> physical world.
Describing something would usually entail specifying the details of the
way something IS something. Such as a description of a car might be 'Its
got four wheels and is blue'. Science can do this by observation and
experiment. An explanation of something is a description of how
something came to be something, such as 'The car has four wheels as this
gives it an optimisd power transmission:stability ratio, and is blue
because current market forces favour blue as a desirable colour,
increasing sales of cars of that colour'. Science also does this, by
theory and the subsequent testing and verification of what the theory
predicts to see if it matches observation and experiments devised to
test that theory.
If you use the two terms 'description' and 'explanation' differently to
this, please let me know. I want to know if >>>RENAMING OF TERMS<<< is
going to start catching on.
There are currently no observably confirmable descriptions of reality
that adhere to a theory of intelligent design, and also no theory of
intelligent design allows the formulation of testable verifiable
predictions to be drawn from that theory.
What good does intelligent design do us, and if it is true, how can we
test it to make sure?
Matt.
maff91
Scharle) wrote:
>In article <37DD82...@telusplanet.net>, David Johnston <rgo...@telusplanet.net> writes:
>|> david ford wrote:
>
>|> >
>|> > robert <wf...@ptd.net> on 1 Sep 1999, and on 1 Sep 1999:
>|> >
>|> > [snips throughout]
>|> >
>|> > r dave, why, when one does a literature search, does one find NO
>|> > r research being done on creationism ANYWHERE by ANY scientists in
>|> > r the world? could it be it's not science??
>|> >
>|> > Science is about *describing* (_not_ explaining) the physical and
>|> > biological world.
>|>
>|> Geez. Where did you get that definition from? The 16th century?
>
> There is a well known explanation of "fundamentalism" that it
>started in the 19th century as an emulation of science, as
>described by Francis Bacon, as passed through the Scottish "common
>sense philosophers", in the realm of religion.
>
> I think that a lot of the "creationist" objections to
>evolution as science can be understood as a kind of Baconian
>critique. That is, if science is just a collection of regularities,
>if its hypotheses are of the sort "all crows are black", then
>much of science since Bacon, including evolutionary biology, does
>not fit that model.
>
> Perhaps we can understand this model of the world ... there is
>"science", which contains descriptions of natural events, and there
>are "gods" which function as explanations for the events. Benjamin
>Franklin encroached on the realm of Thor when Ben Franklin explained
>lightning as electricity, rather than confining himself to saying
>"there is a phenomenon of lightning."
http://x1.dejanews.com/getdoc.xp?AN=454219236
--
L.P.#0000000001
david ford
david ford:
df Science is about *describing* (_not_ explaining) the physical
df and biological world. Intelligent design theory is about
df _explaining_ the physical world. Hence, intelligent design
df theory is not science. Evolution theory is similarly not
df science because it's all about _explaining_ the biological
df world. The question then becomes, Does evolution theory or
df intelligent design theory more simply/ compactly/
df economically explain what we see in the realm of biology? In
df short, both intelligent design theory and evolution theory
df are not science.
WRE In short, David Ford is only a few decades and a few
WRE philosophies out of date. Robert Pennock thoroughly explodes
WRE this "describing" versus "explaining" view of science in his
WRE book, "Tower of Babel". Adherence to a "description only"
WRE view of science is a tell-tale sign of positivism.
Positivism can't be all that bad. After all, it helped Einstein
develop relativity.
WRE Pennock notes that Hempel's work beginning in 1948 changed
WRE the view concerning explanation, since he put it on an empirical
WRE rather than necessarily metaphysical basis.
Keith Doyle
Matt <mat...@netgates.co.uk> wrote:
>david ford wrote:
>
>> Science is about *describing* (_not_ explaining) the physical and
>> biological world. Intelligent design theory is about _explaining_ the
>> physical world.
>
>way something IS something. Such as a description of a car might be 'Its
>got four wheels and is blue'. Science can do this by observation and
>experiment. An explanation of something is a description of how
>something came to be something, such as 'The car has four wheels as this
>gives it an optimisd power transmission:stability ratio, and is blue
>because current market forces favour blue as a desirable colour,
>increasing sales of cars of that colour'. Science also does this, by
>theory and the subsequent testing and verification of what the theory
>predicts to see if it matches observation and experiments devised to
>test that theory.
>If you use the two terms 'description' and 'explanation' differently to
>this, please let me know. I want to know if >>>RENAMING OF TERMS<<< is
>going to start catching on.
>There are currently no observably confirmable descriptions of reality
>that adhere to a theory of intelligent design, and also no theory of
>intelligent design allows the formulation of testable verifiable
>predictions to be drawn from that theory.
>What good does intelligent design do us, and if it is true, how can we
>test it to make sure?
It seems that this "explain" vs "describe" issue is consistent with
usual Creationist tactics:
a) If evolution is science, creationism is too.
b) if creationism is not science, neither is evolution.
c) if creationism can't explain, science can't either.
Its just another pathetic attempt to redefine science in order to level
the playing field between creationism and evolution. However, as pointed
out in other responses to the original article, item "c" has been shown
to be a bogus argument decades ago, along with all the others.
--
Keith Doyle
(remove underbars in reply address for E-mail)
"The most exciting phrase to hear in science, the one that heralds new
discoveries, is not 'Eureka!' (I found it!) but 'That's funny ...'"
-- Isaac Asimov
Elroy Willis
> david ford <dfo...@gl.umbc.edu> wrote:
>> robert <wf...@ptd.net> on 1 Sep 1999, and on 1 Sep 1999:
>> [snips throughout]
>> r except, of course, creationism has a problem: how DID diversity
>> r happen? science has a mechanism...evolution thru natural selection
>> r (inter alia). creationism's mechanism? magic.
>> See this sequence of letters? What's the mechanism behind this
>> sequence of letters' appearance? Look now at your computer. What's the
>> mechanism behind its appearance? magic? intelligence? what?
>The mechanism is well-known physics and chemistry: neurons firing in
>the brain - motoric nerve fibers - muscle fibers contracting - keys
>struck - various unspeakable things done by a confused operating system
>(i.e. solid state physics) - various things done to electrons coming
>from the monitor cathode - photons emitted from the screen.
>Which mechanisms did the supposed creator use for implementation of his
>design ?
>Morale: Intelligent design (a volitional activity) is only the first
>part of the story; it must be implemented by *mechanisms*. This second
>part is usually neglected by the I.D. crowd.
Is "wishing" or "thinking" stuff into existence considered a mechanism
for some omnipotent god? Hmm...
david ford
<http://www.talkorigins.org/origins/welcome.html>
"How do I know the contents of this archive are reliable?"
Visitors to the archive should be aware that essays and FAQs
appearing in the archive have generally not undergone a
rigorous peer review procedure by scientific experts.
Rather, they have been commented on and critiqued by the
readership of the talk.origins newsgroup. While many of the
participants in talk.origins are well regarded scientists,
this informal procedure is not as demanding as the process a
scientist goes through to publish a paper in a scientific
journal. It is important to keep this fact in mind when
reading the contents of this archive. Because most of the
essays have not undergone rigorous peer review, some of them
may contain errors or misstatements of fact. Any errors you
identify should be reported to the authors or to the editor.
As a general rule, you should never rely too heavily on
anything you read on the Internet. Read the primary,
reviewed literature before making up your mind on any topic.
Most of the archive's essays provide references to primary
sources to make it easier for you to do this.
It has recently been alleged by 2 individuals in talk.origins
that the theory of natural selection has as much support as the
law of gravity. Our best theory of gravity is the general theory
of relativity. GTR has proved enormously successful, with its
predictions repeatedly matching up with observation. These
smashing successes are recorded in and touted as successes in the
peer-reviewed scientific literature. Two questions for adherents
of the plausibility of the neo-Darwinian mechanism:
Does the theory of NS make predictions that match up with
observation?
If "yes," what are the references to the literature wherein the
successes are detailed and touted as successes?
wf...@ptd.net
>robert <wf...@ptd.net> on 1 Sep 1999, and on 1 Sep 1999:
>
>[snips throughout]
>
>r dave, why, when one does a literature search, does one find NO
>r research being done on creationism ANYWHERE by ANY scientists in
>r the world? could it be it's not science??
>
>Science is about *describing* (_not_ explaining) the physical and
>biological world.
nope, i disagree. thats why theories have mechanisms. thats why
there's quantum gravity, and not a purely operational view of gravity
like newtonian mechanics.
Intelligent design theory is about _explaining_ the
>physical world. Hence, intelligent design theory is not science.
except its advocates, like dembski, say it is.
>Evolution theory is similarly not science because it's all about
>_explaining_ the biological world.
this is pure nonsense. absolute, chemically pure nonsense.
The question then becomes, Does
>evolution theory or intelligent design theory more simply/ compactly/
>economically explain what we see in the realm of biology? In short,
>both intelligent design theory and evolution theory are not science.
wrong.
you're saying there is no mechanism in science.
but science is all about mechanism. so you're completely, dead wrong.
>
>===============begin inserted text===============
>Isham, C.J. 1996. "Quantum Theories of the Creation of the Universe"
>in _Quantum Cosmology and the Laws of Nature: Scientific Perspectives on
>Divine Action_, Russell, Murphy, and Isham, ed., 53:
> The distinction between _explaining_ and _describing_ opens up a
> Pandora's box of questions concerning the status and role of
> mathematical theories of physics. Nevertheless, the distinction
> is one with which most practicing physicists are familiar, even if
> it _is_ somewhat ambiguous.
except, implicitly, by your own quote, we see both are science.
newtonian mechanics described the world. concepts like quantum gravity
and darwinian evolution explain the world. both are science, unlike
intelligent design which relies on a deux ex machina view of science.
>Penzias, Arno. In a 4 May 1994 interview with Fred Heeren, in Heeren's
>_Show Me God: What the Message From Space is Telling Us About God_
>(1995), 129:
> And since science can't _explain_ anything--it can only _describe_
> things--that's perfectly sensible.
i think this is taken out of context. you make it sound like science
does not explain mechanisms. chemical kinetics, for example, is all
about mechanisms. thats its raison d'etre.
If every time you wanted to
> describe a new phenomenon and you found an explanation for it,
> you'd be in a lot of trouble. Because you'd say the tree gets
> green because it _wants_ to. Or it gets green because nature
> wanted it that way. Or a fairy comes there every March, or
> something like that. Each one of those are explanations.
and here you prove my case. a mechanistic (or as johnson would have
it, a 'materialist') view of science is exactly what science is about.
what penzias is saying here is saying explains HOW, not WHY.
>
>If you don't see the distinction between "description" and "explanation"
>there's not much I can do. Supposing you do see the distinction, can
>you think of anything in science where we have explanation but no
>description?
you've herniated the very concepts penzias talks about out of
existence.
>
>> So, how does your "God" explanation work? Does it explain why bat
>> wings have one structure and bird wings have another and pteranodon
>> wings had yet a third?
>
>Same concept of flight, 3 different implementations. The same thing
>happens when an engineer conceives of attaching wings to a container and
>proceeds to design an F-16 fighter, a commercial jet, and a helicopter.
except the engineer has the luxury of designing from scratch.
evolution doesnt. thats why its not intelligent design. it takes what
happens to be lying around and builds on it.
>
>> Does it explain why there are no native snakes
>> in Hawaii? Does it help us understand under what circumstances
>> antibiotic resistance or pesticide resistance develop? What, exactly,
>> is "God" supposed to explain about the history of life on earth?
>
>For the "history of life" question, after creating Adam and Eve, God
>ceased from His creative activity.
um, with all due respect this is crap. how do you know this? what is a
'god created activity'? why did he cease then?
Thus we do not see new organisms
>appearing today,
actually we do. N. Accuminata, for example, speciated within 30 yrs.
so this statement is wrong.
unlike was the case in the past, when God at various
>intervals of time created different sets of creatures, whose appearance
>was recorded by the fossil record.
except we see transitionals between them, so god must have been kinda
lazy to keep recreating different variations on a theme
>
>If you want a "for what reason?" of resistance development, my
>explanation would be that the master Programmer's programs were designed
>to allow for a limited degree of change; this change occasionally
>expresses itself when the environment changes.
actually i realize you're pulling our leg. this ad hoc justification
which attempts to destroy science bends on itself to beg the question
However, there are limits to the amount of variability,
>and the DNA program can only change so much before the thing crashes.
>Though a say pea plant may become friends with heavy metals, it'll never
>become an oak tree.
in a sense this is right. extinction, predicted by darwin, is the
outcome of this limit. but there is no guarantee that all species have
the same limit. in fact the recent discovery of genes that allow fast
evolution within 2 or 3 generations suggests the limits are quite
broad.
>
>I'd like to emphasize that these are very minor explanations flowing
>from the Designer hypothesis.
there is no designer hypothesis because there is no designer and no
mechanism. for example, in big bang cosmology we have gravity as the
force shapping the existence of superstructures of galaxies. in
darwinian evolution we have the mechanism of natural selection.
intelligent design has nothing. nothing at all.
>================end inserted text================
>
>r if evolution is wrong, and creationism right, why is there NO
>r research being done on creationism by any scientists ANYWHERE
>r in the world. why is research being done ONLY on evolution?
>
>Julie T. is a scientist and has conducted research using intelligent
>design thought.
>links to Julie T. posts
> http://www.deja.com/=dnc/getdoc.xp?AN=506979684
i commend her. however, she's not newton or einstein. if her theory
was scientific it would be used by the scientific community. quantum
theory replaced newtonian mechanics in a generation. intelligent
design is older than darwinian evolution and it's led nowhere. its
christian apologetics, not science.
so my statement stands: the scientific community is doing no research
on ID. that you can name a singular 'scientist' merely proves my
point.
>
>r except, of course, creationism has a problem: how DID diversity
>r happen? science has a mechanism...evolution thru natural selection
>r (inter alia). creationism's mechanism? magic.
>
>See this sequence of letters? What's the mechanism behind this sequence
>of letters' appearance? Look now at your computer. What's the
>mechanism behind its appearance? magic? intelligence? what?
we know what the mechanism is behind the typewriter. your 'intelligent
designer' is conspicuous by his/her absence. and the absence of his
mechanism.
>
>Please list the mechanisms you have in mind by [r]"inter alia."
genetic drift, etc
so ID, unlike evolution, is not science. and science is both
descriptive and explanatory. it does NOT, however, explain WHY...thats
why ID is not science.
>
wf...@ptd.net
>Wesley R. Elsberry <w...@cx33978-a.dt1.sdca.home.com> on 14 Sep 1999:
>david ford:
>
>df Science is about *describing* (_not_ explaining) the physical
>df and biological world. Intelligent design theory is about
>df _explaining_ the physical world. Hence, intelligent design
>df theory is not science. Evolution theory is similarly not
>df science because it's all about _explaining_ the biological
>df world. The question then becomes, Does evolution theory or
>df intelligent design theory more simply/ compactly/
>df economically explain what we see in the realm of biology? In
>df short, both intelligent design theory and evolution theory
>df are not science.
>
>WRE In short, David Ford is only a few decades and a few
>WRE philosophies out of date. Robert Pennock thoroughly explodes
>WRE this "describing" versus "explaining" view of science in his
>WRE book, "Tower of Babel". Adherence to a "description only"
>WRE view of science is a tell-tale sign of positivism.
>
>Positivism can't be all that bad. After all, it helped Einstein
>develop relativity.
>
and left einstein behind in the revolution on quantum mechanics.
wf...@ptd.net
>
>Does the theory of NS make predictions that match up with
> observation?
>If "yes," what are the references to the literature wherein the
> successes are detailed and touted as successes?
>
hoisted by his own petard i'd say.
im not an evolutionary biologist, merely a chemist. but i'd be
delighted if intelligent designers could meet this standard they want
to set for the science of evolutionary biology.
wf...@ptd.net
Scharle) wrote:
>In article <37DD82...@telusplanet.net>, David Johnston <rgo...@telusplanet.net> writes:
>|> david ford wrote:
>
>|> >
>|> > robert <wf...@ptd.net> on 1 Sep 1999, and on 1 Sep 1999:
>|> >
>|> > [snips throughout]
>|> >
>|> > r dave, why, when one does a literature search, does one find NO
>|> > r research being done on creationism ANYWHERE by ANY scientists in
>|> > r the world? could it be it's not science??
>|> >
>|> > Science is about *describing* (_not_ explaining) the physical and
>|> > biological world.
>|>
>|> Geez. Where did you get that definition from? The 16th century?
>
> There is a well known explanation of "fundamentalism" that it
>started in the 19th century as an emulation of science, as
>described by Francis Bacon, as passed through the Scottish "common
>sense philosophers", in the realm of religion.
>
this is true, and its become canon for creationists like phillip
johnson. unfortunately johnson's argument would require that chemistry
and physics are not sciences either since the same critique he applies
to evolutionary bio can be applied to them.
Peter van Velzen
wf...@ptd.net wrote in article <37e6d7ee....@news.ptd.net>...
> On 20 Sep 1999 12:41:37 -0400, david ford <dfo...@gl.umbc.edu> wrote:
>
> >
> >Does the theory of NS make predictions that match up with
> > observation?
> >If "yes," what are the references to the literature wherein the
> > successes are detailed and touted as successes?
> >
1. It predicts that some genes will die out,
because they are not fit to survive.
The proof of this is so evident,
that nobody ever cared to go into the details.
and the statement itselve is so self-evident
that nobody would ever brag about any proof at all.
On the other hand
I have never heard a creationist,
point to a single species with genes
that couldn't produce any offspring,
2. It predicts that favourable genes will multiply
more rapidly and gradually replace the old ones.
If you really need references about the succes of this prediction
you probably have the genes of Homo Erectus.
>
> hoisted by his own petard i'd say.
>
> im not an evolutionary biologist, merely a chemist. but i'd be
> delighted if intelligent designers could meet this standard they want
> to set for the science of evolutionary biology.
>
How on earth can you become a chemist
and not know the thirst thing about DNA?
The discovery of DNA was the greatest succes of the theory thus far.
As most people do not seem to realize
Darwin had no idea on how features were passed from one generation to
another.
He simply presumed they did somehow.
He would have been overjoyed that people nowadays can show you exactly
where they are.
Peter van Velzen
Amstelveen
The Netherlands
wf...@ptd.net
<pba...@worldonline.nl> wrote:
>This is funny
>
>
>wf...@ptd.net wrote in article <37e6d7ee....@news.ptd.net>...
>> On 20 Sep 1999 12:41:37 -0400, david ford <dfo...@gl.umbc.edu> wrote:
>>
>> >
>> >Does the theory of NS make predictions that match up with
>> > observation?
>> >If "yes," what are the references to the literature wherein the
>> > successes are detailed and touted as successes?
>> >
>
>1. It predicts that some genes will die out,
> because they are not fit to survive.
>
>The proof of this is so evident,
>that nobody ever cared to go into the details.
>and the statement itselve is so self-evident
>that nobody would ever brag about any proof at all.
whatever this means. i think you have david and me mixed up.
>
>
>
>2. It predicts that favourable genes will multiply
> more rapidly and gradually replace the old ones.
>
>If you really need references about the succes of this prediction
>you probably have the genes of Homo Erectus.
>
>
>>
>> hoisted by his own petard i'd say.
>>
>> im not an evolutionary biologist, merely a chemist. but i'd be
>> delighted if intelligent designers could meet this standard they want
>> to set for the science of evolutionary biology.
>>
>
>How on earth can you become a chemist
>and not know the thirst thing about DNA?
>
>The discovery of DNA was the greatest succes of the theory thus far.
again, you have me mixed up with dave. he's the one saying magic
causes speciation
>As most people do not seem to realize
>Darwin had no idea on how features were passed from one generation to
>another.
i'm not sure that's true. everyone is pretty much up to speed on
mendel's work
david ford
1) credentials.
Colin Patterson (1933 - 1998) was a zoologist whose specialty was
fossil fishes. Starting in 1962, he was at the British Museum
(Natural History), where he was a senior paleontologist and for which
he wrote the official general book on evolution, _Evolution_ (1978),
197pp. He was a Research Associate of the American Museum of Natural
History, NY, was Alexander Agassiz Visiting Lecturer at Harvard
University in 1970, and had a B.Sc. and Ph.D. from London University.
He published 150 papers, books, and reviews.[cover of his _Evolution_;
obituary at <http://www.linnean.org.uk/special.htm>]
2) recent comments by Patterson about the talk; the talk's audience.
From a letter by Patterson to Lionel Theunissen dated 16 Aug 1993,
which is in Theunissen's "Patterson Misquoted: A Tale of Two 'Cites'"
<http://www.talkorigins.org/faqs/patterson.html>, last updated 24 June
1997:
That brush with Sunderland (I had never heard of him before) was
my first experience of creationists. The famous "keynote
address" at the American Museum of Natural History in 1981 was
nothing of the sort [nothing of what sort? -df]. It was a talk
to the "Systematics Discussion Group" in the Museum, an
(extremely) informal group. I had been asked to talk to them on
"Evolutionism and creationism"; fired up by a paper by Ernst Mayr
published in Science just the week before. I gave a fairly
rumbustious talk, arguing that the theory of evolution had done
more harm than good to biological systematics (classification).
Unknown to me, there was a creationist in the audience with a
hidden tape recorder. So much the worse for me. But my talk was
addressed to professional systematists, and concerned
systematics, nothing else.
I hope that by now I have learned to be more circumspect in
dealing with creationists, cryptic or overt. But I still
maintain that scepticism is the scientist's duty, however much
the stance may expose us to ridicule.
Yours Sincerely, [signed] Colin Patterson
[Patterson]"fired up by a paper by Ernst Mayr published in _Science_
just the week before" Patterson refers to Mayr's "Biological
Classification: Toward a Synthesis of Opposing Methodologies"
_Science_ 214: 510-16 (30 Oct 1981). The talk occurred on 5 Nov 1981.
Patterson's statement that "my talk... concerned systematics, nothing
else" is inaccurate, as you'll find out shortly. The talk has not
been published, but one or more transcripts of it are floating around.
The talk was delivered to the Systematics Discussion Group at the
American Museum of Natural History. The Discussion Group met once a
month in an upstairs classroom opposite the museum's dinosaur exhibit
hall, and is usually composed of museum staff, grad students from
nearby schools, and "the occasional amateur like Norman Macbeth, the
author of _Darwin Retried_," with attendance ranging from under 16 to
over 150, depending on the topic and speaker. "Systematics" deals
with classification/ taxonomy.[Bethell (Feb 1985), 49-50]
3) Johnson's remarks about the talk.
Johnson, Phillip E. 1993. _Darwin on Trial_ (Ill: InterVarsity
Press), 220pp. On 173:
Colin Patterson's 1981 lecture was not published, but I have
reviewed a transcript and Patterson restated his position, which
I would label "evolutionary nihilism," in an interview with the
journalist Tom Bethell. (See Bethell, "Deducing from
Materialism," _National Review_, Aug. 29, 1986, p. 43.) I
discussed evolution with Patterson for several hours in London in
1988. He did not retract any of the specific sceptical
statements he has made, but he did say that he continues to
accept "evolution" as the only conceivable explanation for
certain features of the natural world.
On 9, 10:
His lecture compared creationism (not creation-science) with
evolution, and characterized both as scientifically vacuous
concepts which are held primarily on the basis of faith. ....
Patterson suggested that both evolution and creation are forms of
pseudo-knowledge, concepts which seem to imply information but do
not. One point of comparison was particularly striking. A
common objection to creationism in pre-Darwinian times was that
no one could say anything about the mechanism of creation.
Creationists simply pointed to the "fact" of creation and
conceded ignorance of the means. But now, according to
Patterson, Darwin's theory of natural selection is under fire and
scientists are no longer sure of its general validity.
Evolutionists increasingly talk like creationists in that they
point to a fact but cannot provide an explanation of the means.
4) actual quotations from Patterson's fall 1981 address.
Bethell, Tom. Feb 1985. "Agnostic Evolutionists: The taxonomic case
against Darwin" _Harper's_, 49-61. On 50:
Patterson's address was titled "Evolutionism and Creationism."
Patterson is not a creationist, but he had been trying to think
like one as a sort of experiment. "It's true," he told his
audience, "that for the last eighteen months or so I've been
kicking around non-evolutionary or even anti-evolutionary ideas."
He went on:
I think always before in my life when I've got up to speak
on a subject I've been confident of one thing-- that I know
more about it than anybody in the room, because I've worked
on it. Well, this time it isn't true. I'm speaking on two
subjects, evolutionism and creationism, and I believe it's
true to say that I know nothing whatever about either of
them. One of the reasons I started taking this
anti-evolutionary view, or let's call it a non-evolutionary
view, was that last year I had a sudden realization. For
over twenty years I had thought I was working on evolution
in some way. One morning I woke up and something had
happened in the night, and it struck me that I had been
working on this stuff for more than twenty years, and there
was not one thing I knew about it. It's quite a shock to
learn that one can be misled for so long. Either there was
something wrong with me or there was something wrong with
evolutionary theory. Naturally I know there is nothing
wrong with me, so for the last few weeks I've tried putting
a simple question to various people and groups. Question
is: Can you tell me anything you know about evolution? Any
one thing, any one thing that is true?
Johnson. _Darwin on Trial_. On 10, with Johnson's ellipsis, we
continue with 1 line repeated:
"Can you tell me [Patterson] anything you know about evolution,
any one thing... that is true? I tried that question on the
geology staff at the Field Museum of Natural History and the only
answer I got was silence. I tried it on the members of the
Evolutionary Morphology seminar in the University of Chicago, a
very prestigious body of evolutionists, and all I got there was
silence for a long time and eventually one person said, 'I do
know one thing-- it ought not to be taught in high school.' "
5) Patterson's remarks about the aftermath, and some additional
thoughts of his on the theory of evolution. Bethell (Feb 1985), 52:
"I really put my foot in it," Patterson told me that day I first
met him nearly two years ago. We were in a restaurant on
Columbus Avenue near the Museum of Natural History, and he was
recalling the talk he had given eighteen months earlier to the
systematics discussion group. "I compared evolution and creation
and made a case that the two were equivalent. I was all fired
up, and I said what I thought. I went through merry hell for
about a year. Almost everybody except the people at the museum
objected. Lots of academics wrote. Deluges of mail. 'Here we
are trying to combat a political argument,' they said, 'and you
give them ammunition!'"
He ordered something from the menu and said: "One has to live
with one's colleagues. They hold the theory very dear. I found
out that what you say will be taken in 'political' rather than
rational terms."
Patterson told me that he regarded the theory of evolution as
"often unnecessary" in biology. "In fact," he said, "they could
do perfectly well without it." Nevertheless, he said, it was
presented in textbooks as though it were "the unified field
theory of biology," holding the whole subject together-- and
binding the profession to it. "Once something has that status,"
he said, "it becomes like religion."
Bethell, Tom. 29 Aug 1986. "Deducing from Materialism" _National
Review_, 43-45. On 43-44, with Bethell's bracket:
Patterson seems not to have recanted. In a recent issue of the
_Creation/Evolution Newsletter_ he writes: "The awful question:
'Can you tell me anything you know about evolution...' Well, I
still think it's a reasonable one. Ed Wiley [of the University
of Kansas] answered that it generates hierarchy, but I find that
a bit too vague. My own current answer would be, 'I know that
the majority of change in the information transmitted (DNA)
occurs in spite of natural selection, not because of it.' "
In 1984 I interviewed Patterson in London and asked him if, in
the voluminous mail (much of it irate) he had received in
response to his heretical comments, anyone had pointed to
unequivocal evidence for evolution. He told me that someone had
claimed, "We do know that the polar bear evolved from the brown
bear." "Do we know that?" I asked. "No."
[Johnson]"But now, according to Patterson.... Evolutionists
increasingly talk like creationists in that they point to a fact but
cannot provide an explanation of the means."
Dobzhansky, Theodosius. 1958. "Evolution at Work" _Science_ 127:
1091-8. On 1092:
Darwin did not eschew making hypotheses concerning the forces
which bring evolution about. Without a plausible explanation of
how of evolution might happen it would be hard to accept the idea
that it did happen. The theory of natural selection was Darwin's
answer, and from the vantage point of modern knowledge it can be
seen that the answer was substantially correct.
Gould, Stephen Jay. May 1981. "Evolution as Fact and Theory"
_Discover_, 34-7. On 35:
Evolutionists have been clear about this distinction between fact
and theory from the very beginning, if only because we have
always acknowledged how far we are from completely understanding
the mechanisms (theory) by which evolution (fact) occurred. ....
From the 1940s through the 1960s, Darwin's own theory of natural
selection did achieve a temporary hegemony that it never enjoyed
in his lifetime. But renewed debate characterizes our decade,
and, while no biologist questions the importance of natural
selection, many now doubt its ubiquity. In particular, many
evolutionists argue that substantial amounts of genetic change
may not be subject to natural selection and may spread through
populations at random. Others are challenging Darwin's linking
of natural selection with gradual, imperceptible change through
all intermediary degrees; they are arguing that most evolutionary
events may occur far more rapidly than Darwin envisioned. ....
Yet amidst all this turmoil no biologist has been led to doubt
the fact that evolution occurred; we are debating _how_ it
happened.
[Johnson]"now, according to Patterson, Darwin's theory of natural
selection is under fire and scientists are no longer sure of its
general validity"
Huxley, Lewin, Kemp, Lewontin
http://www.deja.com/=dnc/getdoc.xp?AN=519875648
[Patterson characterizing the irate letters he received]'Here we are
trying to combat a political argument... and you give them
ammunition!'
Davies on abiogenesis researchers' fear of giving creationists
ammunition
http://www.deja.com/=dnc/getdoc.xp?AN=476339191
[Bethell]"Patterson told me that he regarded the theory of evolution
as 'often unnecessary' in biology. 'In fact,' he said, 'they could do
perfectly well without it.'"
evolution needed to make sense of biology?
http://www.deja.com/=dnc/getdoc.xp?AN=506007780
[Patterson]"one's colleagues. They hold the theory [of evolution]
very dear."
a day of talk.origins posts
=======================================================================
"News and Commentary" _Origins & Design_ 17:1
<http://www.arn.org/docs/odesign/od171/colpat171.htm>
[made a few minor changes -df]
"Colin Patterson Revisits His Famous Question about Evolution"
Paul A. Nelson
Authoritative," conveying "an impression of moody rebelliousness," and
"habitually pessimistic"-- thus writer Tom Bethell described the
paleontologist and systematist Colin Patterson, on first meeting him in
1983. 1
Patterson, who works at the British Museum of Natural History in London,
is one of the leaders of the philosophy of biological systematics known
as "transformed cladistics." The public hubbub which surrounded
"transformed" or "pattern" cladistics in the 1980s has now generally
subsided, although the issues lying at the heart of the controversy have
not. Indeed, Patterson has revisited those issues, which were captured
in large measure by a famous question he first posed nearly fifteen
years ago. "Can you tell me anything about evolution," he asked his
listeners, "any one thing, that is true?"
On November 5, 1981, Patterson gave a now infamous talk at the American
Museum of Natural History in New York, to the Systematics Discussion
Group which met monthly at the museum. An unknown creationist in the
audience secretly taped the talk, and a transcript was soon circulating
as samizdat among creationists, and shortly thereafter among the
scientific community at large.
The uncorrected transcript was plainly flawed-- giving "Conbear" for
"von Baer," for instance, and omitting the names of well-known
biologists-- but enough of Patterson's provocative points came through
to ignite the firestorm which followed. Patterson soon came in for
heavy criticism from the evolutionary community. The talk was much
debated: what had he meant; was he simply tweaking noses in New York;
what did he really think about evolution?
As creationist writers trumpeted the speech, Patterson retreated,
understandably annoyed by the episode and the voluminous correspondence
he received in its wake.
In August 1993, at a Systematics Association meeting in London,
Patterson revisited his 1981 talk; specifically, the bearing of
evolution on the practice and philosophy of systematics: ordering the
relationships of organisms. In his recollections (published last year;
see the notes on p.7), Patterson describes the background to the talk:
In November 1981, after an invitation from Donn Rosen [a fish
systematist at the American Museum, now deceased], I gave a talk to
the Systematics Discussion Group in the American Museum of Natural
History. Donn asked me to talk on 'Evolutionism and Creationism',
and it happened that just one week before my talk Ernst Mayr
published a paper on systematics in _Science_ (Mayr 1981). Mayr
pointed out the deficiencies (in his view) of cladistics and
phenetics, and noted that the 'connection with evolutionary
principles is exceedingly tenuous in many recent cladistic
writings.' For Mayr, classifications should incorporate such
things as 'inferences on selection pressures, shifts of adaptive
zones, evolutionary rates, and rates of evolutionary divergence.'
Fired up by Mayr's paper, I gave a fairly radical talk in New York,
comparing the effect of evolutionary theory on systematics with
Gillespie's (1979, p. 8) characterization of pre-Darwinian
creationism: 'not a research governing theory (since its power to
explain was only verbal) but an antitheory, a void that had the
function of knowledge but, as naturalists increasingly came to
feel, conveyed none.' Unfortunately, and unknown to me, there was
a creationist in my audience with a hidden tape recorder. A
transcript of my talk was produced and circulated among
creationists, and the talk has since been widely, and often
inaccurately, quoted in creationist literature. 2
But despite the inaccuracies, Patterson's central question about
evolution came through unmistakably:
But one sentence from the talk was accurately reproduced, and was
perhaps quoted more than any other. The sentence was a rhetorical
question; I quote it from a creationist source (Johnson 1991, p.10):
'Can you tell me anything about evolution, any one thing that is true?'3
The question still matters, Patterson argues, because evolution is still
assumed to be the primary determinant of phylogenetic reasoning. But
Patterson's agnosticism about evolution-- expressed in 1981 as, "I had
been working on this stuff for twenty years, and there was not one thing
I knew about it"-- continues today.
Patterson describes that agnosticism by looking at patterns in molecular
data.
At first, he notes, he thought he had found answers to his own question:
In 1981, I knew of no sensible answer to the question, but in the
ensuing decade I came to believe that there were two things I knew
about evolution. First, that transitions [purines, adenine (A) and
guanine (G), mutating to purines, e.g., A --> G; or pyrimidines,
cytosine (C) and thymine (T), mutating to pyrimidines, e.g., T -->
C] are more frequently fixed than transversions [where a purine
mutates to a pyrimidine, or vice versa] and second, that at the
level of DNA, the great majority of substitutions take place
despite natural selection rather than because of it. 4
However, as Patterson continues, he came to doubt whether in seeing
these patterns he was grasping the process of evolution:
...do transition bias and neutral substitution represent knowledge
about evolution, or something else? Further, and more generally,
why should I, a morphologist, claim to know something about
molecular evolution but nothing of morphological evolution? 5
We must distinguish between patterns to be explained, Patterson urges,
and the process theories by which we explain those patterns-- a
distinction foundational to the "transformed cladistic" perspective on
systematics and phylogeny. The molecular patterns he observed,
Patterson believes, are thus only data awaiting explanation.
"I therefore believe I was mistaken in thinking that I knew something
about molecular evolution," he writes. "Instead, I know (or have
learned) something about the properties of molecular data, and those
properties are amongst the things that must be explained by evolutionary
theory."
Patterson concludes:
...I mentioned a question ('Can you tell me anything you know about
evolution?') that I have put to various biologists, and an answer
that had been given: 'I know that evolution generates hierarchy.'
In the framework of phylogenetic reconstruction and our current
problems with it, another answer comes to mind: 'I know that
evolution generates homoplasy' [or "convergence," in the older
jargon of systematics]. In both cases, the answer is not quite
accurate. It would be truer to say, 'I know that evolution
explains hierarchy' or 'I know that evolution explains homoplasy.'
We must remember the distinction between the cart-- the
explanation-- and the horse-- the data. And where models are
introduced in phylogenetic reconstruction, we should prefer models
dictated by features of the data to models derived from explanatory
theories. 6
Among the issues raised by Patterson's revisiting of his 1981 question,
probably the most significant is how do we know which patterns are real
(and therefore, actually need explaining)? "Transition bias is data,"
he argues-- but only if one assumes the common descent of the gene
sequences in question, meaning, in most cases, macroevolution. For some
design theorists, who doubt that macroevolution is possible, sequence
comparisons between divergent animal phyla (for instance) will not be
data showing a historical relationship from an unknown common ancestor--
a relationship requiring causal explanation. Rather, those data may
reflect any number of causes other than descent.
Data-- "facts" requiring explanation-- emerge against a background of
causal possibility. Because they are highly skeptical of the
possibility of macroevolution, some design theorists would deny that the
systematic hierarchy is real [like who? -df], in the same sense that the
branching pattern of an elm tree or the Hapsburg Dynasty is real, i.e.,
something extending through space and time.
Thus, they would seek a nominalist explanation for the systematic
hierarchy (reflecting, perhaps, our desire to organize data in
bifurcating trees), and would defend that by arguing that the
transformations required by macroevolution are probabilistically
inaccessible. (Other design theorists would accept the hierarchy as
actual, of course, a genuine tree of life, but would argue that the tree
exists only because of a designer's intervention to make the necessary
transitions between forms possible.)
The real crunch between Patterson and design theorists, however, arises
from the possibility of design. The presence of cytochrome c in, say,
echinoderms, and the same protein in humans, gives evolutionists an
historical linkage between the two forms, even in the absence of a
theory of macroevolution, simply because high degrees of molecular
similarity require a common cause.
For most methodological naturalists, that can only be descent with
modification. 7
But suppose, as seems possible, that a designer employed the same
cytochrome molecule in two distinct lineages (echinoderms and humans)?
The usual naturalist response holds while this is certainly possible,
any theory making such predictions is empty. Assertions about the
designer's actions are unconstrained, and would fit whatever data turn
up.
But that does not follow. A designer who is free to employ the same
molecules in constructing diverse organisms is not therefore an agent
who acts capriciously. Furthermore, a design theorist would locate the
empirical content of his theory elsewhere, in those predictions which
distinguish design from naturalistic descent. It is the whole case for
design, taken broadly, that gives the theory empirical content. 8
But the step to the possibility of design, it seems, is a far longer
stride than the shorter step from certainty to agnosticism about
evolution. One hopes, in any case, that Patterson will join the debate,
wherever he ends up standing.
A Colin Patterson Sampler
===============begin inserted text===============
"Colin Patterson Revisits His Famous Question about Evolution"
<http://www.arn.org/docs/odesign/od171/sampler171.htm> _Origins &
Design_ 17:1 [made a few minor changes -df]
"A Colin Patterson Sampler"
1977: "The Contribution of Paleontology to Teleostean Phylogeny," in
_Major Patterns of Vertebrate Evolution_, eds. M.K. Hecht, P.C. Goody,
and B.M. Hecht (New York: Plenum Press, 1977), pp. 579-643.
A major, well-illustrated paper in Patterson's specialty, the
systematics of fishes, which shows his developing skepticism about the
value of evolutionary theory in systematics. Patterson compares the
practices of pre-Darwinians, e.g., Agassiz, with post-Darwinians:
Where Agassiz refrained from linking the converging bases of his
lineages (Fig. 1) since he believed that their junction 'may only
be sought in the creative intelligence,' the theory of evolution
allows a modern author to represent a hypothetical ancestral group
as having the same reality as any other major taxon. Yet the
search for ancestors of the teleosts has hardly been successful,
for every other major branch point in Figure 18 is also occupied by
hypothetical forms or question-marks: these ancestors have no more
reality than the abstract synapomorphy-bearers indicated by the
open circles in Figure 17.
1979: Interview with Luther D. Sunderland, June 30, British Museum of
Natural History, ERIC Document Reproduction Service microfiche ED 228
056 (available at most public libraries), pp. 7-19.
Sunderland, late creationist activist (d. 1987), interviewed several
paleontologists while preparing his book _Darwin's Enigma_. This
interview is marked by a fair amount of miscommunication, but also by
passages such as the following:
Sunderland: ...How do you see that evolution might explain the
origin of fishes?
Patterson: (Pause)
Sunderland: Then you'd rather not say?
Patterson: Ten years ago I'd have been perfectly willing to tell
you, but it so happens that I know someone who is working this
problem for about 15 years-- the starfish end of it-- the
echinoderms. He believes that this development could be traced
from the Cambrian with the echinoderms. I could very easily refer
you to his work and say that I agree with him that fish are related
to echinoderms, but I do not think it is obvious.
1980: "Cladistics," _The Biologist_ 27: 234-240.
A popular article, drafted as the "transformed cladistics" controversy
was growing to its height. "As the theory of cladistics has developed,"
argued Patterson (p. 239), "it has been realized that more and more of
the evolutionary framework is inessential, and may be dropped. The
chief symptom of this change is the significance attached to nodes in
cladistics. In Hennig's book, as in all early works in cladistics, the
nodes are taken to represent ancestral species. This assumption has
been found to be unnecessary, even misleading, and may be dropped."
"Phylogenies and Fossils," _Systematic Zoology_ 29: 216-219.
More skepticism about fossils and phylogeny: "To me, one of the most
astonishing consequences of the furor over cladistics is the realization
that the current account of tetrapod evolution, shown in a thousand
diagrams and everywhere acknowledged as the centerpiece of historical
biology, is a will-o'-the-wisp. For nowhere can one find a clear
statement of how and why the Recent groups are interrelated, and the
textbook stories are replete with phantoms-- extinct, uncharacterizable
groups giving rise one to another" (p. 217).
1981: "Significance of Fossils in Determining Evolutionary
Relationships," _Annual Review of Ecology and Systematics_ 12: 195-223.
Patterson's classic, critical analysis of the role of fossils in
systematics: "...extinct paraphyletic groups [common in neo-Darwinian
phylogenies before the cladistic revolution] seem to me to obscure
rather than illuminate relationships, for they exist not in nature but
in the minds of evolutionists. Such groups lead to a sterile inversion
of problems of relationships, which come to depend not on comparative
analysis of what is accessible-- the Recent biota-- but on juggling with
what is inaccessible-- uncharacterizable abstractions from the fossil
record" (p. 219).
1982: "Morphological Characters and Homology," in _Problems of
Phylogenetic Reconstruction_, eds. K.A. Joysey and A.E. Friday,
Systematics Association Special Vol. No. 21 (New York: Academic Press),
pp. 21-74.
Perhaps the most widely-cited paper on homology of the past two decades,
where Patterson discusses five ways of defining homology (classical,
evolutionary, phenetic, cladistic, and utilitarian), taking issue with
"the evolutionists...for here I do expect disagreement" (p. 62).
Patterson's main complaint is with extinct, paraphyletic groups, which
typically play the role of "transitional forms" in evolutionary
reasoning. "Such groups," Patterson argued, "...are imagined by
evolutionists, those most committed to the confirmation of Darwin's
views. The power of this mystery, extinct paraphyletic groups as the
source of phylogeny, is shown by the fact that we still have no
cladogram, or series of nested homologies, for tetrapods, the group in
which phylogeny is supposed to be best known" (p. 64).
1983: "How does phylogeny differ from ontogeny?" in _Development and
Evolution_, eds. B.C. Goodwin, N. Holder and C. Wylie (Cambridge:
Cambridge Univ. Press), pp. 1-31.
A discussion of the bearing of ontogenetic (developmental) data on
phylogeny: "Phylogeny is generalised transformation, but we have no
empirical experience of phylogeny; the only transformations of which we
have empirical evidence are those of ontogeny" (p. 21).
1988: "Homology in Classical and Molecular Biology," _Molecular Biology
and Evolution_ 5: 603-625.
Patterson applies his 1982 analysis of homology (see above) to molecular
data. This paper is notable for its claim that, at the molecular level
(unlike gross morphology), "there is no detected molecular equivalent of
convergence-- or of misleading similarity-- except in the most trivial
sense" (p. 618).
1993: "Congruence Between Molecular and Morphological Phylogenies,"
_Annual Review of Ecology and Systematics_ 24: 153-188.
In a review written with fellow British Museum staffers David Williams
and Christopher Humphries, Patterson surveys the congruence-- or lack
thereof-- between molecular and morphological phylogenies. He and his
co-authors conclude:
As morphologists with high hopes of molecular systematics, we end
this survey with our hopes dampened. Congruence between molecular
phylogenies is as elusive as it is in morphology and as it is
between molecules and morphology....Partly because of morphology's
long history, congruence between morphological phylogenies is the
exception rather than the rule. With molecular phylogenies, all
generated within the last couple of decades, the situation is
little better. Many cases of incongruence between molecular
phylogenies are documented above; and when a consensus of all trees
within 1% of the shortest in a parsimony analysis is
published...structure or resolution tends to evaporate (p. 180).
Copyright (c) 1996 Paul Nelson. All rights reserved. International
copyright secured. File Date: 6.22.96
This data file may be reproduced in its entirety for non-commercial use.
================end inserted text================
Notes
1. Tom Bethell, "Agnostic Evolutionists," _Harper's_ 270 (Feb 1985):
49-61.
2. Colin Patterson, "Null or minimal models," in _Models in Phylogeny
Reconstruction_, eds. R.W. Scotland, D.J. Siebert, and D.M.
Williams, Systematics Association Special Volume No. 52 (Oxford:
Clarendon Press, 1994), pp. 173-92; p. 174.
3. Ibid.
4. Ibid., p. 175.
5. Ibid.
6. Ibid., pp. 188-89.
7. Patterson, for instance, argues: "Convergence between molecular
sequences is too improbable to occur, just as similarity between
sequences is improbable to be explained except by common ancestry.
Some might view this argument as viciously or vacuously circular,
but the same argument is routinely advocated in morphology....This
is the argument from complexity: if two structures are complex
enough and similar in detail, probability dictates that they must
be homologous rather than convergent." See C. Patterson, "Homology
in Classical and Molecular Biology," _Molecular Biology and
Evolution_ 5 (1988): 603-625; p. 615. This argument, as with all
arguments assuming naturalism, excludes intelligent causation,
which may yield independent similarities in the absence of any
material descent. Doubtless all instances of Colin Patterson's
handwritten signature, for example-- on documents from bank checks
to personal letters-- are spatiotemporally distinct (i.e., not
"descended" from other signatures), yet the signatures themselves
will be remarkably similar, having, as they do, a unitary cause in
Colin Patterson himself.
8. Stephen C. Meyer, "The Methodological Equivalence of Design and
Descent: Can There Be A Scientific Theory of Creation?" in _The
Creation Hypothesis_, ed. J.P. Moreland (Downer's Grove, Illinois:
InterVarsity Press, 1994), pp. 67-112.
Copyright (c) 1996 Paul Nelson. All rights reserved. International
copyright secured. File Date: 6.22.96
This data file may be reproduced in its entirety for non-commercial use.
A return link to the Access Research Network web site would be
appreciated.
Jeff
snip entire post:
On 28 Sep 1999 20:57:32 -0400, david ford <dfo...@gl.umbc.edu> wrote:
snip entire post:
I found a lot of that interesting but was wondering what it was for, or in
response to etc. Also, if you had said any of it or was it all quotes etc.
Did you want any specific type of reply to a point or question of some sort?
I assume it was asking for opinions about the relevance of the Patterson
question and misquote allegations? I think that when someone asks me if
anything in my field (immunology) is "unequivocally" true (as implied here) I
would take a step back also. If they asked was there anything that the vast
bulk of evidence could be used to indicate it was most likely true then that is
different. I think that you have to keep expecting that the next experiment you
do could show how completely wrong you or others were before. I am more certain
of much that is wrong than right. If I had to say the one thing in evolution
that I hold as true it is that if a trait is required for survival in a given
environment that only those in a population with that trait will survive (I.e.
drug resistant cancers, pathogens). Hence vary the selection for more effective
treatment. Seems too simple somehow.
Dan Moore
david ford wrote:
[snip]
> But that does not follow. A designer who is free to employ the same
> molecules in constructing diverse organisms is not therefore an agent
> who acts capriciously.
Why? What evidence can you offer for this? This appears to be mere
conjucture on your part.
>Furthermore, a design theorist would locate the
> empirical content of his theory elsewhere, in those predictions which
> distinguish design from naturalistic descent. It is the whole case for
> design, taken broadly, that gives the theory empirical content. 8
>
This sounds good in theory but in practice design theorists seem to
run away from empirical evidence as it does not support their ideas.
> But the step to the possibility of design, it seems, is a far longer
> stride than the shorter step from certainty to agnosticism about
> evolution. One hopes, in any case, that Patterson will join the debate,
> wherever he ends up standing.
>
Yes, the rejection of one scientific theory for another is a short
step. Rejecting science for silly headed religious stupidity is
a great leap.
> Where Agassiz refrained from linking the converging bases of his
> lineages (Fig. 1) since he believed that their junction 'may only
> be sought in the creative intelligence,' the theory of evolution
> allows a modern author to represent a hypothetical ancestral group
> as having the same reality as any other major taxon. Yet the
> search for ancestors of the teleosts has hardly been successful,
> for every other major branch point in Figure 18 is also occupied by
> hypothetical forms or question-marks: these ancestors have no more
> reality than the abstract synapomorphy-bearers indicated by the
> open circles in Figure 17.
Patterson points out that this cladistic structure has not been
completely filled. Hardly a rejection of the fact of evolution.
> Sunderland, late creationist activist (d. 1987), interviewed several
> paleontologists while preparing his book _Darwin's Enigma_. This
> interview is marked by a fair amount of miscommunication, but also by
> passages such as the following:
> Sunderland: ...How do you see that evolution might explain the
> origin of fishes?
> Patterson: (Pause)
> Sunderland: Then you'd rather not say?
> Patterson: Ten years ago I'd have been perfectly willing to tell
> you, but it so happens that I know someone who is working this
> problem for about 15 years-- the starfish end of it-- the
> echinoderms. He believes that this development could be traced
> from the Cambrian with the echinoderms. I could very easily refer
> you to his work and say that I agree with him that fish are related
> to echinoderms, but I do not think it is obvious.
Patterson appears to be a careful scientist. What do you, David
Ford, think this quote means. You posted it here so I presume
you had a reason for doing so.
> 1980: "Cladistics," _The Biologist_ 27: 234-240.
>
> A popular article, drafted as the "transformed cladistics" controversy
> was growing to its height. "As the theory of cladistics has developed,"
> argued Patterson (p. 239), "it has been realized that more and more of
> the evolutionary framework is inessential, and may be dropped. The
> chief symptom of this change is the significance attached to nodes in
> cladistics. In Hennig's book, as in all early works in cladistics, the
> nodes are taken to represent ancestral species. This assumption has
> been found to be unnecessary, even misleading, and may be dropped."
Learn about cladistics and why this statement in no way
discredits the fact of evolution.
> "Phylogenies and Fossils," _Systematic Zoology_ 29: 216-219.
>
> More skepticism about fossils and phylogeny: "To me, one of the most
> astonishing consequences of the furor over cladistics is the realization
> that the current account of tetrapod evolution, shown in a thousand
> diagrams and everywhere acknowledged as the centerpiece of historical
> biology, is a will-o'-the-wisp. For nowhere can one find a clear
> statement of how and why the Recent groups are interrelated, and the
> textbook stories are replete with phantoms-- extinct, uncharacterizable
> groups giving rise one to another" (p. 217).
>
> 1981: "Significance of Fossils in Determining Evolutionary
> Relationships," _Annual Review of Ecology and Systematics_ 12: 195-223.
>
> Patterson's classic, critical analysis of the role of fossils in
> systematics: "...extinct paraphyletic groups [common in neo-Darwinian
> phylogenies before the cladistic revolution] seem to me to obscure
> rather than illuminate relationships, for they exist not in nature but
> in the minds of evolutionists. Such groups lead to a sterile inversion
> of problems of relationships, which come to depend not on comparative
> analysis of what is accessible-- the Recent biota-- but on juggling with
> what is inaccessible-- uncharacterizable abstractions from the fossil
> record" (p. 219).
Now go read up on the battle between the cladists and the
P.E. crowd. This statement was in no way a rejection of the
fact of evolution.
>
> 1982: "Morphological Characters and Homology," in _Problems of
> Phylogenetic Reconstruction_, eds. K.A. Joysey and A.E. Friday,
> Systematics Association Special Vol. No. 21 (New York: Academic Press),
> pp. 21-74.
>
> Perhaps the most widely-cited paper on homology of the past two decades,
> where Patterson discusses five ways of defining homology (classical,
> evolutionary, phenetic, cladistic, and utilitarian), taking issue with
> "the evolutionists...for here I do expect disagreement" (p. 62).
> Patterson's main complaint is with extinct, paraphyletic groups, which
> typically play the role of "transitional forms" in evolutionary
> reasoning. "Such groups," Patterson argued, "...are imagined by
> evolutionists, those most committed to the confirmation of Darwin's
> views. The power of this mystery, extinct paraphyletic groups as the
> source of phylogeny, is shown by the fact that we still have no
> cladogram, or series of nested homologies, for tetrapods, the group in
> which phylogeny is supposed to be best known" (p. 64).
Define what group Patterson meant by "evolutionists" in this context.
Describe how his narrow use of the term here differs from how
creationists
use the term.
>
> 1983: "How does phylogeny differ from ontogeny?" in _Development and
> Evolution_, eds. B.C. Goodwin, N. Holder and C. Wylie (Cambridge:
> Cambridge Univ. Press), pp. 1-31.
>
[snip]
> Patterson applies his 1982 analysis of homology (see above) to molecular
> data. This paper is notable for its claim that, at the molecular level
> (unlike gross morphology), "there is no detected molecular equivalent of
> convergence-- or of misleading similarity-- except in the most trivial
> sense" (p. 618).
Point?
>
> 1993: "Congruence Between Molecular and Morphological Phylogenies,"
> _Annual Review of Ecology and Systematics_ 24: 153-188.
>
> In a review written with fellow British Museum staffers David Williams
> and Christopher Humphries, Patterson surveys the congruence-- or lack
> thereof-- between molecular and morphological phylogenies. He and his
> co-authors conclude:
> As morphologists with high hopes of molecular systematics, we end
> this survey with our hopes dampened. Congruence between molecular
> phylogenies is as elusive as it is in morphology and as it is
> between molecules and morphology....Partly because of morphology's
> long history, congruence between morphological phylogenies is the
> exception rather than the rule. With molecular phylogenies, all
> generated within the last couple of decades, the situation is
> little better. Many cases of incongruence between molecular
> phylogenies are documented above; and when a consensus of all trees
> within 1% of the shortest in a parsimony analysis is
> published...structure or resolution tends to evaporate (p. 180).
Point?
[snip]
> 7. Patterson, for instance, argues: "Convergence between molecular
> sequences is too improbable to occur, just as similarity between
> sequences is improbable to be explained except by common ancestry.
> Some might view this argument as viciously or vacuously circular,
> but the same argument is routinely advocated in morphology....This
> is the argument from complexity: if two structures are complex
> enough and similar in detail, probability dictates that they must
> be homologous rather than convergent." See C. Patterson, "Homology
> in Classical and Molecular Biology," _Molecular Biology and
> Evolution_ 5 (1988): 603-625; p. 615. This argument, as with all
> arguments assuming naturalism, excludes intelligent causation,
> which may yield independent similarities in the absence of any
> material descent. Doubtless all instances of Colin Patterson's
> handwritten signature, for example-- on documents from bank checks
> to personal letters-- are spatiotemporally distinct (i.e., not
> "descended" from other signatures), yet the signatures themselves
> will be remarkably similar, having, as they do, a unitary cause in
> Colin Patterson himself.
I would think you would have wanted this up front with the
rest of your Patterson quotes. But then you, David Ford, didn't
write any of this, you jeust copied it, appartantly blindly assuming
it would be somehow meaningful except as an excellent example of
using words without context.
As you seem to ignore rebuttals to the silliness you post here, I
assume you will ignore this as well and continue pissing into the
wind.
> Copyright (c) 1996 Paul Nelson. All rights reserved. International
> copyright secured. File Date: 6.22.96
>
Try writing your own stuff if you have anything to offer.
Dan
david ford
Philosophy of Modern Biology_, translated from the 1970 French edition
by Austryn Wainhouse. (NY: Vintage Books), 199pp. On 138, the first
two paragraphs of the chapter "The Frontiers":
WHEN ONE wonders on the tremendous journey of evolution over the
past three billion years or so, the prodigious wealth of
structures it has engendered, and the extraordinarily effective
teleonomic performances of living beings, from bacteria to man,
one may well find oneself beginning to doubt again whether all
this could conceivably be the product of an enormous lottery
presided over by natural selection, blindly picking the rare
winners from among numbers drawn at utter random.
While one's conviction may be restored by a detailed review of
the accumulated modern evidence that this conception alone is
compatible with the facts (notably with the molecular mechanisms
of replication, mutation, and translation), it affords no
synthetic, intuitive, and immediate grasp of the vast sweep of
evolution. The miracle stands "explained"; it does not strike us
as any less miraculous. As Francois Mauriac wrote, "What this
professor says is far more incredible than what we poor
Christians believe."
zoologist Gray
http://www.deja.com/=yahoo/getdoc.xp?AN=437813267
According to neo-Darwinism, mutations in organisms' DNA sequences is the
raw material natural selection works with to produce blindwatchmaking,
yet mutations are routinely observed to result in _cancer_ and genetic
diseases, not the arrival of novel body structures and organs. Could
someone please tell me how exactly the neo-Darwinian mechanism is
compatible with the fact that mutation routinely causes cancer and
disease? Refs to the literature would be great.
Charles Dye
>According to neo-Darwinism, mutations in organisms' DNA sequences is the
>raw material natural selection works with to produce blindwatchmaking,
>yet mutations are routinely observed to result in _cancer_ and genetic
>diseases, not the arrival of novel body structures and organs. Could
>someone please tell me how exactly the neo-Darwinian mechanism is
>compatible with the fact that mutation routinely causes cancer and
>disease? Refs to the literature would be great.
Obvious logical error: confusing "routinely" with "always."
Less obvious error: confusing the effects of a mutation on an adult
organism with the effects on a developing embryo.
Re the title: I'll take the theory of natural selection. You can
keep the Versus Reality; thanks anyway.
Ian Musgrave & Peta O'Donohue
Address altered to avoid spam, delete RemoveInsert
On 5 Oct 1999 16:52:12 -0400, david ford <dfo...@gl.umbc.edu> wrote:
<snip out of context quote>
>According to neo-Darwinism, mutations in organisms' DNA sequences is the
>raw material natural selection works with to produce blindwatchmaking,
>yet mutations are routinely observed to result in _cancer_ and genetic
>diseases, not the arrival of novel body structures and organs.
Does david ever read any of the replies to his posts. A number of
posts earlier this year deal with these issues.
>Could
>someone please tell me how exactly the neo-Darwinian mechanism is
>compatible with the fact that mutation routinely causes cancer and
>disease? Refs to the literature would be great.
As someone else pointed out, mutation (of somatic DNA) can cause
cancer, but it doesn't ONLY cause cancer. Context is everything. A
deletion event can knock out p53, and lead to cancer, or a deletion
event in an ISO18000 sequence can lead to the expression of a novel
nylon hydrolysis enzyme.
Similarly, a mutation in an apolioprotien can lead to a form that
renders the carrier more susceptible to heart attacks, a different
mutation in the apolipoprotein makes the carriers more resistant.
Duplication of homoebox genes (and/or differences in the timing of
their expression) can result in significant novelty.
(repeated) Literature references to these items (and more, eg
d-ala-d-serine ligases) can be found in this very thread, via
DejaNews.
Cheers! Ian
=====================================================
Ian Musgrave Peta O'Donohue,Jack Francis and Michael James Musgrave
reyn...@werple.mira.net.au http://werple.mira.net.au/~reynella/
a collection of Dawkins inspired weasle programs http://www-personal.monash.edu.au/~ianm/whale.htm
Southern Sky Watch http://www.abc.net.au/science/space/default.htm
Jack King
> G'Day All
> Address altered to avoid spam, delete RemoveInsert
>
> On 5 Oct 1999 16:52:12 -0400, david ford <dfo...@gl.umbc.edu> wrote:
>
> <snip out of context quote>
>
>
>
> >Could
> >someone please tell me how exactly the neo-Darwinian mechanism is
> >compatible with the fact that mutation routinely causes cancer and
> >disease? Refs to the literature would be great.
>
> As someone else pointed out, mutation (of somatic DNA) can cause
> cancer, but it doesn't ONLY cause cancer. Context is everything. A
> deletion event can knock out p53, and lead to cancer, or a deletion
> event in an ISO18000 sequence can lead to the expression of a novel
> nylon hydrolysis enzyme.
The deletion of a nucleotide will lead to a frameshift. It is virtially always
lethal. But for the sake of argument, let's say that it is not repaired by
corrective enzymes, and it results in a "nylon hydrolysis enzyme". Asuuming
this is a mutation to a germ cell (a very small target indeed), this would
be passed on. The argument goes that eventually over, say, 10 million years,
a small land carnivor while explode into a 50 foot sea going bohemouth like
Basilosaurus (for example). This theory is supposedly supported by "nice little
sequences" in the fossil record. But the fact that there are genetic barriers is totally
ignored. Mutations can and do result in natural varients, but nothing beyond
that has ever been demonstrated. The only reason this theory flies at all is
because the True Believers refuse to entertain any other hypothesis other than
common descent.
> Similarly, a mutation in an apolioprotien can lead to a form that
> renders the carrier more susceptible to heart attacks, a different
> mutation in the apolipoprotein makes the carriers more resistant.
Of course....and that means that they eventually start sprouting new organs?!
>
>
> Duplication of homoebox genes (and/or differences in the timing of
> their expression) can result in significant novelty.
When homebox and homeotic genes are affected by mutation, this can cause
entire body parts to be misplaced or duplicated. This is because homeotic
mutations disrupt the master "program", and cause genetic "subroutines" to be
placed in different locations. Thus when we bombard Drosophila with radiation,
we see abberations like wings being duped, and legs growing out of backs, etc.
We never see new unique structures.
--
Jack King
jack...@nortelnetworks.com
http://www.bit-net.com/~jackking
Check out a GREAT vacation villa in the Caribbean
http://www.stjohnusvi.com/coralmoonvilla/
Jennie Hazen
Jack King <jack...@nortelnetworks.com> wrote in message
news:37FB5E4A...@nortelnetworks.com...
> Ian Musgrave & Peta O'Donohue wrote:
Asuuming
> this is a mutation to a germ cell (a very small target indeed), this would
> be passed on. The argument goes that eventually over, say, 10 million
years,
> a small land carnivor while explode into a 50 foot sea going bohemouth
like
> Basilosaurus (for example). This theory is supposedly supported by "nice
little
> sequences" in the fossil record. But the fact that there are genetic
barriers is totally
> ignored. Mutations can and do result in natural varients, but nothing
beyond
> that has ever been demonstrated. The only reason this theory flies at all
is
> because the True Believers refuse to entertain any other hypothesis other
than
> common descent.
What genetic barriers are you referring to? The only ones I know of prevent
sufficiently distant species from interbreeding, and clearly that is not
what you mean here, as you are talking about changes within a species.
Germ cells, BTW, are the result of cell division like any other cell; and
are as likely to have the mutations inherent to that process as any other
cell. The size of the tissue is irrelevant.
Jack King
>
>
> What genetic barriers are you referring to? The only ones I know of prevent
> sufficiently distant species from interbreeding, and clearly that is not
> what you mean here, as you are talking about changes within a species.
Of course it is what I mean. Breeding experiments show clearly the hard genetic
barriers. In short, the reason dogs (for example) don't become as big as elephants,
much less change into elephants, is not that we just haven't been breeding them long
enough. Dogs do not have the genetic capacity for that degree of change, and they
stop getting bigger when the genetic limit is reached.
>
>
> Germ cells, BTW, are the result of cell division like any other cell; and
> are as likely to have the mutations inherent to that process as any other
> cell. The size of the tissue is irrelevant.
Of course. But we can have point mutations all over the body, but unless it
changes a codon in a germ cell, it will have no hereditary significance. Of
all the mutations that can occur, the number than affect germ cells are
infinitesimally
small.
Adam Noel Harris
:Jennie Hazen wrote:
:
:>
:>
:> What genetic barriers are you referring to? The only ones I know of prevent
:> sufficiently distant species from interbreeding, and clearly that is not
:> what you mean here, as you are talking about changes within a species.
:
:Of course it is what I mean. Breeding experiments show clearly the hard
:genetic barriers. In short, the reason dogs (for example) don't become
:as big as elephants, much less change into elephants, is not that we
:just haven't been breeding them long enough. Dogs do not have the
:genetic capacity for that degree of change, and they stop getting
:bigger when the genetic limit is reached.
How big can dogs get?
Are mutations which would increase the size of dogs that have reached the
"limit" possible?
:> Germ cells, BTW, are the result of cell division like any other cell; and
:> are as likely to have the mutations inherent to that process as any other
:> cell. The size of the tissue is irrelevant.
:
:Of course. But we can have point mutations all over the body, but unless it
:changes a codon in a germ cell, it will have no hereditary significance. Of
:all the mutations that can occur, the number than affect germ cells are
:infinitesimally
:small.
How small? Do you have an estimate? I'm asking about the post-repair,
germline point mutations which have the potential to contribute to the
next generation. Please give your answer in units of
mutations/site/generation.
-Adam
--
Opinions expressed are not necessarily those of Stanford University.
PGP Fingerprint = C0 65 A2 BD 8A 67 B3 19 F9 8B C1 4C 8E F2 EA 0E
Clark Dorman
Jack King <jack...@nortelnetworks.com> writes:
> Jennie Hazen wrote:
> > What genetic barriers are you referring to? The only ones I know of prevent
> > sufficiently distant species from interbreeding, and clearly that is not
> > what you mean here, as you are talking about changes within a species.
>
> Of course it is what I mean. Breeding experiments show clearly
> the hard genetic barriers.
Can you discuss the length of the breeding experiments in
relation to the known mutation rate? In the breeding experiment,
were they selecting for present mutations or did the experiment
go on for, say, 20,000 years, to take into account mutations?
> In short, the reason dogs (for
> example) don't become as big as elephants, much less change
> into elephants, is not that we just haven't been breeding them
> long enough. Dogs do not have the genetic capacity for that
> degree of change, and they stop getting bigger when the genetic
> limit is reached.
Ok, what is the limit? As is well known, dogs are very close
relatives to wolfs. How big can a wolf get? How about 200 lb
wolves? Is that reasonable?
Do you think that the same argument would apply to, say, sloths?
Why or why not? I think the answer would be an obvious yes, it
would apply. Gosh, you just can't make an animal, like a sloth
or a dog, into a gigantic animal. What do you think?
What is the maximum size of, say, an ostrich-like bird? 200 lbs?
300 lbs?
> > Germ cells, BTW, are the result of cell division like any other cell; and
> > are as likely to have the mutations inherent to that process as any other
> > cell. The size of the tissue is irrelevant.
>
> Of course. But we can have point mutations all over the body, but unless it
> changes a codon in a germ cell, it will have no hereditary significance. Of
> all the mutations that can occur, the number than affect germ cells are
> infinitesimally
> small.
'infinitesimally small'? I suppose germ-line mutations make up a
small percentage, but only because germ-line cells are a small
percentage of the body. But, you should realize in the germ line
are not rare. Each person inherits (on average) from several to
a couple of dozen in their genome. I would not call that
infinitesimally small at all.
See, for example:
http://www.tiac.net/users/cri/mutate.html
--
Clark Dorman "Evolution is cleverer than you are."
http://cns-web.bu.edu/pub/dorman/D.html -Francis Crick
Jack King
> Jack King <jack...@nortelnetworks.com> wrote:
> :Jennie Hazen wrote:
> :
> :>
> :>
> :> What genetic barriers are you referring to? The only ones I know of prevent
> :> sufficiently distant species from interbreeding, and clearly that is not
> :> what you mean here, as you are talking about changes within a species.
> :
> :Of course it is what I mean. Breeding experiments show clearly the hard
> :genetic barriers. In short, the reason dogs (for example) don't become
> :as big as elephants, much less change into elephants, is not that we
> :just haven't been breeding them long enough. Dogs do not have the
> :genetic capacity for that degree of change, and they stop getting
> :bigger when the genetic limit is reached.
>
> How big can dogs get?
>
> Are mutations which would increase the size of dogs that have reached the
> "limit" possible?
I tell you what. It sounds like an excellent doctoral thesis. Why don't you get
the biggest canine you can find and bombard him with X-rays and see what
happens. Don't let PETA know about it, however.
>
>
> :> Germ cells, BTW, are the result of cell division like any other cell; and
> :> are as likely to have the mutations inherent to that process as any other
> :> cell. The size of the tissue is irrelevant.
> :
> :Of course. But we can have point mutations all over the body, but unless it
> :changes a codon in a germ cell, it will have no hereditary significance. Of
> :all the mutations that can occur, the number than affect germ cells are
> :infinitesimally
> :small.
>
> How small? Do you have an estimate? I'm asking about the post-repair,
> germline point mutations which have the potential to contribute to the
> next generation. Please give your answer in units of
> mutations/site/generation.
Any mutation is rare. When it occurs, it is almost always fixed by repair
enzymes. What few do get through are almost always either deleterious
or neutral. Some may end up being "beneficial". But most of a genome consists on
somatic (non-germ) cells. The chances of a beneficial mutation getting into somatic
cells is tiny. But now we have to shrink the target even further for this mutated
codon to be passed on.
I have never seen this number quantified. Sounds like another good topic for a
doctoral thesis.
Felipe
Jack King <jack...@nortelnetworks.com> wrote in message
news:37FB5E4A...@nortelnetworks.com...
> Ian Musgrave & Peta O'Donohue wrote:
>
> > Address altered to avoid spam, delete RemoveInsert
> >
> > On 5 Oct 1999 16:52:12 -0400, david ford <dfo...@gl.umbc.edu> wrote:
> >
> > <snip out of context quote>
> >
> >
> >
> > >Could
> > >someone please tell me how exactly the neo-Darwinian mechanism is
> > >compatible with the fact that mutation routinely causes cancer and
> > >disease? Refs to the literature would be great.
> >
> > As someone else pointed out, mutation (of somatic DNA) can cause
> > cancer, but it doesn't ONLY cause cancer. Context is everything. A
> > deletion event can knock out p53, and lead to cancer, or a deletion
> > event in an ISO18000 sequence can lead to the expression of a novel
> > nylon hydrolysis enzyme.
>
> The deletion of a nucleotide will lead to a frameshift. It is virtially
always
> lethal.
Blatant falsehood. It *might* lead to lethality, if it occurs in the exon
of an important enough polypeptide. But plenty of genes are disabled in one
form or another, and organisms suffer little if any consequences. (Hence
many a recessive allele, whose effect -- or lack of effect -- is masked
because of the other functioning copy.) Further, frame shifts may only
affect a portion of a polypeptide, and maybe not even near the active site
of the appropriate protein/enzyme. And, as if that weren't enough,
deletions can also happen in introns, and never affect expression at all.
Boy.
But for the sake of argument, let's say that it is not repaired by
> corrective enzymes, and it results in a "nylon hydrolysis enzyme".
My guess is that Ian has an example in mind, and that we'll find out the
gorey details shortly. Don't put that smug smile on just yet.
Asuuming
> this is a mutation to a germ cell (a very small target indeed), this would
> be passed on.
Or, it could happen in replicating the gametes themselves. And how many rep
lication events lead to gametes? How many chances are there for copying
errors?
Mutations can and do result in natural varients, but nothing beyond
> that has ever been demonstrated.
Thing is, natural variants are sometimes enough to cause reproductive
barriers.
Keith Doyle
Jack King <jack...@nortelnetworks.com> wrote:
>Jennie Hazen wrote:
>
>>
>>
>> What genetic barriers are you referring to? The only ones I know of prevent
>> sufficiently distant species from interbreeding, and clearly that is not
>> what you mean here, as you are talking about changes within a species.
>
>Of course it is what I mean. Breeding experiments show clearly the hard genetic
>barriers.
No they don't, in fact quite the contrary. Horses and donkeys are the most well
known example-- offspring are sometimes sterile, sometimes fertile.
--
Keith Doyle
(remove underbars in reply address for E-mail)
"Beware the man of one book." -- St. Thomas Aquinas
Dunk
>Jennie Hazen wrote:
>> What genetic barriers are you referring to?
>Of course it is what I mean. Breeding experiments show clearly the hard genetic
>barriers. In short, the reason dogs (for example) don't become as big as elephants,
>much less change into elephants, is not that we just haven't been breeding them long
>enough. Dogs do not have the genetic capacity for that degree of change, and they
>stop getting bigger when the genetic limit is reached.
Brown and short faced bears are/were the largest terrestial mamallian
carnivores. The size limit seems to come from ecology. You may be
thinking of artificial selection. It goes like this: first you can get
a lot of variation in a multigene trait from recombination of existing
genes. Later you have to wait for mutations so change slows way down.
Then if you *artificially* select for new mutants with a chosen trait,
regardless of whether they would do well in the wild, you start to get
organisms that wouldn't. So you wouldn't get precisely those organisms
from *natural* selection, and further change in that trait would take
longer.
Various garden flowers achieve tree-like proportions on islands.
Pete
Adam Noel Harris
:Adam Noel Harris wrote:
:> How big can dogs get?
:>
:> Are mutations which would increase the size of dogs that have reached the
:> "limit" possible?
:
:I tell you what. It sounds like an excellent doctoral thesis. Why don't you get
:the biggest canine you can find and bombard him with X-rays and see what
:happens. Don't let PETA know about it, however.
There simply wouldn't be enough time or dogs to get far. However, any
progress that was made would simply be admitted by you to be within the
dog-size-limit, which you can't define a priori, and would be dismissed.
Let's approach it this way - given what is known about developmental
genetics, why would such a mutation be impossible? If your argument is
not that such a mutation is impossible, but rather that mutations are so
rare that we could never expect to see such, that is different and will
require a different response.
Elsewhere in this thread you write that mutation cannot produce a new
structure, only rearrange existing structures (such as homeotic
mutations). Do you believe mutation can change the shape of a structure?
Do you believe mutation can change the size of a structure? Can natural
selection fix mutations which lead to advantageous sizes and shapes of
structures, including duplications of previous structures which might now
be selected for a new function? I'm trying to figure out exactly where
you think the limits can be found.
[...]
:> How small? Do you have an estimate? I'm asking about the post-repair,
:> germline point mutations which have the potential to contribute to the
:> next generation. Please give your answer in units of
:> mutations/site/generation.
:
:Any mutation is rare. When it occurs, it is almost always fixed by repair
:enzymes. What few do get through are almost always either deleterious
:or neutral. Some may end up being "beneficial". But most of a genome consists on
:somatic (non-germ) cells. The chances of a beneficial mutation getting into somatic
:cells is tiny. But now we have to shrink the target even further for this mutated
:codon to be passed on.
:I have never seen this number quantified. Sounds like another good topic for a
:doctoral thesis.
If you have not seen this number quantified, then you are not the person
who should be advancing arguments about mutations being too rare to
account for evolution.
I have been struck by this problem in your argument in the past (along
with my perception that you equate junk DNA with intron). I might as well
argue that traffic accident fatalities are so rare as to not be a concern
to anyone. Afterall, when two vehicles are on a collision course, one or
the other of the drivers almost always reacts and is able to evade the
collision. If the cars do collide, then the occupants are almost always
saved by their safety belts or airbags. If they are seriously injured,
they usually can be saved by emergency crews.
All of this is nice, but it is irrelevant when we look at the actual
fatality rate. Scientists are able to estimate the actual mutation rate,
and all the repair and somatic cells in the world won't mean much to the
calculations that are made based on this rate. Population genetics tells
us that the rates are (as best they can be estimated) in line with the
amount of diversification we see in extant species based on their protein
or DNA sequences and paleontological estimates of their time of
divergence. Making excuses about the fate of most mutations doesn't
address the ones that DO get passed on.
Jack King
> > The deletion of a nucleotide will lead to a frameshift. It is virtially
> always
> > lethal.
>
> Blatant falsehood. It *might* lead to lethality, if it occurs in the exon
> of an important enough polypeptide.
Of course, it would have no effect if it landed on, say, an intron. For some
reason you're throwing up needless smoke screens. The issue was that point mutation
deletions can lead to benicial changes. This is virtually impossible (see _The New
Healers_; p.54 William R. Clark (1997))
> But for the sake of argument, let's say that it is not repaired by
> > corrective enzymes, and it results in a "nylon hydrolysis enzyme".
>
> My guess is that Ian has an example in mind, and that we'll find out the
> gorey details shortly. Don't put that smug smile on just yet.
I see, a tag team match is it? I have one (myself); you have (it would appear
from the responses) dozens. Obviously I don't have time to respond to everyone.
You appear to be one of the lucky ones (this time).
>
> Asuuming
> > this is a mutation to a germ cell (a very small target indeed), this would
> > be passed on.
>
> Or, it could happen in replicating the gametes themselves. And how many rep
> lication events lead to gametes? How many chances are there for copying
> errors?
Copying errors result in "information leakage". Are you claiming that this is
a mechanism which will result in a new organ?!
>
> Mutations can and do result in natural varients, but nothing beyond
> > that has ever been demonstrated.
>
> Thing is, natural variants are sometimes enough to cause reproductive
> barriers.
Like sterility of hybrids. Exactly.
Syvanen
unless it
> > :changes a codon in a germ cell, it will have no hereditary
significance. Of
> > :all the mutations that can occur, the number than affect germ cells
are
> > :infinitesimally
> > :small.
> >
post-repair,
> > germline point mutations which have the potential to contribute to
the
> > next generation. Please give your answer in units of
> > mutations/site/generation.
>
> Any mutation is rare. When it occurs, it is almost always fixed by
>repair enzymes.
Yes, DNA replication produces about 10^-3 errors
per replication cycle per site. For every 10^6
errors, all but a few are repaired.
> What few do get through are almost always either deleterious
> or neutral.
The net result at neutral sites is about 10^-8 per
generation per site.
> Some may end up being "beneficial". But most of a genome
>consists on somatic (non-germ) cells. The chances of a beneficial
mutation getting into somatic
> cells is tiny. But now we have to shrink the target even further for
this mutated
> codon to be passed on.
> I have never seen this number quantified. Sounds like another good
topic for a
> doctoral thesis.
>
I just gave you the numbers. Now if we have a population
of 10^6 individuals, then there is a probability of .01
that in any given generation, one mutant will appear that
has mutated any given site and, further, if there are about
5 x 10^8 neutral sites (the value for most mammals) then this
population will generate 5,000,000 neutral mutants each
generation. Based on fairly rough estimate, we can guess
that the number of mutatns that changes the phenotype of the
organism is about .1% of the neutral rate, then it
seems fairly clear that the population is continuously giving
rise to about 5000 mutants each generation that have the
potential to be selected, provided the new phenotype has a
selective advantage.
Do you still have a point here?
Mike Syvanen
Sent via Deja.com http://www.deja.com/
Before you buy.
KD
Dunk wrote in message <37fbb93...@fl.news.verio.net>...
>Brown and short faced bears are/were the largest terrestial mamallian
>carnivores. The size limit seems to come from ecology. You may be
>thinking of artificial selection. It goes like this: first you can get
>a lot of variation in a multigene trait from recombination of existing
>genes. Later you have to wait for mutations so change slows way down.
>Then if you *artificially* select for new mutants with a chosen trait,
>regardless of whether they would do well in the wild, you start to get
>organisms that wouldn't. So you wouldn't get precisely those organisms
>from *natural* selection, and further change in that trait would take
>longer. Various garden flowers achieve tree-like proportions on islands.
There was a Sim City-like game put out by Maxis several years ago which
modeled this sort of thing, and while it was boring as heck to play it did a
good job of showing how natural selection is supposed to work. Mutation and
ecology are necessary variables, if nothing else the game showed how in
changing environments a plant or animal with traits which are suddenly
advantageous will take over the eco niche very quickly (the answer, I think,
to why there is so little fossil evidence of transitional species, in
geologic time these changes happen too quickly, either a species makes it or
gets wiped out quickly).
Ian Musgrave & Peta O'Donohue
In article <37FB5E4A...@nortelnetworks.com>,
Jack King <jack...@nortelnetworks.com> wrote:
> Ian Musgrave & Peta O'Donohue wrote:
>
> > G'Day All
> > Address altered to avoid spam, delete RemoveInsert
> >
> > On 5 Oct 1999 16:52:12 -0400, david ford <dfo...@gl.umbc.edu> wrote:
> >
> > <snip out of context quote>
> > >Could
> > >someone please tell me how exactly the neo-Darwinian mechanism is
> > >compatible with the fact that mutation routinely causes cancer and
> > >disease? Refs to the literature would be great.
> >
> > As someone else pointed out, mutation (of somatic DNA) can cause
> > cancer, but it doesn't ONLY cause cancer. Context is everything. A
> > deletion event can knock out p53, and lead to cancer, or a deletion
> > event in an ISO18000 sequence can lead to the expression of a novel
> > nylon hydrolysis enzyme.
>
> The deletion of a nucleotide will lead to a frameshift. It is
> virtially always lethal. But for the sake of argument, let's say
> that it is not repaired by corrective enzymes, and it results in a
> "nylon hydrolysis enzyme".
Oh, but it does happen, see
Ohno S. (1984 Apr). Birth of a unique enzyme from an alternative
reading frame of the preexisted, internally repetitious coding sequence.
Proc Natl Acad Sci U S A , 81, 2421-5.
A 60 base pair deletion in a non-functional DNA sequence frame
shifts the sequence resulting in the nylon degrading enzyme
6-aminohexanoic acid linear oligomer hydrolase, which hydrolyses nylon
oligomers stranegly enough :-). Nylon was conspicuosly absent from the
natural environment until quite recently. This mutation has been
duplicated in the lab.
Prijambada ID, Negoro S, Yomo T, and Urabe I. (1995 May). Emergence of
nylon oligomer degradation enzymes in Pseudomonas aeruginosa PAO through
experimental evolution. Appl Environ Microbiol , 61, 2020-2.
A similar thing has happened to create the sperm specific dynenin gene
(this was a tandem-duplication with fusion by deletion, the protien
coding sequence is derived from the non-coding sequence of the parent
genes. Hows that for cool)
Capy P. (1998 Dec 10). Evolutionary biology. A plastic genome. Nature,
396, 522-3.
> Assuming this is a mutation to a germ cell (a very small target
> indeed),
A germ cell is no smaller target than any other cell, and a large number
of mutations are copy errors during DNA replication, the rate (roughly
10^-8 per nucleotide) is the same for all cells, and as sperm precursor
cells undergo very many replications, the chance of mutation is not so
small at all.
> this would be passed on. The argument goes that eventually
> over, say, 10 million years, a small land carnivor while explode into
> a 50 foot sea going bohemouth like Basilosaurus (for example).
This is the result of the combination of existing variation and new
mutations, rather than mutation alone.
> This
> theory is supposedly supported by "nice little
> sequences" in the fossil record. But the fact that there are genetic
> barriers is totally ignored.
What genetics barriers, can you reference a paper showing these
barriers.
> Mutations can and do result in natural varients, but nothing
> beyond that has ever been demonstrated. The only reason this theory
> flies at all is because the True Believers refuse to entertain any
> other hypothesis other than common descent.
Varients is all you really need, you don't need anything dramatic.
> > Similarly, a mutation in an apolioprotien can lead to a form that
> > renders the carrier more susceptible to heart attacks, a different
> > mutation in the apolipoprotein makes the carriers more resistant.
>
> Of course....and that means that they eventually start sprouting new
> organs?!
No, that's homeotic mutants silly. This was in reply to a question about
whether mutations can be benifical.
Not that we need "new" organs, most of what we have are variants of old
organs or other structures.
Our ear bones are modifcations of jaw bones which are modifications of
stiffenings for gill arches, and gee, <irony>it would be _so_ hard to
get stiffening rods in gill arches via mutation </irony>
Our 4 chambered hearts are modifications of three chambered hearts which
are modifications of two chambered hearts whiich are modifcationsof
valves in muscular blood vessels which are modifications of the blood
vessels _per_se_.
Wings are modifcations of forelegs which are modications of lobe fins
which are due to a duplication of a segmentation polarity homeobox gene.
> > Duplication of homoebox genes (and/or differences in the timing of
> > their expression) can result in significant novelty.
>
> When homebox and homeotic genes are affected by mutation, this can
> cause entire body parts to be misplaced or duplicated. This is
> because homeotic mutations disrupt the master "program", and cause
> genetic "subroutines" to be placed in different locations.
<snip>
So that when you duplicate the segmentation polarity gene, you get nice
little bilaterally paired appendages that can be utilized as fins, (and
then on to legs and wings etc.)
Cheers! Ian
=====================================================
Ian Musgrave Peta O'Donohue,Jack Francis and Michael James Musgrave
reyn...@werple.mira.net.au http://werple.mira.net.au/~reynella/
a collection of Dawkins inspired weasle programs
http://www-personal.monash.edu.au/~ianm/whale.htm
Southern Sky Watch http://www.abc.net.au/science/space/default.htm
cz...@ecn.ab.ca
Organization: Edmonton Community Network
Distribution:
X-Newsreader: TIN [version 1.2 PL2.6]
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Date: 7 Oct 99 12:30:10 GMT
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[piggybacked]
: Dunk wrote in message <37fbb93...@fl.news.verio.net>...
: >Brown and short faced bears are/were the largest terrestial mamallian
: >carnivores.
I don't know abvout "short-faced" bears, but by brown bears, do you mean
kodiaks?
The largest bears on earth are kodiaks (an isolated off-shoot of
grizzlies on the Alaskan island of the same name) and polar bears,
as is my understanding.
--
*************************************************************
In science, "fact" can only mean "confirmed to such a
degree that it would be perverse to withold provisional
assent." I suppose that apples might start to rise
tomorrow, but the possibility does not merit equal time
in physics classrooms.
-Stephen Jay Gould
*************************************************************
Jack King
>
> >
> > The deletion of a nucleotide will lead to a frameshift. It is
> > virtially always lethal. But for the sake of argument, let's say
> > that it is not repaired by corrective enzymes, and it results in a
> > "nylon hydrolysis enzyme".
>
> Oh, but it does happen, see
>
> Ohno S. (1984 Apr). Birth of a unique enzyme from an alternative
> reading frame of the preexisted, internally repetitious coding sequence.
> Proc Natl Acad Sci U S A , 81, 2421-5.
My statement stands. A frameshift is lethal virtually 100% of the time.
Are you disputing that? If so, than please see _The New Healers_; p. 53, 54;
William Clark
Nonetheless, in spite of the odds, I'm not saying that it is impossible. I
also made that clear in my post. It will be so rare, however, that to assume
that it is a mechanism of evolution requires faith that only a True Believer
can muster.
> > Assuming this is a mutation to a germ cell (a very small target
> > indeed),
>
> A germ cell is no smaller target than any other cell,
This has already been discussed in detail with other posters (as have most
of the other issues you raise in your post). Of course it is no smaller a target.
The point is that if it is the ONLY target that has evolutionary significance
then the odds of having a mutation that is meaningful is tiny. An organism
could experience 100 mutations, and none may affect a germ cell.
> and a large number
> of mutations are copy errors during DNA replication, the rate (roughly
> 10^-8 per nucleotide) is the same for all cells, and as sperm precursor
> cells undergo very many replications, the chance of mutation is not so
> small at all.
Also mentioned in another post. Copying errors result in information
leakage. There is no way that will end up being an effective evolutionary
mechanism. Better stick to gene duping. You've got a little more
credibility there.
>
>
> > this would be passed on. The argument goes that eventually
> > over, say, 10 million years, a small land carnivor while explode into
> > a 50 foot sea going bohemouth like Basilosaurus (for example).
>
> This is the result of the combination of existing variation and new
> mutations, rather than mutation alone.
Of course! How else could a small land mammal end up being a whale?
If you believe in common descent than you have have painted yourself into
a corner. Accumulation of mutations becomes the magic allixer that transforms
lead into gold.
> > This
> > theory is supposedly supported by "nice little
> > sequences" in the fossil record. But the fact that there are genetic
> > barriers is totally ignored.
>
> What genetics barriers, can you reference a paper showing these
> barriers.
I hope I don't have to cite papers on anything so obvious as the genetic
barriers in the reproductive systems of various species. There are wide
varient swings in genus/species which will show a rainbow of slightly modified
creatures. But then we hit a genetic wall. We can only produce varients within
a certain range.
> > Mutations can and do result in natural varients, but nothing
> > beyond that has ever been demonstrated. The only reason this theory
> > flies at all is because the True Believers refuse to entertain any
> > other hypothesis other than common descent.
>
> Varients is all you really need, you don't need anything dramatic.
Yes...that is the party line of the True Believers which has been repeated
so many times that it has become a mantra.
>
>
> > > Similarly, a mutation in an apolioprotien can lead to a form that
> > > renders the carrier more susceptible to heart attacks, a different
> > > mutation in the apolipoprotein makes the carriers more resistant.
> >
> > Of course....and that means that they eventually start sprouting new
> > organs?!
>
> No, that's homeotic mutants silly. This was in reply to a question about
> whether mutations can be benifical.
Oh, great....so we have finally agreed on something. There may be a mutation
to the allele of a elephant seal which makes them a little less tastey to a Killer
Whale. That enables their numbers to increase. But then the True Believers assume
that just add a few million years and more mutations, and the elephant seal will turn
into an elephant, totally ignoring the hard coded genetic barriers.
> Not that we need "new" organs, most of what we have are variants of old
> organs or other structures.
>
> Our ear bones are modifcations of jaw bones which are modifications of
> stiffenings for gill arches, and gee, <irony>it would be _so_ hard to
> get stiffening rods in gill arches via mutation </irony>
We should not forget that one of the main reasons that people are mislead
that all organisms are related is the genuine relationship among similar
species of a distinct organism. Despite the fact that most creatures are
clearly unique and distict, this has been the main reason for the persistence
of evolutionary theory. A good example is the superficial similarity
between the Brachiopod lampshell bivalves (phylum Brachiapoda) and the
totally unrelated Molluscan bivalves (phylum Mollusca). In fact for a
long time they were grouped within the same phylum based on their similarities.
As a crude example, although we have been building cars for many decades
all are based on moving bodies with wheels. Starting from the unicycle,
bicycle, tricycle, automobiles, and motorcycles, all have the same overall
mechanisms, parts, and appearance. Why? All are constrained by the same
things: gravity and friction. Similar unifying constraints are imposed
on living things, and the result is inevitable similarities.
<snip>
>
> > When homebox and homeotic genes are affected by mutation, this can
> > cause entire body parts to be misplaced or duplicated. This is
> > because homeotic mutations disrupt the master "program", and cause
> > genetic "subroutines" to be placed in different locations.
> <snip>
>
> So that when you duplicate the segmentation polarity gene, you get nice
> little bilaterally paired appendages that can be utilized as fins, (and
> then on to legs and wings etc.)
And then these "bumps" which eventually morphed into fins, where then supposed
to have modified into the limbs of frogs. But the True believers brush off the
fact that the fins of fish and the limbs of frogs are completely distinct, containing
different numbers and arrangments of bones and tissues. As molecular biologist
Parianne Senapathy states:
"Despite this, what the evolutionary biologists do not seem to realize is the fact
that
the genome is absolutely blind to the environment, and therefore an
immense, almost infinate number of random mutations should occur in order
to arrive at some useful structure. But our rich knowledge in the field
of molecular biology and genetics indicates that this many mutations
cannot occur in living organisms even in trillions and trillions of years."
(_Independent Birth of Organisms_; p. 89-90).
Michael
> Ian Musgrave & Peta O'Donohue wrote:
>
>
[SNIP]
>
> > > This
> > > theory is supposedly supported by "nice little
> > > sequences" in the fossil record. But the fact that there are genetic
> > > barriers is totally ignored.
> >
> > What genetics barriers, can you reference a paper showing these
> > barriers.
>
> I hope I don't have to cite papers on anything so obvious as the genetic
> barriers in the reproductive systems of various species.
These are different barriers. Ian was asking for morphologic barriers, you
are answering with reproductive barriers.
> There are wide
> varient swings in genus/species which will show a rainbow of slightly modified
> creatures. But then we hit a genetic wall. We can only produce varients within
> a certain range.
>
> > > Mutations can and do result in natural varients, but nothing
> > > beyond that has ever been demonstrated. The only reason this theory
> > > flies at all is because the True Believers refuse to entertain any
> > > other hypothesis other than common descent.
> >
> > Varients is all you really need, you don't need anything dramatic.
>
> Yes...that is the party line of the True Believers which has been repeated
> so many times that it has become a mantra.
>
> >
> >
> > > > Similarly, a mutation in an apolioprotien can lead to a form that
> > > > renders the carrier more susceptible to heart attacks, a different
> > > > mutation in the apolipoprotein makes the carriers more resistant.
> > >
> > > Of course....and that means that they eventually start sprouting new
> > > organs?!
> >
> > No, that's homeotic mutants silly. This was in reply to a question about
> > whether mutations can be benifical.
>
> Oh, great....so we have finally agreed on something. There may be a mutation
> to the allele of a elephant seal which makes them a little less tastey to a Killer
> Whale. That enables their numbers to increase. But then the True Believers assume
> that just add a few million years and more mutations, and the elephant seal will turn
> into an elephant, totally ignoring the hard coded genetic barriers.
Citations on the specific barriers here, please.
>
>
> > Not that we need "new" organs, most of what we have are variants of old
> > organs or other structures.
> >
> > Our ear bones are modifcations of jaw bones which are modifications of
> > stiffenings for gill arches, and gee, <irony>it would be _so_ hard to
> > get stiffening rods in gill arches via mutation </irony>
>
> We should not forget that one of the main reasons that people are mislead
> that all organisms are related is the genuine relationship among similar
> species of a distinct organism. Despite the fact that most creatures are
> clearly unique and distict, this has been the main reason for the persistence
> of evolutionary theory. A good example is the superficial similarity
> between the Brachiopod lampshell bivalves (phylum Brachiapoda) and the
> totally unrelated Molluscan bivalves (phylum Mollusca). In fact for a
> long time they were grouped within the same phylum based on their similarities.
> As a crude example, although we have been building cars for many decades
> all are based on moving bodies with wheels. Starting from the unicycle,
> bicycle, tricycle, automobiles, and motorcycles, all have the same overall
> mechanisms, parts, and appearance. Why? All are constrained by the same
> things: gravity and friction. Similar unifying constraints are imposed
> on living things, and the result is inevitable similarities.
And systematists try to avoid those constrained similarities. They look for
others. For example, under your argument, birds and bats would be in the
same groups because of their wings. Yet a lot of other evidence places them
in two different groups. And when you look at the wings, you find that they
are designed differently, using different bones. Same constrainsts, different
design. This allows us to tell that wings evolved independently in at least two
different groups (and there is a third, as well). With this in mind, what should
we make of animals that use the same bones to make such structures?
>
>
> <snip>
>
> >
> > > When homebox and homeotic genes are affected by mutation, this can
> > > cause entire body parts to be misplaced or duplicated. This is
> > > because homeotic mutations disrupt the master "program", and cause
> > > genetic "subroutines" to be placed in different locations.
> > <snip>
> >
> > So that when you duplicate the segmentation polarity gene, you get nice
> > little bilaterally paired appendages that can be utilized as fins, (and
> > then on to legs and wings etc.)
>
> And then these "bumps" which eventually morphed into fins, where then supposed
> to have modified into the limbs of frogs. But the True believers brush off the
> fact that the fins of fish and the limbs of frogs are completely distinct, containing
>
> different numbers and arrangments of bones and tissues.
And yet researchers have found that one in the hox gene can result in many
of these changes. By simply extending the growth period of one portion of
the fin, bones qet twisted around in a hook shape that ultimately forms the
amphibian hand. Its not so tough after all.
Jack King
>
> :I tell you what. It sounds like an excellent doctoral thesis. Why don't you get
> :the biggest canine you can find and bombard him with X-rays and see what
> :happens. Don't let PETA know about it, however.
>
> There simply wouldn't be enough time or dogs to get far. However, any
> progress that was made would simply be admitted by you to be within the
> dog-size-limit, which you can't define a priori, and would be dismissed.
Hmm.. I thought it was obvious that my tongue was firmly planted in my
cheek.
>
> Let's approach it this way - given what is known about developmental
> genetics, why would such a mutation be impossible? If your argument is
> not that such a mutation is impossible, but rather that mutations are so
> rare that we could never expect to see such, that is different and will
> require a different response.
I am saying that they are rare, but only lead to natural variants. Genetic
barriers, like what we see in breeding experiments, allow variants only
up to a certain fixed barrier.
> Elsewhere in this thread you write that mutation cannot produce a new
> structure, only rearrange existing structures (such as homeotic
> mutations). Do you believe mutation can change the shape of a structure?
A new genetic developmental genetic pathway (the genetic track switching
which casues a zygote to pop out body parts) would have to be produced in the
genome of the creature. This track switching is rigidly fixed. The bone of a
vertebrate,
for example, which is lacking in an invertebrate, is built with unique and complex
genetic networks. Since the number of unique pathways is immense, the odds against
achieving them by any kind of mutation(s) in a given genome is astronomical. By what
miracle, then do we get from invertebrate to vertebrate??
>
> Do you believe mutation can change the size of a structure?
Sure...but only up to a fixed rigid limit. These are natural varients. We can
achieve the same thing with agressive breeding. But we play by the same
rules. You're eventually going to hit the wall.
> Can natural
> selection fix mutations which lead to advantageous sizes and shapes of
> structures, including duplications of previous structures which might now
> be selected for a new function? I'm trying to figure out exactly where
> you think the limits can be found.
Of course. No one is questions natural selection.
>
> :Any mutation is rare. When it occurs, it is almost always fixed by repair
> :enzymes. What few do get through are almost always either deleterious
> :or neutral. Some may end up being "beneficial". But most of a genome consists on
> :somatic (non-germ) cells. The chances of a beneficial mutation getting into somatic
> :cells is tiny. But now we have to shrink the target even further for this mutated
> :codon to be passed on.
> :I have never seen this number quantified. Sounds like another good topic for a
> :doctoral thesis.
>
> If you have not seen this number quantified, then you are not the person
> who should be advancing arguments about mutations being too rare to
> account for evolution.
Why? Is there some magnetic power that draws cosmic rays the germ cells?
This is silly. If you are standing 50 yards away from a target, the chances
are you will hit it once in a while with your arrow. But the chances are much
smaller that you will hit a dime sized circle in the middle of the bulls eye.
> I have been struck by this problem in your argument in the past (along
> with my perception that you equate junk DNA with intron). I might as well
> argue that traffic accident fatalities are so rare as to not be a concern
> to anyone. Afterall, when two vehicles are on a collision course, one or
> the other of the drivers almost always reacts and is able to evade the
> collision. If the cars do collide, then the occupants are almost always
> saved by their safety belts or airbags. If they are seriously injured,
> they usually can be saved by emergency crews.
Very funny. Kind of like the Faith in evolution being equated to an infinite number of
rednecks riding in an infinite number of pickup trucks firing an infinite number of
shotgun rounds at an infinite number of highway signs, they will eventually produce all
the world's
great literary works in Braille.
>
> All of this is nice, but it is irrelevant when we look at the actual
> fatality rate. Scientists are able to estimate the actual mutation rate,
> and all the repair and somatic cells in the world won't mean much to the
> calculations that are made based on this rate. Population genetics tells
> us that the rates are (as best they can be estimated) in line with the
> amount of diversification we see in extant species based on their protein
> or DNA sequences and paleontological estimates of their time of
> divergence. Making excuses about the fate of most mutations doesn't
> address the ones that DO get passed on.
No one is questioning that every once in a while a mutation does get passed
on. I wish people would stop accusing me of things I have never said. What
I am saying is that to then take truth extrapolate wild conclusion is not science.
Ian Musgrave & Peta O'Donohue
Address altered to avoid spam, delete RemoveInsert
On 5 Oct 1999 16:52:12 -0400, david ford <dfo...@gl.umbc.edu> wrote:
<snip out of context quote>
>According to neo-Darwinism, mutations in organisms' DNA sequences is the
>raw material natural selection works with to produce blindwatchmaking,
>yet mutations are routinely observed to result in _cancer_ and genetic
>diseases, not the arrival of novel body structures and organs.
Does david ever read any of the replies to his posts. A number of
posts earlier this year deal with these issues.
>Could
>someone please tell me how exactly the neo-Darwinian mechanism is
>compatible with the fact that mutation routinely causes cancer and
>disease? Refs to the literature would be great.
As someone else pointed out, mutation (of somatic DNA) can cause
cancer, but it doesn't ONLY cause cancer. Context is everything. A
deletion event can knock out p53, and lead to cancer, or a deletion
event in an ISO18000 sequence can lead to the expression of a novel
nylon hydrolysis enzyme.
Similarly, a mutation in an apolioprotien can lead to a form that
renders the carrier more susceptible to heart attacks, a different
mutation in the apolipoprotein makes the carriers more resistant.
Duplication of homoebox genes (and/or differences in the timing of
their expression) can result in significant novelty.
(repeated) Literature references to these items (and more, eg
d-ala-d-serine ligases) can be found in this very thread, via
DejaNews.
Cheers! Ian
Keith Doyle
Jack King <jack...@nortelnetworks.com> wrote:
>
>Sure...but only up to a fixed rigid limit. These are natural varients. We can
>achieve the same thing with agressive breeding. But we play by the same
>rules. You're eventually going to hit the wall.
>
There's no evidence whatsoever of this. Further, the fossil record is ample
evidence that at least both reptiles and mammals are within the same set of
"walls."
--
Keith Doyle
(remove underbars in reply address for E-mail)
"Often a non-Christian knows something about the earth, the
heavens, and the other parts of the world, about the motions and
orbits of the stars and even their sizes and distances,... and
this knowledge he holds with certainty from reason and
experience. It is thus offensive and disgraceful for an
unbeliever to hear a Christian talk nonsense about such things,
claiming that what he is saying is based in Scripture. We should
do all that we can to avoid such an embarrassing situation, lest
the unbeliever see only ignorance in the Christian and laugh to
scorn."
-- St. Augustine, "De Genesi ad litteram libri duodecim"
(The Literal Meaning of Genesis)
Keith Doyle
Jack King <jack...@nortelnetworks.com> wrote:
>Oh, great....so we have finally agreed on something. There may be a mutation
>to the allele of a elephant seal which makes them a little less tastey to a Killer
>Whale. That enables their numbers to increase. But then the True Believers assume
>that just add a few million years and more mutations, and the elephant seal will turn
>into an elephant, totally ignoring the hard coded genetic barriers.
Ridiculous. Nothing is hard coded in DNA, as everything is subject to
mutations. Note that a mutation that affects a recessive gene may be
neutral for the individual, but can be specifically selected for or against
in the individuals progeny. Reproductive barriers are not always absolute--
as in the horse/donkey example. Also reproductive barriers are produced over
time by reproductive isolation-- this has been reproduced in laboratory
experiments. Therefore reproductive barriers are not inherently absolute
or "hard coded."
>We should not forget that one of the main reasons that people are mislead
>that all organisms are related is the genuine relationship among similar
>species of a distinct organism. Despite the fact that most creatures are
>clearly unique and distict, this has been the main reason for the persistence
>of evolutionary theory. A good example is the superficial similarity
>between the Brachiopod lampshell bivalves (phylum Brachiapoda) and the
>totally unrelated Molluscan bivalves (phylum Mollusca). In fact for a
>long time they were grouped within the same phylum based on their similarities.
No, one of the main reasons that scientists have concluded that evolution
is correct is that it explains the connection between an organism's genetic
relationships with its morphological relationships and its temporal relationships.
The reptile to mammal transition is well documented in the fossil record
including the jawbone to inner ear bone transition-- a modification of
an existing structure for a completely unrelated function. No observable
"barriers" here.
Perhaps if you keep chanting that there are hard genetic barriers enough,
the people in your parish will keep believing it, but that isn't going to
make it any less the mere figment of your wishful thinking that it is.
--
Keith Doyle
(remove underbars in reply address for E-mail)
Ignorance is the soil in which belief in miracles grows.
-- Robert G. Ingersoll
Keith Doyle
Ian Musgrave & Peta O'Donohue <reyn...@RemoveInsert.werple.mira.net.au> wrote:
>G'Day All
>Address altered to avoid spam, delete RemoveInsert
>
>On 5 Oct 1999 16:52:12 -0400, david ford <dfo...@gl.umbc.edu> wrote:
>
><snip out of context quote>
>
>>According to neo-Darwinism, mutations in organisms' DNA sequences is the
>>raw material natural selection works with to produce blindwatchmaking,
>>yet mutations are routinely observed to result in _cancer_ and genetic
>>diseases, not the arrival of novel body structures and organs.
>
>Does david ever read any of the replies to his posts. A number of
>posts earlier this year deal with these issues.
It's the Usenet equivalent to keeping your fingers in your ears and
your eyes shut.
Jack King
> In article <37FCA974...@nortelnetworks.com>,
> Jack King <jack...@nortelnetworks.com> wrote:
>
> >Oh, great....so we have finally agreed on something. There may be a mutation
> >to the allele of a elephant seal which makes them a little less tastey to a Killer
> >Whale. That enables their numbers to increase. But then the True Believers assume
> >that just add a few million years and more mutations, and the elephant seal will turn
> >into an elephant, totally ignoring the hard coded genetic barriers.
>
> Ridiculous. Nothing is hard coded in DNA, as everything is subject to
> mutations. Note that a mutation that affects a recessive gene may be
> neutral for the individual, but can be specifically selected for or against
> in the individuals progeny.
You have obviously not been following this thread. Sure any part of the genome
is subject to mutation. Of course most of a genome consists of non-coding regions
(thus making the target for relevant mutations even smaller). But these mutations
bring about only natural variations.
> Reproductive barriers are not always absolute--
> as in the horse/donkey example.
Horse & donkey are close enough genetically to breed a hybrid. The hybrid itself
is sterile and can no longer pass subsequent genes into the gene pool.
> Also reproductive barriers are produced over
> time by reproductive isolation-- this has been reproduced in laboratory
> experiments. Therefore reproductive barriers are not inherently absolute
> or "hard coded."
Yes, of course. New genetic barriers can be errected. They cannot be torn
down.
>
>
> >We should not forget that one of the main reasons that people are mislead
> >that all organisms are related is the genuine relationship among similar
> >species of a distinct organism. Despite the fact that most creatures are
> >clearly unique and distict, this has been the main reason for the persistence
> >of evolutionary theory. A good example is the superficial similarity
> >between the Brachiopod lampshell bivalves (phylum Brachiapoda) and the
> >totally unrelated Molluscan bivalves (phylum Mollusca). In fact for a
> >long time they were grouped within the same phylum based on their similarities.
>
> No, one of the main reasons that scientists have concluded that evolution
> is correct is that it explains the connection between an organism's genetic
> relationships with its morphological relationships and its temporal relationships.
> The reptile to mammal transition is well documented in the fossil record
> including the jawbone to inner ear bone transition-- a modification of
> an existing structure for a completely unrelated function. No observable
> "barriers" here.
Well documented? Only to those whose narrow thinking refuse to consider
anything other than common descent. Body hair, Mammary glands to nurse,
warm blooded, bear young alive, placenta, etc, etc. The two are so far
apart, that about all you can claim is that they are in the same phyla.
> Perhaps if you keep chanting that there are hard genetic barriers enough,
> the people in your parish will keep believing it, but that isn't going to
> make it any less the mere figment of your wishful thinking that it is.
And have you bowed before and sprinkled some incense to your icon C. Darwin
yet today? Have you been regulary reading his holy book? If you'de like to
break free, I can set you up with a de-programmer.
Adam Noel Harris
:Adam Noel Harris wrote:
:> There simply wouldn't be enough time or dogs to get far. However, any
:> progress that was made would simply be admitted by you to be within the
:> dog-size-limit, which you can't define a priori, and would be dismissed.
:
:Hmm.. I thought it was obvious that my tongue was firmly planted in my
:cheek.
Yep. My point was that even if we went to the ridiculous lengths that you
would require for evidence, you could hand wave the results away.
:> Let's approach it this way - given what is known about developmental
:> genetics, why would such a mutation be impossible? If your argument is
:> not that such a mutation is impossible, but rather that mutations are so
:> rare that we could never expect to see such, that is different and will
:> require a different response.
:
:I am saying that they are rare, but only lead to natural variants.
I agree. We just differ on what we think is an acceptable "natural
variant," and we differ on what is too rare to work and what is not.
Since you don't really even know _how_ rare, I doubt you've seriously
considered if the mutation rate is sufficient to explain common descent in
the time frames available. IOW, you are pretty sure they are too rare but
haven't done the math.
:Genetic barriers, like what we see in breeding experiments, allow
:variants only up to a certain fixed barrier.
If you mean that after x generations of artificial selection, the trait
being selected seems to plateau out, we do see this "barrier." However,
this barrier is explained in population genetics models by the fixation of
selected "natural variants." Going further would require new mutants.
But those new mutants would fall around the NEW population mean, not the
old one. Natural variants that arise that increase the size of a great
dane or decrease the size of a chihuahua are quite different than natural
variants that arise in wolf populations.
Mutation builds on prior adaptions, and that's not something you can
simply wave your hands over and say only "natural variants" are allowed.
:> Elsewhere in this thread you write that mutation cannot produce a new
:> structure, only rearrange existing structures (such as homeotic
:> mutations). Do you believe mutation can change the shape of a structure?
:
:A new genetic developmental genetic pathway (the genetic track switching
:which casues a zygote to pop out body parts) would have to be produced in the
:genome of the creature.
That depends on the scope of the change we are talking about. Do whale
flippers require new developmental genetic pathways from the limbs of
terrestrial mammals?
For larger scale changes, the conventional argument is that these "new"
pathways are really just duplications and alterations of old pathways.
Indeed, we see similar genes involved in multiple developmental pathways
in model organisms studied.
:This track switching is rigidly fixed.
Evidence?
:The bone of a vertebrate, for example, which is lacking in an
:invertebrate, is built with unique and complex genetic networks.
But how "unique?" Why do the bone morphogenetic proteins in vertebrates
have counterparts in invertebrates that function in similar developmental
genetic pathways, have similar primary sequences, and in some cases can be
substituted for each other in transgenic animals? Seems more like these
complex genetic networks are repititions of simpler networks.
:Since the number of unique pathways is immense, the odds against
:achieving them by any kind of mutation(s) in a given genome is
:astronomical. By what miracle, then do we get from invertebrate to
:vertebrate??
The miracle of cumulative selection. By what miracle do invertebrates
share so many sequences with vertebrates? Senapathy's ideas, from what I
have seen of them, are what requires highly improbable one-step selection
to create new creatures. Conventional wisdom sees the power of cumulative
selection over many smaller steps.
Surely, the invertebrate to vertebrate transistion is well beyond what you
allow for "natural variants," so perhaps we should look at something
closer to the rigid barrier. What's just beyond the power of mutation,
selection, and drift to explain?
:> Do you believe mutation can change the size of a structure?
:
:Sure...but only up to a fixed rigid limit. These are natural varients. We can
:achieve the same thing with agressive breeding. But we play by the same
:rules. You're eventually going to hit the wall.
But the math says that the wall comes from using up natural variants.
What is the barrier that stops the production of new variants around the
new population mean, given that those would simply be "natural variants"
too.
:> Can natural
:> selection fix mutations which lead to advantageous sizes and shapes of
:> structures, including duplications of previous structures which might now
:> be selected for a new function? I'm trying to figure out exactly where
:> you think the limits can be found.
:
:Of course. No one is questions natural selection.
So mutation can produce natural variants and natural selection can select
them. When the whole population has shifted to one extreme due to the
action of selection, what is the limit - the rigid barrier - that limits
what natural variants are produced?
[about mutation rates]
:> If you have not seen this number quantified, then you are not the person
:> who should be advancing arguments about mutations being too rare to
:> account for evolution.
:
:Why? Is there some magnetic power that draws cosmic rays the germ cells?
Why does there need to be? Germ cells are hit by cosmic rays. The soma
is hit by cosmic rays. We're interested in the germ cell hits, we have
estimates of the germ cell hits, and you're concerned about the relative
size of the soma vs. germline. Why? I don't know what proportion of
mutations are caused by cosmic rays, but I know that it's not all.
Polymerases are imperfect, and bases can be incorporated inappropriately.
The repair machinery _does not_ get them all.
:This is silly. If you are standing 50 yards away from a target, the chances
:are you will hit it once in a while with your arrow. But the chances are much
:smaller that you will hit a dime sized circle in the middle of the bulls eye.
But we have estimates for the number of arrows that strike the bulls eye.
Why do you think these are irrelevant because of the rest of the target?
:> I have been struck by this problem in your argument in the past (along
:> with my perception that you equate junk DNA with intron). I might as well
:> argue that traffic accident fatalities are so rare as to not be a concern
:> to anyone. Afterall, when two vehicles are on a collision course, one or
:> the other of the drivers almost always reacts and is able to evade the
:> collision. If the cars do collide, then the occupants are almost always
:> saved by their safety belts or airbags. If they are seriously injured,
:> they usually can be saved by emergency crews.
:
:Very funny. Kind of like the Faith in evolution being equated to an
:infinite number of rednecks riding in an infinite number of pickup
:trucks firing an infinite number of shotgun rounds at an infinite
:number of highway signs, they will eventually produce all the world's
:great literary works in Braille.
There is no need for "Faith" in mutations happening in germ cells, which
is what I was analogizing. There is observation. That the mutation rates
are appropriate for the divergence in sequences seen over time is not my
problem. It's yours. How many ways can I emphasize this? Germ cells
and DNA repair mechanisms are already factored in.
:> All of this is nice, but it is irrelevant when we look at the actual
:> fatality rate. Scientists are able to estimate the actual mutation rate,
:> and all the repair and somatic cells in the world won't mean much to the
:> calculations that are made based on this rate. Population genetics tells
:> us that the rates are (as best they can be estimated) in line with the
:> amount of diversification we see in extant species based on their protein
:> or DNA sequences and paleontological estimates of their time of
:> divergence. Making excuses about the fate of most mutations doesn't
:> address the ones that DO get passed on.
:
:No one is questioning that every once in a while a mutation does get passed
:on. I wish people would stop accusing me of things I have never said. What
:I am saying is that to then take truth extrapolate wild conclusion is
:not science.
I don't accuse you of denying mutation. I accuse you of saying it does
not happen at a fast enough rate when you do not know what the rate is and
don't know what the molecular changes mutations are supposed to account
for are.
Jack King
> :> Let's approach it this way - given what is known about developmental
> :> genetics, why would such a mutation be impossible? If your argument is
> :> not that such a mutation is impossible, but rather that mutations are so
> :> rare that we could never expect to see such, that is different and will
> :> require a different response.
> :
> :I am saying that they are rare, but only lead to natural variants.
>
> I agree. We just differ on what we think is an acceptable "natural
> variant," and we differ on what is too rare to work and what is not.
> Since you don't really even know _how_ rare, I doubt you've seriously
> considered if the mutation rate is sufficient to explain common descent in
> the time frames available. IOW, you are pretty sure they are too rare but
> haven't done the math.
Well I didn't really want to get into the math. Nonethelss, you (and others)
keep bringing it up. Senapathy (who also has advanced degrees in mathematics)
calculates:
"Consider a developmental genetic pathway consisting of only ten genes.
If we are given 100 genes in a gene pool, the probability of arriving
at this specific genetic network is 1-100^(10), or 1-10^(-20). This
is an extremely low probability. This means that 1-10^(-20) combin-
ations of 100 given genes, taken ten at a time, would be the desired
order of genes for a new developmental pathway leading to a new structure.
In reality the number of genes in the developmental genetic pathway
for an organ is over 100, tremendously reducing the probability of
arriving at a specific developmental genetic pathway to 1-10^(-200),
an insurmountably low level." p.35 _Independent Birth of Organisms_
>
>
> :Genetic barriers, like what we see in breeding experiments, allow
> :variants only up to a certain fixed barrier.
>
> If you mean that after x generations of artificial selection, the trait
> being selected seems to plateau out, we do see this "barrier."
No, that is not what I mean. You cannot mate Genus Canis with Genus
Felis. There is a rigid wall. You can come up with all kinds of natural
varients, you can isolate species, you can do whatever you wish. It
doesn't change anything. Those barriers do not change just because
of mutations. The wall is too high.
> Mutation builds on prior adaptions, and that's not something you can
> simply wave your hands over and say only "natural variants" are allowed.
And you cannot simply wave your hand and say mutations are the magic
bullet. You simply assume it is because there is nothing else.
>
>
> :A new genetic developmental genetic pathway (the genetic track switching
> :which casues a zygote to pop out body parts) would have to be produced in the
> :genome of the creature.
>
> That depends on the scope of the change we are talking about. Do whale
> flippers require new developmental genetic pathways from the limbs of
> terrestrial mammals?
Considering how trivial the differences in morphology usually are
between well defines species today, taking in account all the modifications
necessary to convert a land mammal into a whale -- forelimb modifications,
the evolution of tail flukes, the streamlining, reduction of hindlimbs,
modifications of skull to bring nostrils to the top of the head,
modification of trachea, modifications of behavior patterns, specialized
nipples so that the young could feed underwater (a complete list would
be enormous) -- one is inclined to think in terms of possibly hundereds,
even thousands of transitional species on the most direct path between
a hypothetical land ancestor and the common ancestor of modern whales.
>
>
> For larger scale changes, the conventional argument is that these "new"
> pathways are really just duplications and alterations of old pathways.
> Indeed, we see similar genes involved in multiple developmental pathways
> in model organisms studied.
With gene duping all you are doing is copying a genetic subroutine (say for
a limb), to another part of the master genetic "program". Nothing new has
been created. You simply end up with a duplicate of an already existing
organ. It is truely amazing how people can possible conceive that this is
actually a mechanism of evolution. The only reason why they keep pounding
this drum is because they have very little else.
>
> :This track switching is rigidly fixed.
>
> Evidence?
The genetic barriers is demonstrated time & time again in breeding. Now why
don't you provide the evidence that these rigid barriers crumble away in the
face of a very rare cumulative mutations which are lucky enough to land in
coding regions of germ cells which happen to slip by corrective enzymes, and
which do not turn out to be deliterious or neutral.
>
> :The bone of a vertebrate, for example, which is lacking in an
> :invertebrate, is built with unique and complex genetic networks.
>
> But how "unique?" Why do the bone morphogenetic proteins in vertebrates
> have counterparts in invertebrates that function in similar developmental
> genetic pathways, have similar primary sequences, and in some cases can be
> substituted for each other in transgenic animals? Seems more like these
> complex genetic networks are repititions of simpler networks.
Spoken like a True Believer. Vertebrates first appeared very suddenly circa
400+ mya. The first appearance of this group was already highly differentiated.
None of them could be considered remotely intermediate to the other. We see the
same thing with invertebrates during the Cambrian explosion. At that time virtually
every known phyla was birthed. Phyla are completely unconnected at the top
of the taxonomical hierarchy. Please explain the common descent.
> :Since the number of unique pathways is immense, the odds against
> :achieving them by any kind of mutation(s) in a given genome is
> :astronomical. By what miracle, then do we get from invertebrate to
> :vertebrate??
>
> The miracle of cumulative selection.
I'm glad you admit it is a miracle.
> By what miracle do invertebrates
> share so many sequences with vertebrates? Senapathy's ideas, from what I
> have seen of them, are what requires highly improbable one-step selection
> to create new creatures. Conventional wisdom sees the power of cumulative
> selection over many smaller steps.
The reason why invertebrates & vertebrates share so many "sequences" is that
they come from a common templete. It's that simple.
>
>
> :> If you have not seen this number quantified, then you are not the person
> :> who should be advancing arguments about mutations being too rare to
> :> account for evolution.
> :
> :Why? Is there some magnetic power that draws cosmic rays the germ cells?
>
> Why does there need to be? Germ cells are hit by cosmic rays. The soma
> is hit by cosmic rays. We're interested in the germ cell hits, we have
> estimates of the germ cell hits, and you're concerned about the relative
> size of the soma vs. germline. Why? I don't know what proportion of
> mutations are caused by cosmic rays, but I know that it's not all.
> Polymerases are imperfect, and bases can be incorporated inappropriately.
> The repair machinery _does not_ get them all.
Of course it doesn't get them all. That's why we end up with genetic diseases
like sickle cell when germ cells are mutated, and that's why we end up with
cancers when somatic cells are mutated. Yes, on rare occasions you may
have a mutation in the germ line that is "beneficial" resulting in a varient. Big
deal.
<snip circular discussion>
Michael
> Adam Noel Harris wrote:
>
>
> Considering how trivial the differences in morphology usually are
> between well defines species today, taking in account all the modifications
> necessary to convert a land mammal into a whale -- forelimb modifications,
> the evolution of tail flukes, the streamlining, reduction of hindlimbs,
> modifications of skull to bring nostrils to the top of the head,
> modification of trachea, modifications of behavior patterns, specialized
> nipples so that the young could feed underwater (a complete list would
> be enormous) -- one is inclined to think in terms of possibly hundereds,
> even thousands of transitional species on the most direct path between
> a hypothetical land ancestor and the common ancestor of modern whales.
Doesn't strike you as odd, then, that all of the skeletal transitions you mention
are found in the fossil record, right around the time we would expect to
find them? For example: shortening of limbs, movement of nostrils to top
of head, changes to vertebrae consistent with freeing spine for propulsion,
etc.
>
>
> >
> >
> > For larger scale changes, the conventional argument is that these "new"
> > pathways are really just duplications and alterations of old pathways.
> > Indeed, we see similar genes involved in multiple developmental pathways
> > in model organisms studied.
>
> With gene duping all you are doing is copying a genetic subroutine (say for
> a limb), to another part of the master genetic "program". Nothing new has
> been created. You simply end up with a duplicate of an already existing
> organ. It is truely amazing how people can possible conceive that this is
> actually a mechanism of evolution. The only reason why they keep pounding
> this drum is because they have very little else.
In the problems for whale evolution you listed, there are no new organs.
Mostly its just rearranging the skeleton. Tail flukes? Just big slabs of meat
on the tail. The specialized nipples? Nothing new there, except for a little
pressure. They're all just modifications. Now, I'm sure that there are some
new features, (the melon, perhaps), but the majority of the change does not
involve anything "new".
>
>
> >
> > :This track switching is rigidly fixed.
> >
> > Evidence?
>
> The genetic barriers is demonstrated time & time again in breeding. Now why
> don't you provide the evidence that these rigid barriers crumble away in the
> face of a very rare cumulative mutations which are lucky enough to land in
> coding regions of germ cells which happen to slip by corrective enzymes, and
> which do not turn out to be deliterious or neutral.
Would a mutation to a mosquito that allows it to live through pesticides count?
Note that in humans this is the equivalent of being able to breath nerve gas. If
this is not a novel and beneficial feature, I don't know what is. If not, why not?
How about the one mutation to a hox gene that converts a fin into a primitive
hand?
Mike
Adam Noel Harris
:Adam Noel Harris wrote:
:> I agree. We just differ on what we think is an acceptable "natural
:> variant," and we differ on what is too rare to work and what is not.
:> Since you don't really even know _how_ rare, I doubt you've seriously
:> considered if the mutation rate is sufficient to explain common descent in
:> the time frames available. IOW, you are pretty sure they are too rare but
:> haven't done the math.
:
:Well I didn't really want to get into the math. Nonethelss, you (and others)
:keep bringing it up. Senapathy (who also has advanced degrees in mathematics)
Another one, eh? :)
:calculates:
:
:"Consider a developmental genetic pathway consisting of only ten genes.
:If we are given 100 genes in a gene pool, the probability of arriving
:at this specific genetic network is 1-100^(10), or 1-10^(-20). This
:is an extremely low probability. This means that 1-10^(-20) combin-
:ations of 100 given genes, taken ten at a time, would be the desired
:order of genes for a new developmental pathway leading to a new structure.
:In reality the number of genes in the developmental genetic pathway
:for an organ is over 100, tremendously reducing the probability of
:arriving at a specific developmental genetic pathway to 1-10^(-200),
:an insurmountably low level." p.35 _Independent Birth of Organisms_
Senapathy is using his advanced degrees in mathematics to convert garbage
into garbage. Why is he using a model which assembles genetic pathways at
random and beginning with ten genes? You may think the step-by-step
gradualism of conventional evolutionary theory is bunk, but if you're
going to use calculations to dismiss it, they should be calculations which
address it.
Senapathy is using the "747 in a junkyard" argument on developmental
genetic pathways, which ignores cumulative selection.
:> If you mean that after x generations of artificial selection, the trait
:> being selected seems to plateau out, we do see this "barrier."
:
:No, that is not what I mean.
Then I was being far too generous.
:You cannot mate Genus Canis with Genus Felis. There is a rigid wall.
SFW? Which part of conventional evolutionary theory requires
hybridization of diverged species? The rigid wall you describe above has
NOTHING TO DO with the wall you were talking about earlier, the one
involving the limit of morphological change a species can undergo.
:You can come up with all kinds of natural
:varients, you can isolate species, you can do whatever you wish. It
:doesn't change anything. Those barriers do not change just because
:of mutations. The wall is too high.
Since we never need to cross this wall, how is it relevant? You're
supposed to be demonstrating the wall between the last common ancestor of
dogs and cats and the extant groups, not between dogs and cats themselves.
:> Mutation builds on prior adaptions, and that's not something you can
:> simply wave your hands over and say only "natural variants" are allowed.
:
:And you cannot simply wave your hand and say mutations are the magic
:bullet. You simply assume it is because there is nothing else.
I accept mutation as the means for producing divergence over time because
it is an observable mechanism and it is adequate. It is not that I assume
that there is nothing else; it's that nothing else appears to be needed
nor plausible. Did you have something in mind? How are genomes created
under Senapathy's model?
:> That depends on the scope of the change we are talking about. Do whale
:> flippers require new developmental genetic pathways from the limbs of
:> terrestrial mammals?
:
: Considering how trivial the differences in morphology usually are
:between well defines species today, taking in account all the modifications
:necessary to convert a land mammal into a whale -- forelimb modifications,
:the evolution of tail flukes, the streamlining, reduction of hindlimbs,
:modifications of skull to bring nostrils to the top of the head,
:modification of trachea, modifications of behavior patterns, specialized
:nipples so that the young could feed underwater (a complete list would
:be enormous) -- one is inclined to think in terms of possibly hundereds,
:even thousands of transitional species on the most direct path between
:a hypothetical land ancestor and the common ancestor of modern whales.
No comment. I'm arguing beyond my field.
:> For larger scale changes, the conventional argument is that these "new"
:> pathways are really just duplications and alterations of old pathways.
:> Indeed, we see similar genes involved in multiple developmental pathways
:> in model organisms studied.
:
:With gene duping all you are doing is copying a genetic subroutine (say for
:a limb), to another part of the master genetic "program". Nothing new has
:been created. You simply end up with a duplicate of an already existing
:organ. It is truely amazing how people can possible conceive that this is
:actually a mechanism of evolution. The only reason why they keep pounding
:this drum is because they have very little else.
Your amazement aside, what might the "natural variants" of the new limb or
organ look like? What sort of limits to changes in size, shape, and
function are there? Since you haven't established where the barrier is
yet, I don't see why "natural variants" cannot be selected to form a
flipper from a leg.
:> Evidence?
:
:The genetic barriers is demonstrated time & time again in breeding. Now why
:don't you provide the evidence that these rigid barriers crumble away in the
:face of a very rare cumulative mutations which are lucky enough to land in
:coding regions of germ cells which happen to slip by corrective enzymes, and
:which do not turn out to be deliterious or neutral.
You overstate the degree of luck necessary, because you don't have an
appreciation of real mutation rates. Are you, above, accepting the
barriers I described or not? If you're still talking about the inability
of diverged species to interbreed, then I don't need to describe any
crumbling - these barriers do not need to be overcome.
:> But how "unique?" Why do the bone morphogenetic proteins in vertebrates
:> have counterparts in invertebrates that function in similar developmental
:> genetic pathways, have similar primary sequences, and in some cases can be
:> substituted for each other in transgenic animals? Seems more like these
:> complex genetic networks are repititions of simpler networks.
:
:Spoken like a True Believer. Vertebrates first appeared very suddenly circa
:400+ mya. The first appearance of this group was already highly differentiated.
:None of them could be considered remotely intermediate to the other. We see the
:same thing with invertebrates during the Cambrian explosion. At that time virtually
:every known phyla was birthed. Phyla are completely unconnected at the top
:of the taxonomical hierarchy. Please explain the common descent.
Please address my point. You call it "faith" when I argue that new
developmental genetic networks are natural variants of older ones, then
when I bring up real world observation of what might have been considered
entirely different networks, you jump to the Cambrian explosion. I know
that together with your rigid barriers, introns, and DNA repair mechanisms
that the Cambrian is one of your favorite topics, but why not deal with
what I wrote? Given DNA and protein homologies, the Cambrian "problem"
looks like an artefact of fossilization. The phyla _are_ connected by
sequence homology.
:> The miracle of cumulative selection.
:
:I'm glad you admit it is a miracle.
:> By what miracle do invertebrates
:> share so many sequences with vertebrates? Senapathy's ideas, from what I
:> have seen of them, are what requires highly improbable one-step selection
:> to create new creatures. Conventional wisdom sees the power of cumulative
:> selection over many smaller steps.
:
:The reason why invertebrates & vertebrates share so many "sequences" is that
:they come from a common templete. It's that simple.
Interesting. How are they assembled from this template (e.g. how are new
developmental genetic pathways constructed from the template?). Why are
they assembled in a nested hierarchical organization.
:> Why does there need to be? Germ cells are hit by cosmic rays. The soma
:> is hit by cosmic rays. We're interested in the germ cell hits, we have
:> estimates of the germ cell hits, and you're concerned about the relative
:> size of the soma vs. germline. Why? I don't know what proportion of
:> mutations are caused by cosmic rays, but I know that it's not all.
:> Polymerases are imperfect, and bases can be incorporated inappropriately.
:> The repair machinery _does not_ get them all.
:
:Of course it doesn't get them all. That's why we end up with genetic diseases
:like sickle cell when germ cells are mutated, and that's why we end up with
:cancers when somatic cells are mutated. Yes, on rare occasions you may
:have a mutation in the germ line that is "beneficial" resulting in a
:varient. Big deal.
Well, if those are enough to explain evolution, then it is a big deal.
JMGoodguy
>an existing structure for a completely unrelated function. No observable
>"barriers" her
Is this documented on the net?
Wesley R. Elsberry
JMGoodguy <jmgo...@aol.com> wrote:
?>including the jawbone to inner ear bone transition-- a
?>modification of an existing structure for a completely
?>unrelated function. No observable "barriers" her
JMG>Is this documented on the net?
I hope not. The transition goes to the bones of the
*middle ear*.
--
Wesley R. Elsberry, Student in Wildlife & Fisheries Sciences, Tx A&M U.
Visit the Online Zoologists page (http://www.rtis.com/nat/user/elsberry)
Email to this account is dumped to /dev/null, whose Spam appetite is capacious.
"I've been stripped, the insulation's gone\Wish I'd slept to waken in the morn"
John Wilkins
<ke_ith_d@ne_tco_m.com> wrote:
| In article <n=n6N7NIGOmll+O...@4ax.com>,
| Ian Musgrave & Peta O'Donohue <reyn...@RemoveInsert.werple.mira.net.au>
| wrote:
| >G'Day All
| >Address altered to avoid spam, delete RemoveInsert
| >
| >On 5 Oct 1999 16:52:12 -0400, david ford <dfo...@gl.umbc.edu> wrote:
| >
| ><snip out of context quote>
| >
| >>According to neo-Darwinism, mutations in organisms' DNA sequences is the
| >>raw material natural selection works with to produce blindwatchmaking,
| >>yet mutations are routinely observed to result in _cancer_ and genetic
| >>diseases, not the arrival of novel body structures and organs.
| >
| >Does david ever read any of the replies to his posts. A number of
| >posts earlier this year deal with these issues.
|
| It's the Usenet equivalent to keeping your fingers in your ears and
| your eyes shut.
|
David seems to believe in the Primacy of the Word, particularly the
Published Word. I can't decide if he's a Postmodernist or a Literalist
(or indeed if there's any real distinction there to be made). If the
Sources say it is so, then it is so, and any reply that is not from
those Sources is irrelevant.
He did have a period where he tried to make discursive argument, but it
seemed to be unfulfilling, as exegesis of sacred scripture often is.
Morat
Jack King wrote:
> Keith Doyle wrote:
>
> > In article <37FCA974...@nortelnetworks.com>,
> > Jack King <jack...@nortelnetworks.com> wrote:
> >
> >
<snip>
>
> > No, one of the main reasons that scientists have concluded that evolution
> > is correct is that it explains the connection between an organism's genetic
> > relationships with its morphological relationships and its temporal relationships.
> > The reptile to mammal transition is well documented in the fossil record
> > including the jawbone to inner ear bone transition-- a modification of
> > an existing structure for a completely unrelated function. No observable
> > "barriers" here.
>
> Well documented? Only to those whose narrow thinking refuse to consider
> anything other than common descent. Body hair, Mammary glands to nurse,
> warm blooded, bear young alive, placenta, etc, etc. The two are so far
> apart, that about all you can claim is that they are in the same phyla.
>
I wonder where you place the marsupials.
>
> > Perhaps if you keep chanting that there are hard genetic barriers enough,
> > the people in your parish will keep believing it, but that isn't going to
> > make it any less the mere figment of your wishful thinking that it is.
>
> And have you bowed before and sprinkled some incense to your icon C. Darwin
> yet today? Have you been regulary reading his holy book? If you'de like to
> break free, I can set you up with a de-programmer.
>
> --
>
> Jack King
> jack...@nortelnetworks.com
> http://www.bit-net.com/~jackking
>
> Check out a GREAT vacation villa in the Caribbean
> http://www.stjohnusvi.com/coralmoonvilla/
--
spam blocking in effect. To reply remove "not"
------------------------------------------------------------------
When someone is saved from certain death by a strange
concatenation of circumstances, they say its a miracle.
But of course if someone is killed by a freak chain of
events - that must also be a miracle.
Just because it isn't nice doesn't mean its not miraculous.
--Terry Pratchett "Interesting Times"
------------------------------------------------------------------
Morat
Keith Doyle wrote:
> In article <37FCA974...@nortelnetworks.com>,
> Jack King <jack...@nortelnetworks.com> wrote:
>
> >Oh, great....so we have finally agreed on something. There may be a mutation
> >to the allele of a elephant seal which makes them a little less tastey to a Killer
> >Whale. That enables their numbers to increase. But then the True Believers assume
> >that just add a few million years and more mutations, and the elephant seal will turn
> >into an elephant, totally ignoring the hard coded genetic barriers.
>
> Ridiculous. Nothing is hard coded in DNA, as everything is subject to
> mutations. Note that a mutation that affects a recessive gene may be
> neutral for the individual, but can be specifically selected for or against
> in the individuals progeny. Reproductive barriers are not always absolute--
> as in the horse/donkey example. Also reproductive barriers are produced over
> time by reproductive isolation-- this has been reproduced in laboratory
> experiments. Therefore reproductive barriers are not inherently absolute
> or "hard coded."
>
"Barriers", when used in the sense above (by Jack King), seem to be an attempt to
scientifically prove, by making something up, that microevolution cannot sum to macro over
tiem.
ISo, if you have Point A and Point B, both a meter apart, and you have a toy car that can
move 1 centimeter at a time, and then must rest for 10 seconds..then according to him:
no amount of moving by the car can ever reach point "B" because there is a barrier in the
way. Admittedly, it's an invisible one, and no one has ever seen any proof for it, or even
found an instance where it seemed to stop something, but he claims it's there. Still, I
bet I could get my toy car from A to B...even if a I used a modifed "Drunkard's Walk"
instead of a straight line.
Another point he made that was true, at least as far as I can tell: There is a pratical
limit to how big something can be. But it's more physics than biology. Has to do with
surface area and volume, IIRC.
>
> >We should not forget that one of the main reasons that people are mislead
> >that all organisms are related is the genuine relationship among similar
> >species of a distinct organism. Despite the fact that most creatures are
> >clearly unique and distict, this has been the main reason for the persistence
> >of evolutionary theory. A good example is the superficial similarity
> >between the Brachiopod lampshell bivalves (phylum Brachiapoda) and the
> >totally unrelated Molluscan bivalves (phylum Mollusca). In fact for a
> >long time they were grouped within the same phylum based on their similarities.
>
> No, one of the main reasons that scientists have concluded that evolution
> is correct is that it explains the connection between an organism's genetic
> relationships with its morphological relationships and its temporal relationships.
> The reptile to mammal transition is well documented in the fossil record
> including the jawbone to inner ear bone transition-- a modification of
> an existing structure for a completely unrelated function. No observable
> "barriers" here.
>
> Perhaps if you keep chanting that there are hard genetic barriers enough,
> the people in your parish will keep believing it, but that isn't going to
> make it any less the mere figment of your wishful thinking that it is.
>
> --
>
> Keith Doyle
> (remove underbars in reply address for E-mail)
>
> Ignorance is the soil in which belief in miracles grows.
> -- Robert G. Ingersoll
--
Jack King
> Jack King wrote:
>
> > Adam Noel Harris wrote:
> >
> >
> > Considering how trivial the differences in morphology usually are
> > between well defines species today, taking in account all the modifications
> > necessary to convert a land mammal into a whale -- forelimb modifications,
> > the evolution of tail flukes, the streamlining, reduction of hindlimbs,
> > modifications of skull to bring nostrils to the top of the head,
> > modification of trachea, modifications of behavior patterns, specialized
> > nipples so that the young could feed underwater (a complete list would
> > be enormous) -- one is inclined to think in terms of possibly hundereds,
> > even thousands of transitional species on the most direct path between
> > a hypothetical land ancestor and the common ancestor of modern whales.
>
> Doesn't strike you as odd, then, that all of the skeletal transitions you mention
> are found in the fossil record, right around the time we would expect to
> find them? For example: shortening of limbs, movement of nostrils to top
> of head, changes to vertebrae consistent with freeing spine for propulsion,
The so-called sequence [Carnivora (small land mammal) -->Pakicetus-->Ambulocetus
-->Rodhocetus kasrani (about 10' long) -->Indocetus ramani-->Basilosaurus] is
taking a half truth of vaguely similar structures which can easily be explained by
convergence, and worshiping as a full blown reality. These were independently
birthed creatures.
Let's look at Exhibit A. In the early Cambrian we see the sudden appearance of
all the major phyla we see today. Burgessochaeta, Dinomischus, Pikaia, Anomalocaris,
Marrella, etc, etc...Totally new unique creatures and unrelated to one another. Where
is the common descent?
>
> > With gene duping all you are doing is copying a genetic subroutine (say for
> > a limb), to another part of the master genetic "program". Nothing new has
> > been created. You simply end up with a duplicate of an already existing
> > organ. It is truely amazing how people can possible conceive that this is
> > actually a mechanism of evolution. The only reason why they keep pounding
> > this drum is because they have very little else.
>
> In the problems for whale evolution you listed, there are no new organs.
> Mostly its just rearranging the skeleton. Tail flukes? Just big slabs of meat
> on the tail. The specialized nipples? Nothing new there, except for a little
> pressure. They're all just modifications. Now, I'm sure that there are some
> new features, (the melon, perhaps), but the majority of the change does not
> involve anything "new".
Unlike the so-called transition from reptile to mammal, the morphing of one
mammal to another kind of mammal would not be as profound. But the True
Believers don't even flinch when they make their assumptions. They picture
bones being re-arranged as if we were like watching the morphing going on
in American Werewolf in Paris. If a Fundy showed that kind of Faith, he
would be laughed out of this News group.
>
> >
> > The genetic barriers is demonstrated time & time again in breeding. Now why
> > don't you provide the evidence that these rigid barriers crumble away in the
> > face of a very rare cumulative mutations which are lucky enough to land in
> > coding regions of germ cells which happen to slip by corrective enzymes, and
> > which do not turn out to be deliterious or neutral.
>
> Would a mutation to a mosquito that allows it to live through pesticides count?
> Note that in humans this is the equivalent of being able to breath nerve gas. If
> this is not a novel and beneficial feature, I don't know what is. If not, why not?
It could have been a mutation, sure. Just as Sickle Cell Anemia helps Africans
better survive Malaria. So your point is?
> How about the one mutation to a hox gene that converts a fin into a primitive
> hand?
Hox genes simply determine when a particular group of genes are expressed during
development. I have never heard of any mutation of the homebox converting
a fin into a hand. Please give me a reference as I'de love to read about it. It
is fairly easy, however to do gene duping of the hox which will result in a second
fin. Nothing new or profound about duping already existing organs.
Felipe
Jack King <jack...@nortelnetworks.com> wrote in message
news:37FCA974...@nortelnetworks.com...
> Ian Musgrave & Peta O'Donohue wrote:
>
> >
> > >
> > > The deletion of a nucleotide will lead to a frameshift. It is
> > > virtially always lethal. But for the sake of argument, let's say
> > > that it is not repaired by corrective enzymes, and it results in a
> > > "nylon hydrolysis enzyme".
> >
> > Oh, but it does happen, see
> >
> > Ohno S. (1984 Apr). Birth of a unique enzyme from an alternative
> > reading frame of the preexisted, internally repetitious coding sequence.
> > Proc Natl Acad Sci U S A , 81, 2421-5.
>
> My statement stands. A frameshift is lethal virtually 100% of the time.
> Are you disputing that? If so, than please see _The New Healers_; p. 53,
54;
> William Clark
I just want to point out that this is different than your original claim
that "a deletion of a nucleotide will lead to a frame shift. It is
virtually always lethal." If you had originally meant that frame shifts
were virtually always lethal (a rather debatable claim in its own right), we
might have expecte you to use "which is virtually always lethal". Your
original claim strongly suggests that deletions are "virtually always
lethal" which simply is not at all true. Likewise, I rather doubt that
frame shifts are "virtually always lethal" for a variety of reasons. They
CAN be lethal, of course, but I wonder if you could suggest a source that
estimates the "virtual 100%" lethality ... ?
> Nonetheless, in spite of the odds, I'm not saying that it is impossible.
I
> also made that clear in my post. It will be so rare, however, that to
assume
> that it is a mechanism of evolution requires faith that only a True
Believer
> can muster.
>
>
> > > Assuming this is a mutation to a germ cell (a very small target
> > > indeed),
> >
> > A germ cell is no smaller target than any other cell,
>
> This has already been discussed in detail with other posters (as have most
> of the other issues you raise in your post). Of course it is no smaller a
target.
> The point is that if it is the ONLY target that has evolutionary
significance
> then the odds of having a mutation that is meaningful is tiny. An
organism
> could experience 100 mutations, and none may affect a germ cell.
Yes, but the mutations people count, i.e. where those estimates of 4-10 new
mutations per individual come from, are heritable ones, ones in the germ
line. People undoubtedly suffer many more than 100 mutations in their
somatic tissues, but they aren't inherited. You might want to review the
literature about how those estimates are obtained. There are very recent
estimates in humans (which are of about the same order of magnitude, IIRC),
but any population genetics text would refer you to the original Drosophila
experiments.
> > and a large number
> > of mutations are copy errors during DNA replication, the rate (roughly
> > 10^-8 per nucleotide) is the same for all cells, and as sperm precursor
> > cells undergo very many replications, the chance of mutation is not so
> > small at all.
>
> Also mentioned in another post. Copying errors result in information
> leakage. There is no way that will end up being an effective evolutionary
> mechanism.
This is an assertion that I think Ian successfully refuted with his
references. How does that crow taste, by the way?
[snip]
> > Our ear bones are modifcations of jaw bones which are modifications of
> > stiffenings for gill arches, and gee, <irony>it would be _so_ hard to
> > get stiffening rods in gill arches via mutation </irony>
>
> We should not forget that one of the main reasons that people are mislead
> that all organisms are related is the genuine relationship among similar
> species of a distinct organism. Despite the fact that most creatures are
> clearly unique and distict, this has been the main reason for the
persistence
> of evolutionary theory.
[snip car example]
Why? All are constrained by the same
> things: gravity and friction. Similar unifying constraints are imposed
> on living things, and the result is inevitable similarities.
Then how would you explain the multiple nested heirarchies among taxonomic
lineages in neutral and unexpressed portions of the genome ... ?
[snip]
Jack King
>
>
> Senapathy is using his advanced degrees in mathematics to convert garbage
> into garbage. Why is he using a model which assembles genetic pathways at
> random and beginning with ten genes? You may think the step-by-step
> gradualism of conventional evolutionary theory is bunk, but if you're
> going to use calculations to dismiss it, they should be calculations which
> address it.
>
> Senapathy is using the "747 in a junkyard" argument on developmental
> genetic pathways, which ignores cumulative selection.
What I posted was just a small snippet of his analysis. He starts out with just
ten genes in the initial analysis and builds upon it. But if you are really interested
in the math, get the book and read it for yourself. If you would then like to
challenge the math, I'de be glad to give you his email address (off-line) and
you can dialog directly with him. I don't claim to have even close to his knowledge
or expertise in molecular biology or mathematics. Given that, if you are truely
interested, make the effort. You may learn something.
>
>
> :You cannot mate Genus Canis with Genus Felis. There is a rigid wall.
>
> SFW? Which part of conventional evolutionary theory requires
> hybridization of diverged species? The rigid wall you describe above has
> NOTHING TO DO with the wall you were talking about earlier, the one
> involving the limit of morphological change a species can undergo.
>
Sorry...it has everything to do with it. Genetic barriers are genetic barriers,
regardless of whether you are talking about the potency of copulation, or
the efficacy of mutations. Macro changes have never been empirically
demonstrated. It has always been assumed that the reason is because there
is not enough time, so in a very unscientific manner, wild assumptions are
made.
> :You can come up with all kinds of natural
> :varients, you can isolate species, you can do whatever you wish. It
> :doesn't change anything. Those barriers do not change just because
> :of mutations. The wall is too high.
>
> Since we never need to cross this wall, how is it relevant? You're
> supposed to be demonstrating the wall between the last common ancestor of
> dogs and cats and the extant groups, not between dogs and cats themselves.
Here all along I'm stating loud and clear that common descent is a sham, and
now you make a statement like the above? Perhaps I'm misunderstanding
your question.
>
>
> :> Mutation builds on prior adaptions, and that's not something you can
> :> simply wave your hands over and say only "natural variants" are allowed.
> :
> :And you cannot simply wave your hand and say mutations are the magic
> :bullet. You simply assume it is because there is nothing else.
>
> I accept mutation as the means for producing divergence over time because
> it is an observable mechanism and it is adequate. It is not that I assume
> that there is nothing else; it's that nothing else appears to be needed
> nor plausible. Did you have something in mind? How are genomes created
> under Senapathy's model?
For those that believe in common descent, mutations are the whole ball game.
Senapathy's model claims independent births. There are also holes in Senapath's
overall thesis, but they are not nearly as wide as common descent.
> :
> : Considering how trivial the differences in morphology usually are
> :between well defines species today, taking in account all the modifications
> :necessary to convert a land mammal into a whale -- forelimb modifications,
> :the evolution of tail flukes, the streamlining, reduction of hindlimbs,
> :modifications of skull to bring nostrils to the top of the head,
> :modification of trachea, modifications of behavior patterns, specialized
> :nipples so that the young could feed underwater (a complete list would
> :be enormous) -- one is inclined to think in terms of possibly hundereds,
> :even thousands of transitional species on the most direct path between
> :a hypothetical land ancestor and the common ancestor of modern whales.
>
> No comment. I'm arguing beyond my field.
And your field is?
>
> :
> :With gene duping all you are doing is copying a genetic subroutine (say for
> :a limb), to another part of the master genetic "program". Nothing new has
> :been created. You simply end up with a duplicate of an already existing
> :organ. It is truely amazing how people can possible conceive that this is
> :actually a mechanism of evolution. The only reason why they keep pounding
> :this drum is because they have very little else.
>
> Your amazement aside, what might the "natural variants" of the new limb or
> organ look like? What sort of limits to changes in size, shape, and
> function are there? Since you haven't established where the barrier is
> yet, I don't see why "natural variants" cannot be selected to form a
> flipper from a leg.
Let me give you a simple example and then let you use your imagination.
Breed a German Shepard with a large Poddle. Think of the possibilities
for change. Lots of nice varients here. But there are clear rigid limits to
that change, correct?
> :The genetic barriers is demonstrated time & time again in breeding. Now why
> :don't you provide the evidence that these rigid barriers crumble away in the
> :face of a very rare cumulative mutations which are lucky enough to land in
> :coding regions of germ cells which happen to slip by corrective enzymes, and
> :which do not turn out to be deliterious or neutral.
>
> You overstate the degree of luck necessary, because you don't have an
> appreciation of real mutation rates. Are you, above, accepting the
> barriers I described or not? If you're still talking about the inability
> of diverged species to interbreed, then I don't need to describe any
> crumbling - these barriers do not need to be overcome.
OK. You've made a pretty bold claim. The above must be based on some
emperical data. We can show experimentally that genetic barriers exist.
You are claiming that they crumble in the face of mutations. Please cite
the reference which proves your point above.
> :> But how "unique?" Why do the bone morphogenetic proteins in vertebrates
> :> have counterparts in invertebrates that function in similar developmental
> :> genetic pathways, have similar primary sequences, and in some cases can be
> :> substituted for each other in transgenic animals? Seems more like these
> :> complex genetic networks are repititions of simpler networks.
> :
> :Spoken like a True Believer. Vertebrates first appeared very suddenly circa
> :400+ mya. The first appearance of this group was already highly differentiated.
> :None of them could be considered remotely intermediate to the other. We see the
> :same thing with invertebrates during the Cambrian explosion. At that time virtually
> :every known phyla was birthed. Phyla are completely unconnected at the top
> :of the taxonomical hierarchy. Please explain the common descent.
>
> Please address my point.
Because vertebrates come from a common templete. We see similarities all
over the place in nature among totally unrelated creatures. The forelimbs of
a mole, and a molecricket look similar. Does that mean they are related?!
> You call it "faith" when I argue that new
> developmental genetic networks are natural variants of older ones, then
> when I bring up real world observation of what might have been considered
> entirely different networks, you jump to the Cambrian explosion. I know
> that together with your rigid barriers, introns, and DNA repair mechanisms
> that the Cambrian is one of your favorite topics, but why not deal with
> what I wrote? Given DNA and protein homologies, the Cambrian "problem"
> looks like an artefact of fossilization. The phyla _are_ connected by
> sequence homology.
What in heavens name are you talking about?! We have zero soft tissue
from Cambrian. Please justify your statement of how you can demonstrate
the connection between all the phyla we see suddenly appear. By definition
phyla are totally distinct. And yet there they are, suddenly appearing in
the fossil record. But you must have some great new data. Show how Chordates
are related to Arthropods and Gastropods and Annelids and etc, etc
<snip circular arguments>
Clark Dorman
Jack King <jack...@nortelnetworks.com> writes:
> Michael wrote:
> > Jack King wrote:
> > > Adam Noel Harris wrote:
>> Doesn't strike you as odd, then, that all of the skeletal
>> transitions you mention are found in the fossil record, right
>> around the time we would expect to find them? For example:
>> shortening of limbs, movement of nostrils to top of head,
>> changes to vertebrae consistent with freeing spine for
>> propulsion,
>
> The so-called sequence [Carnivora (small land mammal)
> -->Pakicetus-->Ambulocetus -->Rodhocetus kasrani (about 10'
> long) -->Indocetus ramani-->Basilosaurus] is taking a half
> truth of vaguely similar structures which can easily be
> explained by convergence, and worshiping as a full blown
> reality. These were independently birthed creatures.
Independently from where? And where did modern whales come from?
The point is that we don't find _Basilosaurus_ in older or newer
strata. So, either it evolved from something, or it appeared out
of nowhere, or somehow we have just completely missed the fossils
of them in other strata. Which do you think the explanation is?
The same argument applies to most fossils in the fossil record.
They occur in limited ranges of strata. How do you think they
got there? I think they evolved from earlier life forms.
--
Clark
howard hershey
>
> Jack King <jack...@nortelnetworks.com> wrote in message
> news:37FCA974...@nortelnetworks.com...
> >
> > >
> > > >
> > > > The deletion of a nucleotide will lead to a frameshift. It is
> > > > virtially always lethal. But for the sake of argument, let's say
> > > > that it is not repaired by corrective enzymes, and it results in a
> > > > "nylon hydrolysis enzyme".
> > >
> > > Oh, but it does happen, see
> > >
> > > Ohno S. (1984 Apr). Birth of a unique enzyme from an alternative
> > > reading frame of the preexisted, internally repetitious coding sequence.
> > > Proc Natl Acad Sci U S A , 81, 2421-5.
> >
> > My statement stands. A frameshift is lethal virtually 100% of the time.
> > Are you disputing that? If so, than please see _The New Healers_; p. 53,
> 54;
> > William Clark
>
> that "a deletion of a nucleotide will lead to a frame shift. It is
> virtually always lethal."
Frame shift mutations *almost* always result in a *loss-of-function*
mutation for the allele that has the mutation. Loss-of-function means
that that sequence no longer produces a functional product. [Some frame
shift mutations can result in a gain-of-function, often because the
partial protein made interferes with the normal protein's function. The
nylon digesting gene is another example of a gain-of-function.] Most
loss-of-function mutations, regardless of whether they are due to
frameshift, deletion, insertion, or point mutation, are phenotypically
recessive. That is, no phenotypic effect at all is observed unless the
mutation is rendered homozygous with another loss-of-function allele
(not necessarily an identical mutation). [There are exceptions to all of
these points.] *Lethality* is *not* a necessary or even common
consequence of a loss-of-function mutation, even when the mutant
phenotype is expressed (that is, typically, made homozygous). *Some*
loss-of-function mutations, indeed, are, in particular environmental
circumstances, selectively favored, as in the eyeless cave fish, certain
neotenous salamanders, various forms of resistance to toxins,
antibiotics, and pesticides due to loss of particular receptors. Please
try to distinguish between loss-of-function and lethality, at the very
least.
> If you had originally meant that frame shifts
> were virtually always lethal (a rather debatable claim in its own right), we
> might have expecte you to use "which is virtually always lethal". Your
> original claim strongly suggests that deletions are "virtually always
> lethal" which simply is not at all true. Likewise, I rather doubt that
> frame shifts are "virtually always lethal" for a variety of reasons. They
> CAN be lethal, of course, but I wonder if you could suggest a source that
> estimates the "virtual 100%" lethality ... ?
I too suspect someone is unable to distinguish between loss-of-function
and lethality and doesn't understand diploid genetics (with its
homozygosity and heterozygosity).
>
> > Nonetheless, in spite of the odds, I'm not saying that it is impossible.
> I
> > also made that clear in my post. It will be so rare, however, that to
> assume
> > that it is a mechanism of evolution requires faith that only a True
> Believer
> > can muster.
Is every genetic disease lethal? Is every genetic variation lethal?
> >
[snip]
Clark Dorman
jmgo...@aol.com (JMGoodguy) writes:
> >including the jawbone to inner ear bone transition-- a modification of
> >an existing structure for a completely unrelated function. No observable
> >"barriers" her
>
Which part? That mammals evolved from synapsid reptiles? See:
http://www.talkorigins.org/faqs/faq-transitional/part1b.html#mamm
It has discussions of the inner ear parts (coming from the jaw)
in there. If you want pictures of them, no that's not there,
you'll have to go to the primary literature (cited in the FAQ).
--
Clark Dorman "Evolution is cleverer than you are."
http://cns-web.bu.edu/pub/dorman/D.html -Francis Crick
Jack King
>
> > The so-called sequence [Carnivora (small land mammal)
> > -->Pakicetus-->Ambulocetus -->Rodhocetus kasrani (about 10'
> > long) -->Indocetus ramani-->Basilosaurus] is taking a half
> > truth of vaguely similar structures which can easily be
> > explained by convergence, and worshiping as a full blown
> > reality. These were independently birthed creatures.
>
> Independently from where? And where did modern whales come from?
>
> The point is that we don't find _Basilosaurus_ in older or newer
> strata. So, either it evolved from something, or it appeared out
> of nowhere, or somehow we have just completely missed the fossils
> of them in other strata. Which do you think the explanation is?
Where did Anomalocaris come from? It appeared out of nowhere in
early Cambrian. The answer is, like Basilosauras, it was independently
birthed with no pre-cursors.
Michael
> Michael wrote:
>
> > Jack King wrote:
> >
> > > Adam Noel Harris wrote:
> > >
> > >
> > > Considering how trivial the differences in morphology usually are
> > > between well defines species today, taking in account all the modifications
> > > necessary to convert a land mammal into a whale -- forelimb modifications,
> > > the evolution of tail flukes, the streamlining, reduction of hindlimbs,
> > > modifications of skull to bring nostrils to the top of the head,
> > > modification of trachea, modifications of behavior patterns, specialized
> > > nipples so that the young could feed underwater (a complete list would
> > > be enormous) -- one is inclined to think in terms of possibly hundereds,
> > > even thousands of transitional species on the most direct path between
> > > a hypothetical land ancestor and the common ancestor of modern whales.
> >
> > Doesn't strike you as odd, then, that all of the skeletal transitions you mention
> > are found in the fossil record, right around the time we would expect to
> > find them? For example: shortening of limbs, movement of nostrils to top
> > of head, changes to vertebrae consistent with freeing spine for propulsion,
>
> The so-called sequence [Carnivora (small land mammal) -->Pakicetus-->Ambulocetus
> -->Rodhocetus kasrani (about 10' long) -->Indocetus ramani-->Basilosaurus] is
> taking a half truth of vaguely similar structures which can easily be explained by
> convergence, and worshiping as a full blown reality. These were independently
> birthed creatures.
OK, explain how they converged (and from what?). I'd also like to hear why they
are in the order that they are in the stratigraphic record.
>
>
> Let's look at Exhibit A. In the early Cambrian we see the sudden appearance of
> all the major phyla we see today. Burgessochaeta, Dinomischus, Pikaia, Anomalocaris,
> Marrella, etc, etc...Totally new unique creatures and unrelated to one another. Where
> is the common descent?
Are you arguing that each phylum was "independently birthed" and evolved form there?
That certainly puts your (Senepathy's?) theory at odds with less of the evidence. If
so
why are we talking about whales? They are obviously all in one phylum.
>
>
> >
> > > With gene duping all you are doing is copying a genetic subroutine (say for
> > > a limb), to another part of the master genetic "program". Nothing new has
> > > been created. You simply end up with a duplicate of an already existing
> > > organ. It is truely amazing how people can possible conceive that this is
> > > actually a mechanism of evolution. The only reason why they keep pounding
> > > this drum is because they have very little else.
> >
> > In the problems for whale evolution you listed, there are no new organs.
> > Mostly its just rearranging the skeleton. Tail flukes? Just big slabs of meat
> > on the tail. The specialized nipples? Nothing new there, except for a little
> > pressure. They're all just modifications. Now, I'm sure that there are some
> > new features, (the melon, perhaps), but the majority of the change does not
> > involve anything "new".
>
> Unlike the so-called transition from reptile to mammal, the morphing of one
> mammal to another kind of mammal would not be as profound. But the True
> Believers don't even flinch when they make their assumptions. They picture
> bones being re-arranged as if we were like watching the morphing going on
> in American Werewolf in Paris. If a Fundy showed that kind of Faith, he
> would be laughed out of this News group.
And oddly enough, we see this morphing unfolding in the fossil record. Of course,
its all just convergent evolution right? Key point, biologists can and do
recognize convergent evolution in other examples -- what are they missing ,
since they don't see the "obvious" convergence in whales?
>
>
> >
> > >
> > > The genetic barriers is demonstrated time & time again in breeding. Now why
> > > don't you provide the evidence that these rigid barriers crumble away in the
> > > face of a very rare cumulative mutations which are lucky enough to land in
> > > coding regions of germ cells which happen to slip by corrective enzymes, and
> > > which do not turn out to be deliterious or neutral.
> >
> > Would a mutation to a mosquito that allows it to live through pesticides count?
> > Note that in humans this is the equivalent of being able to breath nerve gas. If
> > this is not a novel and beneficial feature, I don't know what is. If not, why not?
>
> It could have been a mutation, sure. Just as Sickle Cell Anemia helps Africans
> better survive Malaria. So your point is?
My point is that the magnitude of the change (IIRC the chemical nature of the
nerves was changed) is evidence of the crumbling of your "barriers". Its not
morphologic, but its still a big jump to suddenly be able to breathe nerve gas.
>
>
> > How about the one mutation to a hox gene that converts a fin into a primitive
> > hand?
>
> Hox genes simply determine when a particular group of genes are expressed during
> development. I have never heard of any mutation of the homebox converting
> a fin into a hand. Please give me a reference as I'de love to read about it.
The most readable is _At the Water's Edge_ by Carl Zimmer. Its written for the
general public but does reference the original literature. There is a whole chapter
called "How to Make a Hand". I could probably dig up the original paper refs., if
you really want.
> It
> is fairly easy, however to do gene duping of the hox which will result in a second
> fin. Nothing new or profound about duping already existing organs.
>
If its so easy, why are you arguing about whale evolution? You seem to be really
vague on where these barriers lie. On one hand, you argue that new organs are
impossible, but changes to existing organs are easy. On the other hand, you get
upset about the "morphing" of bones and organs observed in whale evolution.
Can you be more specific?
Mike
Michael
> Clark Dorman wrote:
>
> >
> > > The so-called sequence [Carnivora (small land mammal)
> > > -->Pakicetus-->Ambulocetus -->Rodhocetus kasrani (about 10'
> > > long) -->Indocetus ramani-->Basilosaurus] is taking a half
> > > truth of vaguely similar structures which can easily be
> > > explained by convergence, and worshiping as a full blown
> > > reality. These were independently birthed creatures.
> >
> > Independently from where? And where did modern whales come from?
> >
> > The point is that we don't find _Basilosaurus_ in older or newer
> > strata. So, either it evolved from something, or it appeared out
> > of nowhere, or somehow we have just completely missed the fossils
> > of them in other strata. Which do you think the explanation is?
>
> Where did Anomalocaris come from? It appeared out of nowhere in
> early Cambrian. The answer is, like Basilosauras, it was independently
> birthed with no pre-cursors.
I can maybe see the argument for Anomalocaris, but we do have
good candidates for precursors (or relatives thereof) of basilosaurus. I
suggest you argue for independent birthing of phyla in the Cambrian and
leave it at that (of course, what do you make of the pre-Cambrian life?).
Mike
Jack King
>
> >
> > My statement stands. A frameshift is lethal virtually 100% of the time.
> > Are you disputing that? If so, than please see _The New Healers_; p. 53,
> 54;
> > William Clark
>
> I just want to point out that this is different than your original claim
> that "a deletion of a nucleotide will lead to a frame shift. It is
> virtually always lethal." If you had originally meant that frame shifts
> were virtually always lethal (a rather debatable claim in its own right), we
> might have expecte you to use "which is virtually always lethal". Your
> original claim strongly suggests that deletions are "virtually always
> lethal" which simply is not at all true. Likewise, I rather doubt that
> frame shifts are "virtually always lethal" for a variety of reasons. They
> CAN be lethal, of course, but I wonder if you could suggest a source that
> estimates the "virtual 100%" lethality ... ?
If I delete a nucleotide from a coden, there will always be a frameshift. The
source I cite above states very clearly that it is almost always has negative
implications. Have you checked the cited source? If you have a source that
is disputing that, please cite it.
>
>
> > Nonetheless, in spite of the odds, I'm not saying that it is impossible.
> I
> > also made that clear in my post. It will be so rare, however, that to
> assume
> > that it is a mechanism of evolution requires faith that only a True
> Believer
> > can muster.
> >
> >
> > > > Assuming this is a mutation to a germ cell (a very small target
> > > > indeed),
> > >
> > > A germ cell is no smaller target than any other cell,
> >
> > This has already been discussed in detail with other posters (as have most
> > of the other issues you raise in your post). Of course it is no smaller a
> target.
> > The point is that if it is the ONLY target that has evolutionary
> significance
> > then the odds of having a mutation that is meaningful is tiny. An
> organism
> > could experience 100 mutations, and none may affect a germ cell.
>
> Yes, but the mutations people count, i.e. where those estimates of 4-10 new
> mutations per individual come from, are heritable ones, ones in the germ
> line. People undoubtedly suffer many more than 100 mutations in their
> somatic tissues, but they aren't inherited. You might want to review the
> literature about how those estimates are obtained. There are very recent
> estimates in humans (which are of about the same order of magnitude, IIRC),
> but any population genetics text would refer you to the original Drosophila
> experiments.
>
Yes, poor Drosophila has been bombarded with radiation for decades. We've
mutated the hell out of him. We end up with all kinds of hopeless monsters,
primarily from gene duplications -- antenae growing out of the back, wings
growing out of the head -- a totally disruption of the homebox. If you can tell
me the evolutionary implications of this, I'm all ears.
> > > and a large number
> > > of mutations are copy errors during DNA replication, the rate (roughly
> > > 10^-8 per nucleotide) is the same for all cells, and as sperm precursor
> > > cells undergo very many replications, the chance of mutation is not so
> > > small at all.
> >
> > Also mentioned in another post. Copying errors result in information
> > leakage. There is no way that will end up being an effective evolutionary
> > mechanism.
>
> This is an assertion that I think Ian successfully refuted with his
> references. How does that crow taste, by the way?
Well, I've got one lonely response from someone named Ian which was
basically a repeat of what others had already posted. I also replied to
his post. Your statement above sounds like Sadam Insane declaring victory
in Desert Storm, and withdrawing his troops.
>
>
> Then how would you explain the multiple nested heirarchies among taxonomic
> lineages in neutral and unexpressed portions of the genome ... ?
I've seen these esoteric sentence expressed many times in this newsgroup.
Looks like a cut and paste. Do you really know what it means? At any rate,
organisms are taxonomically grouped based on evolutionary connections
among them. Organisms are classified into sets of similar organisms first.
These groups are further arranged in a nested manner based on assumed
evolutionary connections -- species into genus, genera into a family, famlies
into an order, etc. However, the larger groupings, or the "higher taxa" are
found to be unconnectable! If there is common descent, then why such huge
gulfs between phyla?
Stephen F. Schaffner
Jack King <jack...@nortelnetworks.com> wrote:
>Clark Dorman wrote:
>
>>
>> > The so-called sequence [Carnivora (small land mammal)
>> > -->Pakicetus-->Ambulocetus -->Rodhocetus kasrani (about 10'
>> > long) -->Indocetus ramani-->Basilosaurus] is taking a half
>> > truth of vaguely similar structures which can easily be
>> > explained by convergence, and worshiping as a full blown
>> > reality. These were independently birthed creatures.
>>
>> Independently from where? And where did modern whales come from?
>>
>> The point is that we don't find _Basilosaurus_ in older or newer
>> strata. So, either it evolved from something, or it appeared out
>> of nowhere, or somehow we have just completely missed the fossils
>> of them in other strata. Which do you think the explanation is?
>
>Where did Anomalocaris come from? It appeared out of nowhere in
>early Cambrian. The answer is, like Basilosauras, it was independently
>birthed with no pre-cursors.
Was every species independently "birthed" (whatever that might mean)?
If so, why do species tend to look so much like other
independently-birthed species that were around just before their
birth? And why do independently birthed species on islands, say, look
so much like other independently birthed species on the same island,
and not like independently birthed species on the mainland?
-------
Steve Schaffner s...@genome.wi.mit.edu
SLAC and I have a deal: they don't || Immediate assurance is an excellent sign
pay me, and I don't speak for them. || of probable lack of insight into the
|| topic. Josiah Royce
howard hershey
>
> Clark Dorman wrote:
>
> >
> > > The so-called sequence [Carnivora (small land mammal)
> > > -->Pakicetus-->Ambulocetus -->Rodhocetus kasrani (about 10'
> > > long) -->Indocetus ramani-->Basilosaurus] is taking a half
> > > truth of vaguely similar structures which can easily be
> > > explained by convergence, and worshiping as a full blown
> > > reality. These were independently birthed creatures.
> >
> > Independently from where? And where did modern whales come from?
> >
> > The point is that we don't find _Basilosaurus_ in older or newer
> > strata. So, either it evolved from something, or it appeared out
> > of nowhere, or somehow we have just completely missed the fossils
> > of them in other strata. Which do you think the explanation is?
>
> Where did Anomalocaris come from? It appeared out of nowhere in
> early Cambrian.
What features of an anomalocaris precursor species would be readily
fossilizable? How frequent are complete anomalocaris fossils?
> The answer is, like Basilosauras, it was independently
> birthed with no pre-cursors.
Basilosaurus, then, would be poofed into existence at a different point
in the fossil record. And Basilosaurus does have potential precursors
that left a fossil record. Are you imagining that each organism was
created in a magical poof of creative smoke at all these different times
in the fossil record? Sort of like a travelling magic show (Dr.
Pangloss's Magic Species-Making Show and Longevity Elixir) over the
millenia of the earth's time and space. Here, at this time, a burst of
creative poofing, followed by irregular new poofings and dissappearances
here and there over both time and space. Then a major removal of
organisms at this time followed by another burst of species poofings.
Yes, I agree that one can certainly read the fossil record that way...if
you are totally unconcerned that every time a new species appears in the
record you have to posit another magical poofing and presume, in the
cases with the best preserved record, that each new poof was based on
the model of a previously existing poofed species. Here a poof. There a
poof. Everywhere a poof, poof.
Now this 'irregularly-poofed-into-existence-over-the-aeons' model is
decidedly non-Biblical, but I am sure that doesn't trouble you a bit,
since you are only logically deducing this model from the evidence and
facts alone rather than from some deep-rooted belief in the words on
particular pages.
Oh, and there is that persistent nasty problem of the appearance of
common descent in the molecular sequences of the survivors. But I guess
if you are positing the 'poofed-into-existence' mechanism there is
nothing preventing Dr. Pangloss from poofing in the appearance of common
descent into the DNA.
Clark Dorman
Jack King <jack...@nortelnetworks.com> writes:
> Clark Dorman wrote:
> > > The so-called sequence [Carnivora (small land mammal)
> > > -->Pakicetus-->Ambulocetus -->Rodhocetus kasrani (about 10'
> > > long) -->Indocetus ramani-->Basilosaurus] is taking a half
> > > truth of vaguely similar structures which can easily be
> > > explained by convergence, and worshiping as a full blown
> > > reality. These were independently birthed creatures.
> >
> > Independently from where? And where did modern whales come from?
> >
> > The point is that we don't find _Basilosaurus_ in older or newer
> > strata. So, either it evolved from something, or it appeared out
> > of nowhere, or somehow we have just completely missed the fossils
> > of them in other strata. Which do you think the explanation is?
>
> Where did Anomalocaris come from?
If we knew, it wouldn't be called Anomalocaris :-)
For a discussion of the fossils found in Cambrian and
pre-Cambrian times, I can only refer you to Andrew MacRae's post
http://x32.deja.com/getdoc.xp?AN=410067902&CONTEXT=939395174.1132462209&hitnum=0
and the following discussion. But, I thought we were discussing
whale evolution (or their non-evolution).
> It appeared out of nowhere
> in early Cambrian. The answer is, like Basilosauras, it was
> independently birthed with no pre-cursors.
So, your position is that Basilosaurs was 'independently birthed'
from nothing about 45 million years ago and then it died out.
Is the same true for the Mesonychids, Pakicetus, Ambulocetus,
Rodhocetus, Indocetus and modern whales? That is, somebody or
something 'independently birthed' them, but at different times,
and they sequentially died out?
And that the sequence of 'independently birthed' creatures just
happens to look vaguely like evolution towards modern whales?
I'm trying to put myself in your mindset. It might make some
sense that something or somebody who is doing 'independent
birthing' of creatures might try a shotgun approach to life. The
'independent birther' might try a wide variety of body structures
and something like the Cambrian explosion might result.
Alternately, a wide variety of independently evolved organisms (a
la Senapathy) might develop at about the same time, especially if
there is large-scale transfer of whatever allows them to develop
more complex bodies. But, the idea that a succession of similar
but different creatures somehow appeared 'independently birthed'
at different times, but in a pattern that just happens to fit an
evolutionary hypothesis seems absurd.
Jack King
>
> > Where did Anomalocaris come from? It appeared out of nowhere in
> > early Cambrian. The answer is, like Basilosauras, it was independently
> > birthed with no pre-cursors.
>
> I can maybe see the argument for Anomalocaris, but we do have
> good candidates for precursors (or relatives thereof) of basilosaurus.
Of course there are "candidates". Those who are tied into a lockstep
belief of common descent have no choice but to come up with something.
> I
>
> suggest you argue for independent birthing of phyla in the Cambrian and
> leave it at that (of course, what do you make of the pre-Cambrian life?).
So...Basilosaurus was extant some 40 mya. Are you saying that common
descent only applied to that time frame and not further back?!!!
Rich Daniel
> Felipe wrote:
[...]
>> Then how would you explain the multiple nested heirarchies among taxonomic
>> lineages in neutral and unexpressed portions of the genome ... ?
> I've seen these esoteric sentence expressed many times in this newsgroup.
> Looks like a cut and paste. Do you really know what it means?...
http://www.talkorigins.org/faqs/molecular-genetics.html
--
Rich Daniel
Jack King
>
> > The so-called sequence [Carnivora (small land mammal) -->Pakicetus-->Ambulocetus
> > -->Rodhocetus kasrani (about 10' long) -->Indocetus ramani-->Basilosaurus] is
> > taking a half truth of vaguely similar structures which can easily be explained by
> > convergence, and worshiping as a full blown reality. These were independently
> > birthed creatures.
>
> OK, explain how they converged (and from what?).
A shark is very similar looking to a dolphin and both birds and bats fly. In both
examples they are totally unrelated, but nonetheless have many similar features.
This is the trap that palentologists often put themselves in. If they had the luxury
of examining soft body tissue where 95% of the biology lies, they would come up
with totally different conclusions.
> I'd also like to hear why they
> are in the order that they are in the stratigraphic record.
They were simply birthed in different epics.
> >
> > Let's look at Exhibit A. In the early Cambrian we see the sudden appearance of
> > all the major phyla we see today. Burgessochaeta, Dinomischus, Pikaia, Anomalocaris,
> > Marrella, etc, etc...Totally new unique creatures and unrelated to one another. Where
> > is the common descent?
>
> Are you arguing that each phylum was "independently birthed" and evolved form there?
Yes and no. They were independently birthed. Most of them died out. There may
have been micro changes through natural variation, but there is no common
descent. This thesis is the only why that the sudden appearance of totally new
unique creatures can be explained.
>
> >
> > Unlike the so-called transition from reptile to mammal, the morphing of one
> > mammal to another kind of mammal would not be as profound. But the True
> > Believers don't even flinch when they make their assumptions. They picture
> > bones being re-arranged as if we were like watching the morphing going on
> > in American Werewolf in Paris. If a Fundy showed that kind of Faith, he
> > would be laughed out of this News group.
>
> And oddly enough, we see this morphing unfolding in the fossil record.
No.. You are pasteing together a sequence which you think is common descent.
For creature A to have similar features as creature B is what would be expected
from being burped out of a similar pond.
>
> > It could have been a mutation, sure. Just as Sickle Cell Anemia helps Africans
> > better survive Malaria. So your point is?
>
> My point is that the magnitude of the change (IIRC the chemical nature of the
> nerves was changed) is evidence of the crumbling of your "barriers". Its not
> morphologic, but its still a big jump to suddenly be able to breathe nerve gas.
Let's ignore the possibility that a certain strain of mosquito with resistence did not
already exist, and then natural selection resulted in that strain proliferating. Let's
assume it was a mutation. We still have a mosquito that is 99.999% the same as
all the other ones. A point mutation may have changed just one little amino
acid into another one, and somehow that enabled him to survive. This is a natural
varient. Big deal.
>
> > Hox genes simply determine when a particular group of genes are expressed during
> > development. I have never heard of any mutation of the homebox converting
> > a fin into a hand. Please give me a reference as I'de love to read about it.
>
> The most readable is _At the Water's Edge_ by Carl Zimmer. Its written for the
> general public but does reference the original literature. There is a whole chapter
> called "How to Make a Hand". I could probably dig up the original paper refs., if
> you really want.
On your advise, I just ordered it from Amazon.com. Of course I will be unable to
comment on your claim as it will take me a few weeks to read it. But if you want
to continue a dialog in this thread, why don't you cite the specific in context quotes
and page references from his book which deal with homebox mutations making a fin
into a hand? I do this all the time. By quoting the material from a respected scientist,
it very powerfully makes your point.
> > It
> > is fairly easy, however to do gene duping of the hox which will result in a second
> > fin. Nothing new or profound about duping already existing organs.
> >
>
> If its so easy, why are you arguing about whale evolution? You seem to be really
> vague on where these barriers lie.
Because to go from a huge water going bohemouth from a small land mammal
requires much more than duplicating an already extant appendage.
> On one hand, you argue that new organs are
> impossible, but changes to existing organs are easy.
Natural minor varients are easy. You don't even need mutations. Just cross over
genes between two similar breeding species.
Michael
> Michael wrote:
>
> >
> > > Where did Anomalocaris come from? It appeared out of nowhere in
> > > early Cambrian. The answer is, like Basilosauras, it was independently
> > > birthed with no pre-cursors.
> >
> > I can maybe see the argument for Anomalocaris, but we do have
> > good candidates for precursors (or relatives thereof) of basilosaurus.
>
> Of course there are "candidates". Those who are tied into a lockstep
> belief of common descent have no choice but to come up with something.
Yet these "candidates" have almost exactly what we would expect from
such transitionals. If they are truly "independently birthed" there is no
reason they should be there at all much less in the order that they are.
Does
your theory address this? IIRC you do claim that animals are similar
temporally because content of the "pools" (am I getting this right?) changes
slowly over time. But this does not explain why fossils tend to be in the
exact order that they are (why, for example does Ambulocetus come
before Basilosaurus?).
>
>
> > I
> >
> > suggest you argue for independent birthing of phyla in the Cambrian and
> > leave it at that (of course, what do you make of the pre-Cambrian life?).
>
> So...Basilosaurus was extant some 40 mya. Are you saying that common
> descent only applied to that time frame and not further back?!!!
No, go back farther. I am saying that based on the lack of ancestor claims,
you should propose independent birthing of each phylum 500mya, with
evolution creating everything since then. That, at least would not ignore
the bulk of fossil evidence as your present assertions do.
Mike
Michael
> Michael wrote:
>
> >
> > > The so-called sequence [Carnivora (small land mammal) -->Pakicetus-->Ambulocetus
> > > -->Rodhocetus kasrani (about 10' long) -->Indocetus ramani-->Basilosaurus] is
> > > taking a half truth of vaguely similar structures which can easily be explained by
> > > convergence, and worshiping as a full blown reality. These were independently
> > > birthed creatures.
> >
> > OK, explain how they converged (and from what?).
>
> A shark is very similar looking to a dolphin and both birds and bats fly. In both
> examples they are totally unrelated, but nonetheless have many similar features.
> This is the trap that palentologists often put themselves in. If they had the luxury
> of examining soft body tissue where 95% of the biology lies, they would come up
> with totally different conclusions.
That's not what I asked. I asked how did your examples converge. But since
you brought it up. Notice that even though the shark is superficially very like
the dolphin, and birds are like bats, biologists can recognize that they are not
closely related. They can even make this identification from fossil remains
as well. So what are they missing in the whale fossils? Be specific.
>
>
> > I'd also like to hear why they
> > are in the order that they are in the stratigraphic record.
>
> They were simply birthed in different epics.
How does that predict the extent to which the classification of animals
matches with the fossil record? I would think it the two would not agree
as well as they do under your theory.
Big deal. Man and Chimp share 99+% of their genes and neither breathe
nerve gas. Only 50 genes are different, IIUC. How did man and chimp get such
closely related genes, yet other things "birthed" at about the same time got so
few in common?
>
>
> >
> > > Hox genes simply determine when a particular group of genes are expressed during
> > > development. I have never heard of any mutation of the homebox converting
> > > a fin into a hand. Please give me a reference as I'de love to read about it.
> >
> > The most readable is _At the Water's Edge_ by Carl Zimmer. Its written for the
> > general public but does reference the original literature. There is a whole chapter
> > called "How to Make a Hand". I could probably dig up the original paper refs., if
> > you really want.
>
> On your advise, I just ordered it from Amazon.com. Of course I will be unable to
> comment on your claim as it will take me a few weeks to read it. But if you want
> to continue a dialog in this thread, why don't you cite the specific in context quotes
> and page references from his book which deal with homebox mutations making a fin
> into a hand? I do this all the time. By quoting the material from a respected scientist,
> it very powerfully makes your point.
It'll take a couple of days, you really need most of the chapter for context, I'm having
trouble finding pithy quotes that don't need pages of context. That and they actually
expect me to work around here. :)
>
>
> > > It
> > > is fairly easy, however to do gene duping of the hox which will result in a second
> > > fin. Nothing new or profound about duping already existing organs.
> > >
> >
> > If its so easy, why are you arguing about whale evolution? You seem to be really
> > vague on where these barriers lie.
>
> Because to go from a huge water going bohemouth from a small land mammal
> requires much more than duplicating an already extant appendage.
That's true, its mostly reshaping existing ones. And this reshaping is found in the
fossil record.
Mike
Stephen F. Schaffner
Jack King <jack...@nortelnetworks.com> wrote:
>
>A shark is very similar looking to a dolphin and both birds and bats fly. In both
>examples they are totally unrelated, but nonetheless have many similar features.
>This is the trap that palentologists often put themselves in. If they had the luxury
>of examining soft body tissue where 95% of the biology lies, they would come up
>with totally different conclusions.
Do you really think that paleontologists would group dolphins and sharks
together, or birds and bats, if they only had skeletons to go by? This
is simply ridiculous. You don't have any idea how paleontologists work,
do you?
Adam Noel Harris
:Adam Noel Harris wrote:
Jack, feel free to snip irrelevant or old material in order to make the
posts more manageable. But please, mark snips which remove content (I
freely snip sigs and blank lines without marking). TIA.
[...]
:> Senapathy is using the "747 in a junkyard" argument on developmental
:> genetic pathways, which ignores cumulative selection.
:
:What I posted was just a small snippet of his analysis. He starts out
:with just ten genes in the initial analysis and builds upon it.
He's starting out with too many. The conventional model should be that
genetic networks are built one gene at a time. If Senapathy wants to show
that a particular ten-gene network is unlikely to spring forth in an
independent birth, that's fine. But you shouldn't use his arguments (or
he shouldn't use them, if he is) to address the conventional model.
Again, he ignores cumulative selection.
:But if you are really interested in the math, get the book and read it
:for yourself.
I don't really understand what his ideas are, but from what I have read
(mostly from your posts in the past), they are pretty kooky. I will
consider getting the book, but a summary of his ideas from you would be
nice. If you can present math from the book that is relevant, do so.
Otherwise I think we're going to be arguing past one another.
[snip]
[about lack of hybridization between cats and dogs]
:> SFW? Which part of conventional evolutionary theory requires
:> hybridization of diverged species? The rigid wall you describe above has
:> NOTHING TO DO with the wall you were talking about earlier, the one
:> involving the limit of morphological change a species can undergo.
:>
:
:Sorry...it has everything to do with it.
Then we have a major communication impasse. I still contend it has
nothing to do with it.
:Genetic barriers are genetic barriers, regardless of whether you are
:talking about the potency of copulation, or the efficacy of mutations.
One genetic barrier is the ability for two groups which have been evolving
through mutation, selection, and drift as separate lineages for some
amount of time such that they no longer are compatible at breeding, and
the other genetic barrier is meant to describe the limit to how much a
single lineage can evolve away from some arbitrary starting point.
They are different. Honest. :)
:Macro changes have never been empirically
:demonstrated. It has always been assumed that the reason is because there
:is not enough time, so in a very unscientific manner, wild assumptions are
:made.
Common descent is not a wild assumption, nor unscientific, since it best
explains rich sets of observations (e.g. genetic similarities). The idea
that currently observable mechanisms of change were also responsible for
historical modifications during descent is conservative, not wild. Wild
assumptions would be that novel, unobserved, and theoretically implausible
mechanisms are responsible.
:> Since we never need to cross this wall, how is it relevant? You're
:> supposed to be demonstrating the wall between the last common ancestor of
:> dogs and cats and the extant groups, not between dogs and cats themselves.
:
:Here all along I'm stating loud and clear that common descent is a sham, and
:now you make a statement like the above? Perhaps I'm misunderstanding
:your question.
I know you don't accept common descent. One of your arguments against
common descent appears to be the inability of the proposed mechanisms
(mutation, selection, drift) to allow for descent because there are rigid
genetic barriers to change. If that is indeed what you are trying to
argue, then I am telling you that you are trying to establish your barrier
in the wrong place.
I claim: ---------> cats
LCA|
---------> dogs
Your claim appears to be that there is a barrier to change that the above
would have to cross to become true. Such a barrier would have to be
This: ---X-----> cats
LCA|
---------> dogs
and/or this: ---------> cats
LCA|
---X-----> dogs:
But the barrier you present is that cats and dogs can't interbreed. Well,
my claim doesn't require dogs and cats to interbreed, so what's the
problem?
:> I accept mutation as the means for producing divergence over time because
:> it is an observable mechanism and it is adequate. It is not that I assume
:> that there is nothing else; it's that nothing else appears to be needed
:> nor plausible. Did you have something in mind? How are genomes created
:> under Senapathy's model?
:
:For those that believe in common descent, mutations are the whole ball game.
:Senapathy's model claims independent births. There are also holes in
:Senapath's overall thesis, but they are not nearly as wide as common descent.
Can you summarize his thesis? The bits I have gathered appear to be
riddled with huge holes, so I must not have it right.
:> No comment. I'm arguing beyond my field.
:
:And your field is?
Molecular biology (and genetics).
:> Your amazement aside, what might the "natural variants" of the new limb or
:> organ look like? What sort of limits to changes in size, shape, and
:> function are there? Since you haven't established where the barrier is
:> yet, I don't see why "natural variants" cannot be selected to form a
:> flipper from a leg.
:
:Let me give you a simple example and then let you use your imagination.
:Breed a German Shepard with a large Poddle. Think of the possibilities
:for change. Lots of nice varients here. But there are clear rigid limits to
:that change, correct?
I would expect such a mix to have quite low variation compared to a large
wild wolf population. I would expect that the variation would be used up
quickly during a strict selection regimen. The limit would come when
there was no more useful variation in the population. But, at least in
the case of wolves, there was enough "natural variation" to produce
poodles and german shepards and many many other breeds. These natural
variants were presumably the result of mutation, right? So what is the
barrier that prevents new mutations from accumulating in a population that
has had its variation reduced by selection? That's the barrier you need
to describe.
:> You overstate the degree of luck necessary, because you don't have an
:> appreciation of real mutation rates. Are you, above, accepting the
:> barriers I described or not? If you're still talking about the inability
:> of diverged species to interbreed, then I don't need to describe any
:> crumbling - these barriers do not need to be overcome.
:
:OK. You've made a pretty bold claim. The above must be based on some
:emperical data. We can show experimentally that genetic barriers exist.
:You are claiming that they crumble in the face of mutations. Please cite
:the reference which proves your point above.
The empirical data is that variation has somehow come to exist in the
first place, that species are genetically related, and that mutation is
an observable source of neutral, deleterious, and beneficial variants.
The theory is that the cause of the initial variation was mutation, and
that mutation will continue to produce variation. Since mutation is
observable, the theory is reasonable. And since "natural variants"
include poodles and german shepards from wolves, natural variants which
subsequently accumulate among german shepards might be expected to produce
something even more different.
On the molecular level, morphological variants are thought to be the
result of differences in expression and function of developmentally
active gene products, and rigid barriers are anything but apparent here.
:> Please address my point.
:
:Because vertebrates come from a common templete. We see similarities all
:over the place in nature among totally unrelated creatures. The forelimbs of
:a mole, and a molecricket look similar. Does that mean they are related?!
No closely, no. A better test of relatedness would involve comparing a
good sampling of DNA sequences. We both agree that vertebrates come from
a common template. I think they come from a common ancestral population.
You think they come from (not sure here) the same birthing pool? But my
explanation also accounts for similarities WITHIN vertebrates. Your
independent births from common templates would have to match the
predictions of common ancestry to match the data. I'd be interested in
hearing how it does this.
:> You call it "faith" when I argue that new
:> developmental genetic networks are natural variants of older ones, then
:> when I bring up real world observation of what might have been considered
:> entirely different networks, you jump to the Cambrian explosion. I know
:> that together with your rigid barriers, introns, and DNA repair mechanisms
:> that the Cambrian is one of your favorite topics, but why not deal with
:> what I wrote? Given DNA and protein homologies, the Cambrian "problem"
:> looks like an artefact of fossilization. The phyla _are_ connected by
:> sequence homology.
:
:What in heavens name are you talking about?! We have zero soft tissue
:from Cambrian. Please justify your statement of how you can demonstrate
:the connection between all the phyla we see suddenly appear. By definition
:phyla are totally distinct. And yet there they are, suddenly appearing in
:the fossil record. But you must have some great new data. Show how Chordates
:are related to Arthropods and Gastropods and Annelids and etc, etc
They share a common biochemistry. They share a common genetic code. They
share sequence and functional similarities in their genes. I'm not
talking about extinct phyla, from which there is no DNA evidence. Rather,
I refer to extant organisms representing many of the Cambrian phyla, such
as the ones you list. Apparently you must think they are related too, by
some common template. How does this template work?
:<snip circular arguments>
Is this part of your sig? ;)
Jack King
> Yet these "candidates" have almost exactly what we would expect from
> such transitionals.
What so-called transition fossils we do have, when compared to the
great divisions we see in nature, they are only convincing to
someone already convinced of the reality of organic evolution.
> If they are truly "independently birthed" there is no
> reason they should be there at all much less in the order that they are.
> Does
> your theory address this?
The composition of the pool would obviously change over time. But a creature birthed
say 45 mya would look much more like on birthed 40 mya than one birthed 30 mya.
>
> >
> > So...Basilosaurus was extant some 40 mya. Are you saying that common
> > descent only applied to that time frame and not further back?!!!
>
> No, go back farther. I am saying that based on the lack of ancestor claims,
> you should propose independent birthing of each phylum 500mya, with
> evolution creating everything since then. That, at least would not ignore
> the bulk of fossil evidence as your present assertions do.
Well, at least I have someone in this group conceding at least one creation
event. You're making progress.