When junk DNA isn't junk (was: Letter to the Editor: 'Intelligent design' moves too far from Scripture)
esw...@yahoo.com
news:1116533975.2...@z14g2000cwz.googlegroups.com...
>
> Jason Spaceman wrote:
> > From the article:
> > ---------------------------
> [snip]
> > Yes, there is an Intelligent Designer, DNA proves that. How could
> > the information encoded in DNA "evolve"?
> > -----------------------------
>
> I guess that's why they say "designer" - an engineer wouldn't've put
> junk DNA in there.
Is it truly junk? By using such a term, are we rushing to judgement
before we fully understand the intricacies of DNA? Or do we know all
there is to know already?
For it to be junk, I'd say someone would have to demonstrate it is not
essential. Demonstrating that it doesn't code isn't sufficient because
this assumes we can't learn in the future other functional (e.g.
structural) uses for these portions of the genome in question. I guess
to get through an experiment: remove the alleged junk DNA, inject the
clean DNA into a Zygote, carry it out to birth and see what you get. My
guess is we would quickly discover whether the junk was necessary or
not.
This article claims that "non-coding" is perhaps a better term. I know
many here would eskew it given the source, but they do seem to point to
quite a few studies/findings showing junk DNA to be anything but.
http://www.godandscience.org/evolution/junkdna.html
Any one know of citations debunking the claims made in this article?
snex
Nóbrega, Marcelo A., Yiwen Zhu, Ingrid Plajzer-Frick, Veena Afzal and
Edward M. Rubin, 2004. Megabase deletions of gene deserts result in
viable mice. Nature 431: 988-993.
John Harshman
> "The Last Conformist" <andr...@gmail.com> wrote in message
> news:1116533975.2...@z14g2000cwz.googlegroups.com...
>
>>Jason Spaceman wrote:
>>
>>>From the article:
>>>---------------------------
>>
>>[snip]
>>
>>>Yes, there is an Intelligent Designer, DNA proves that. How could
>>>the information encoded in DNA "evolve"?
>>>-----------------------------
>>
>>I guess that's why they say "designer" - an engineer wouldn't've put
>>junk DNA in there.
>
>
> Is it truly junk? By using such a term, are we rushing to judgement
> before we fully understand the intricacies of DNA? Or do we know all
> there is to know already?
Yes, no, and no.
> For it to be junk, I'd say someone would have to demonstrate it is not
> essential. Demonstrating that it doesn't code isn't sufficient because
> this assumes we can't learn in the future other functional (e.g.
> structural) uses for these portions of the genome in question.
Quite so. Not all non-coding DNA is junk, and that's not the criterion
used to identify junk DNA either.
> I guess
> to get through an experiment: remove the alleged junk DNA, inject the
> clean DNA into a Zygote, carry it out to birth and see what you get. My
> guess is we would quickly discover whether the junk was necessary or
> not.
That sounds very simple, but in fact it's beyond our current technology.
However, nature has kindly carried out similar experiments. There are
some vertebrates, for example, with genomes a tenth the size of the
average mammal's (including humans). Fugu is one such. It has most of
the same genes we do, but 90% of the non-coding DNA is missing. Yet
fugus work just fine. I'm sure that some of the remainder is junk too,
but it clearly demonstrates that most of the human genome is indeed junk.
> This article claims that "non-coding" is perhaps a better term. I know
> many here would eskew it given the source, but they do seem to point to
> quite a few studies/findings showing junk DNA to be anything but.
Non-coding DNA is a different thing from junk DNA. Though most
non-coding DNA is indeed junk, a small proportion of non-coding DNA is
functional; this is well-known, and that proportion has never been
called junk. The way to tell junk from functional DNA is that the
functional DNA is conserved over evolutionary time. Junk is not. There
are some conserved regions whose function is unknown, but nobody calls
them junk. Occasionally a function arises within DNA that was formerly
junk, and it will start being conserved from that point. Also, some DNA
has a bulk function that doesn't depend on its sequence; you may not
want to call that junk, but it's hard to call it functional either.
> http://www.godandscience.org/evolution/junkdna.html
>
> Any one know of citations debunking the claims made in this article?
The easiest thing to do would be to look up the references in the
article and see what they really say. I doubt the authors of the article
intended anyone to understand what they were talking about; they're just
trying to sound impressive.
Ken Shaw
Not this again.
Some sections of DNA which do not code for proteins do appear to have
regulatory functions. Do you know how to identify those sections? Find
the ones highly conserved in the population. Scientists using a
prediction of the ToE identified these sections of non coding DNA and
discovered what they do. No IDist/creationist ideas were involved just
the good old ToE.
Ken
r norman
In addition, consider the puffer fish, Fugu, with about the same
number of genes as a human but only about 1/8th the amount of DNA.
These guys seem to do quite well in the world. So what is that 7/8 of
our DNA doing?
The Fugu Genomics Project
http://www.fugu-sg.org/
http://fugu.hgmp.mrc.ac.uk/
or google on "Fugu genome"
esw...@yahoo.com
news:ifaq819je6lk3kft1...@4ax.com...
This only means it can't be done yet. We should be able to do this
soon, though. Developments just announced today
(http://www.msnbc.msn.com/id/7904332) show remarkable progress in the
swapping of DNA. My proposed experiment would be a natural extention of
this capability and--whether easy or not--would provide a bullet-proof
way for settling the matter.
> >However, nature has kindly carried out similar experiments. There
are
> >some vertebrates, for example, with genomes a tenth the size of the
> >average mammal's (including humans). Fugu is one such. It has most
of
> >the same genes we do, but 90% of the non-coding DNA is missing. Yet
> >fugus work just fine. I'm sure that some of the remainder is junk
too,
> >but it clearly demonstrates that most of the human genome is indeed
junk.
Only if you assume that humans and fugu need the same DNA. We know this
isn't true for functional DNA, so be careful to say it must be true for
what we think is non-functional (junk) DNA. IOW, until we know more,
this is just a tenuous assumption.
> >> This article claims that "non-coding" is perhaps a better term. I
know
> >> many here would eskew it given the source, but they do seem to
point to
> >> quite a few studies/findings showing junk DNA to be anything but.
> >
> >Non-coding DNA is a different thing from junk DNA. Though most
> >non-coding DNA is indeed junk, a small proportion of non-coding DNA
is
> >functional; this is well-known, and that proportion has never been
> >called junk. The way to tell junk from functional DNA is that the
> >functional DNA is conserved over evolutionary time. Junk is not.
How can we really say that? Three things come to mind:
1) Due to random mutations, new junk DNA may crop up (as opposed to
being dropped) over evolutionary time. So evolution may do the very
opposite of what you claim.
2) If there is such a thing as junk DNA, it must be neutral. If so, it
is by definition not affected by natural selection. Only deleterious
and beneficial DNA are. So how can we say evolution will *necessarily*
drop junk DNA over time when it's selection mechanism isn't operational
for neutral features? At best, junk DNA may be dropped accidentally
(randomly), but not in all cases.
3) The fugu allegedly dropped (or didn't add it in the first place?)
this junk DNA, but humans didn't drop it, so how can you really say
that junk DNA gets dropped as a general rule? It may or it may not, if
I understand the evidence you are presenting correctly.
> > There
> >are some conserved regions whose function is unknown, but nobody
calls
> >them junk. Occasionally a function arises within DNA that was
formerly
> >junk, and it will start being conserved from that point. Also, some
DNA
> >has a bulk function that doesn't depend on its sequence; you may not
> >want to call that junk, but it's hard to call it functional either.
> >
> >> http://www.godandscience.org/evolution/junkdna.html
> >>
> >> Any one know of citations debunking the claims made in this
article?
> >
> >The easiest thing to do would be to look up the references in the
> >article and see what they really say. I doubt the authors of the
article
> >intended anyone to understand what they were talking about; they're
just
> >trying to sound impressive.
>
> In addition, consider the puffer fish, Fugu, with about the same
> number of genes as a human but only about 1/8th the amount of DNA.
> These guys seem to do quite well in the world. So what is that 7/8
of
> our DNA doing?
You guys do realize that the Fugu and the puffer fish may not need all
that "junk" DNA, but the same isn't *necessarily* true for humans,
right? To make such a claim given our current understanding would be to
say that we know all there is to know about DNA and how it works.
esw...@yahoo.com
news:0I9je.793162$w62.2...@bgtnsc05-news.ops.worldnet.att.net...
> Not this again.
Sorry.
> Some sections of DNA which do not code for proteins do appear to have
> regulatory functions. Do you know how to identify those sections?
Find
> the ones highly conserved in the population. Scientists using a
> prediction of the ToE identified these sections of non coding DNA and
> discovered what they do. No IDist/creationist ideas were involved
just
> the good old ToE.
I'm not really interested in taking this discussion into a ToE vs. ID
war. But this statement somewhat begs the question. Is it possible we
are declaring those portions of DNA ToE *didn't* predict as non-coding,
yet functional as dead/junk/whatever when if fact they aren't? Note
this wouldn't necessarily say ToE is wrong; it might be that our
understanding of ToE is incomplete and/or our application not entirely
accurate.
Ken Shaw
esw...@yahoo.com wrote:
We understood quite some time ago how to identify the start and stop
codons that delineate a a gene. When complete chromosomes and genomes
started getting sequenced it was discovered that lots of the base pairs
on a chromosome didn't fall into a gene. At first it was assumed that
these sections didn't do anything. The assumption was those stretches
were the remnants of ancient virus insertions are various large scale
duplication mutations that had drifted to a nonfunctional state. Some
scientists noticed that some of these non coding sections were highly
conserved. If these sections were truly junk then the ToE says those
sections should not be conserved so scientists _using a prediction of
the ToE_ investigated further to find out what was happening. It was
then discovered that those highly conserved non coding segments had
regulatory functions.
So the ToE helped us identify those non coding segments regulatory
function. So in this case our understanding of the ToE was neither
incomplete nor was our application inaccurate. As a matter of fact this
simple discovery should put an end to any rational open minded person
having an objection to the ToE. Only because of the ToE did scientists
have any reason to suspect anything unusual was going on with those non
coding segments.
Someone else has pointed you to a study showing that mice with large
amounts of noncoding DNA removed were viable. This indicates to the open
minded that those enormous segments of non coding DNA which are not
highly conserved are non functional.
Ken
Steven J.
<esw...@yahoo.com> wrote in message
news:1116557477.1...@f14g2000cwb.googlegroups.com...-- [snip]
>
>> >Non-coding DNA is a different thing from junk DNA. Though most
>> >non-coding DNA is indeed junk, a small proportion of non-coding DNA
>> > is
>> >functional; this is well-known, and that proportion has never been
>> >called junk. The way to tell junk from functional DNA is that the
>> >functional DNA is conserved over evolutionary time. Junk is not.
>
> How can we really say that? Three things come to mind:
>
> 1) Due to random mutations, new junk DNA may crop up (as opposed to
> being dropped) over evolutionary time. So evolution may do the very
> opposite of what you claim.
>
species (presumably because natural selection removes most mutations to
these sequences), not simply that some string of DNA happens to be there
still. Much of our coding DNA, for example, is so highly conserved that
there are human genes that are recognizably homologous to (and can even
substitute for) fruit fly genes. There is noncoding DNA in mice that is
very similar (in some cases, more similar than some coding DNA) to noncoding
DNA in humans. Presumably this DNA does something important, even if it is
never transcribed into proteins. Conversely, there are stretches of DNA
that are highly variable even between individual humans, and plenty that
vary so much between species that they seem to be under no particular
selective pressure.
>
> 2) If there is such a thing as junk DNA, it must be neutral. If so, it
> is by definition not affected by natural selection. Only deleterious
> and beneficial DNA are. So how can we say evolution will *necessarily*
> drop junk DNA over time when it's selection mechanism isn't operational
> for neutral features? At best, junk DNA may be dropped accidentally
> (randomly), but not in all cases.
>
bet that this is true of some of it), the obviously it must not be removed
automatically by natural selection. For that matter, it has been suggested
that some sequences are parasitic: they're hanging around in our genome, but
only because they're good at getting themselves copied, not because they
help *us* survive natural selection. Again, the statement that only
functional DNA is "conserved" means merely that mutations to nonfunctional
DNA will accumulate at roughly the base mutation rate, not that the DNA will
disappear entirely.
>
> 3) The fugu allegedly dropped (or didn't add it in the first place?)
> this junk DNA, but humans didn't drop it, so how can you really say
> that junk DNA gets dropped as a general rule? It may or it may not, if
> I understand the evidence you are presenting correctly.
>
>
-- [snip]
>
>> In addition, consider the puffer fish, Fugu, with about the same
>> number of genes as a human but only about 1/8th the amount of DNA.
>> These guys seem to do quite well in the world. So what is that 7/8
> of
>> our DNA doing?
>
> You guys do realize that the Fugu and the puffer fish may not need all
> that "junk" DNA, but the same isn't *necessarily* true for humans,
> right? To make such a claim given our current understanding would be to
> say that we know all there is to know about DNA and how it works.
>
noncoding DNA may provide more elaborate regulation of genes, so that pretty
much the same genes can be used in a greater range of ways. But I could be
wrong.
>
>> The Fugu Genomics Project
>> http://www.fugu-sg.org/
>> http://fugu.hgmp.mrc.ac.uk/
>> or google on "Fugu genome"
>
John Harshman
Tonight on "It's the Mind" we feature deja vu, that strange feeling you
sometimes get that you've seen something before.
r norman
<jharshman....@pacbell.net> wrote:
You don't get the deja until you actually do the vu. The trick on this
news group, one that I seem to have perfected, is to quickly scan a
posting without bothering to actually read all the little details
(sometimes called "content"). That makes life a lot easier!
Sorry, John. To the group: John said it first, far more thoroughly,
and far more elegantly.
John Wilkins
...
> Tonight on "It's the Mind" we feature deja vu, that strange feeling you
> sometimes get that you've seen something before.
>
...
Tonight on "It's the Mind" we feature deja vu, that strange feeling you
sometimes get that you've seen something before.
--
John S. Wilkins, Postdoctoral Research Fellow, Biohumanities Project
University of Queensland - Blog: evolvethought.blogspot.com
"Darwin's theory has no more to do with philosophy than any other
hypothesis in natural science." Tractatus 4.1122
Boikat
"John Wilkins" <j.wil...@uq.edu.au> wrote in message
news:d6knh0$1tbm$1...@bunyip2.cc.uq.edu.au...
> John Harshman wrote:
> ...
>
> > Tonight on "It's the Mind" we feature deja vu, that strange feeling you
> > sometimes get that you've seen something before.
> >
>
> ...
>
> Tonight on "It's the Mind" we feature deja vu, that strange feeling you
> sometimes get that you've seen something before.
Stay tuned for last weeks "It's in the mind", when they featured vu deja,
that strange feeling you get that you've never seen anything like that
before.
Boikat
--
<42><
John Harshman
Sure, in theory it could be done. It would just be extraordinarily
tedious, and would require that you do it twice exactly the same in a
diploid cell. Some day it may be practical. But it's hardly necessary.
>>>However, nature has kindly carried out similar experiments. There
>
> are
>
>>>some vertebrates, for example, with genomes a tenth the size of the
>>>average mammal's (including humans). Fugu is one such. It has most
>
> of
>
>>>the same genes we do, but 90% of the non-coding DNA is missing. Yet
>>>fugus work just fine. I'm sure that some of the remainder is junk
>
> too,
>
>>>but it clearly demonstrates that most of the human genome is indeed
>
> junk.
>
> Only if you assume that humans and fugu need the same DNA. We know this
> isn't true for functional DNA, so be careful to say it must be true for
> what we think is non-functional (junk) DNA. IOW, until we know more,
> this is just a tenuous assumption.
Nonsense. We know that there are only modest differences in need between
humans and fugu. It *is* true for functional DNA. All gnathostomes are
quite similar in most respects, looking at the big picture.
>>>>This article claims that "non-coding" is perhaps a better term. I
>
> know
>
>>>>many here would eskew it given the source, but they do seem to
>
> point to
>
>>>>quite a few studies/findings showing junk DNA to be anything but.
>>>
>>>Non-coding DNA is a different thing from junk DNA. Though most
>>>non-coding DNA is indeed junk, a small proportion of non-coding DNA
>
> is
>
>>>functional; this is well-known, and that proportion has never been
>>>called junk. The way to tell junk from functional DNA is that the
>>>functional DNA is conserved over evolutionary time. Junk is not.
>
> How can we really say that? Three things come to mind:
>
> 1) Due to random mutations, new junk DNA may crop up (as opposed to
> being dropped) over evolutionary time. So evolution may do the very
> opposite of what you claim.
I think you may have mistaken the meaning of "conserved". I mean that
the sequence of bases in the fragment is stable. If you haven't mistaken
the meaning, then I have no idea what you are talking about here.
> 2) If there is such a thing as junk DNA, it must be neutral. If so, it
> is by definition not affected by natural selection. Only deleterious
> and beneficial DNA are. So how can we say evolution will *necessarily*
> drop junk DNA over time when it's selection mechanism isn't operational
> for neutral features? At best, junk DNA may be dropped accidentally
> (randomly), but not in all cases.
Again, you mistake the meaning of "conserved", and this time it's quite
clear how you mistake it. "Conserved" does include general non-deletion,
but that's only a small part of it. However, any given stretch of junk
DNA will accumulate a combination of insertions and deletions over time
that add to the observed amount of change.
> 3) The fugu allegedly dropped (or didn't add it in the first place?)
> this junk DNA, but humans didn't drop it, so how can you really say
> that junk DNA gets dropped as a general rule? It may or it may not, if
> I understand the evidence you are presenting correctly.
No, you don't. Junk DNA doesn't get dropped as a general rule, by which
I mean that the total quantity doesn't necessarily change, though the
sequences themselves are not stable. The quantity obviously does
sometimes change, up or down, in a systematic way, according to
principles that are not clearly understood. But the quantity varies
enormously among groups, and sometimes within groups.
It has nothing to do with the complexity of the organism; that much is
obvious.
No, it merely means that we know *enough* to say certain things. Just
because you don't know everything doesn't mean you know nothing.
Andrew Arensburger
> Stay tuned for last weeks "It's in the mind", when they featured vu deja,
> that strange feeling you get that you've never seen anything like that
> before.
Not to be pedantic or anything, but that's called "jamais vu".
--
Andrew Arensburger, Systems guy University of Maryland
arensb.no-...@umd.edu Office of Information Technology
Abuse only as directed.
John Harshman
> Boikat <boi...@bellsouthnospam.net> wrote:
>
>>Stay tuned for last weeks "It's in the mind", when they featured vu deja,
>>that strange feeling you get that you've never seen anything like that
>>before.
>
>
> Not to be pedantic or anything, but that's called "jamais vu".
>
I thought it was presque vu. I have a feeling that I've never seen
anything like jamais vu before.
hersheyh
esw...@yahoo.com wrote:
> "r norman" <rsn_@_comcast.net> wrote in message
> news:ifaq819je6lk3kft1...@4ax.com...
> > On Thu, 19 May 2005 23:46:01 GMT, John Harshman
> > <jharshman....@pacbell.net> wrote:
> >
> > >esw...@yahoo.com wrote:
> > >
> > >> "The Last Conformist" <andr...@gmail.com> wrote in message
> > >> news:1116533975.2...@z14g2000cwz.googlegroups.com...
> > >>
> > >>>Jason Spaceman wrote:
> > >>>
> > >>>>From the article:
> > >>>>---------------------------
> > >>>
[snip]
> > In addition, consider the puffer fish, Fugu, with about the same
> > number of genes as a human but only about 1/8th the amount of DNA.
> > These guys seem to do quite well in the world. So what is that 7/8
> of
> > our DNA doing?
>
> You guys do realize that the Fugu and the puffer fish may not need
all
> that "junk" DNA, but the same isn't *necessarily* true for humans,
> right? To make such a claim given our current understanding would be
to
> say that we know all there is to know about DNA and how it works.
Remember that all vertebrates have about the same number of coding
genes, from Fugu to Homo. The amount of DNA in genomes has little
relationship to the number of genes or the need for DNA. Fugu (and
another pufferfish) have about 0.4 pg of DNA/genome. Humans have about
3.5 pg. But essentially all mammals tested have between 2.9 and 3.7 pg
of DNA/genome. Bos taurus (domestic cows) and macaques and chips have
more than humans. Cats and dogs have the least. Chickens (Gallus
gallus) has about 1.2 pg, as does a fish closely related to the
pufferfish, Oryzias latipes, or the Japanese medaka. The zebrafish
(Danio rerio) has about 1.7 pg. The amphibian Xenopus tropicalis has
1.7 pg, but the closely related Xenopus laevis has 3.2 (probably due to
polyploidy). There is a nice diagram of this on p. 1284 of a
commentary article by Hedges, S.B. & Kumar, S. Science 2002 297:
1283-1284. You can look it up electronically in Goggle Scholar.
A comparison between humans and mice is sufficient to determine that
only about 5% of the human genome is under evolutionary constraint.
Remember that selection is overwhelmingly conservative rather than
favoring change.
Boikat
"John Harshman" <jharshman....@pacbell.net> wrote in message
news:iboje.1204$mK....@newssvr13.news.prodigy.com...
Actually, I mucked it up anyway. It's supposed to be vu ja de' Mork and
Mindy.
Boikat
Mark Isaak
>esw...@yahoo.com wrote:
>
>> [...]
>> I'm not really interested in taking this discussion into a ToE vs. ID
>> war. But this statement somewhat begs the question. Is it possible we
>> are declaring those portions of DNA ToE *didn't* predict as non-coding,
>> yet functional as dead/junk/whatever when if fact they aren't? Note
>> this wouldn't necessarily say ToE is wrong; it might be that our
>> understanding of ToE is incomplete and/or our application not entirely
>> accurate.
>
>We understood quite some time ago how to identify the start and stop
>codons that delineate a a gene.
There is an exception to this that is not mentioned much, and which is
another nail in the coffin of intelligent design.
The basic explanation of RNA translation is that there are 61 codons
which code for 20 amino acids, plus 3 stop codons. But one of the
stop codons (UGA) is not always a stop codon. Sometimes it codes for
a 21st amino acid, selenocysteine. Which it codes for depends on some
of the RNA downstream of codon, and there are at least a couple
different variations of the downstream RNA that can cause the
selenocystein interpretation. It has not been easy to tell when UGA
means stop and when UGA means selenocystein.
There is plenty of redundancy among the codons to give selenocystine a
codon of its own. That is what we would expect of a deliberate
designer (or maybe one codon which always combines with other DNA to
produce alternate amino acids, leaving room for future enhancements).
The kludge of giving UGA a rare second function is the sort of thing
we expect from evolution, not from intelligent design.
For more info, see G. V. Kryukov et al., 2003, Characterization of
mammalian selenoproteomes. _Science_ 300: 1439-1443.
--
Mark Isaak eciton (at) earthlink (dot) net
"Voice or no voice, the people can always be brought to the bidding of
the leaders. That is easy. All you have to do is tell them they are
being attacked, and denounce the pacifists for lack of patriotism and
exposing the country to danger." -- Hermann Goering
r norman
You underestimate the craftiness of the designer, intent on befuddling
the minds of us satanic and atheistic scientists foolishly trying to
make some sense of the physical universe we find ourselves living in.
Mitchell Coffey
<j.wil...@uq.edu.au> wrote:
>John Harshman wrote:
>...
>
>> Tonight on "It's the Mind" we feature deja vu, that strange feeling you
>> sometimes get that you've seen something before.
>>
>
>...
>
>Tonight on "It's the Mind" we feature deja vu, that strange feeling you
>sometimes get that you've seen something before.
>
>--
Tonight on "It's the Mind" we feature deja vu, that strange feeling
you sometimes get that you've seen something before.
....
eNo
news:sm8s815v86d5j5igd...@4ax.com...
So, bottom line, you don't think designers ever implement dual-use
functions? On what basis do you make such an assertion? I ask, because as a
designer with occasional claims to intelligence, I do this often and see it
in many of my colleagues' designs--especially those that are
adapted/upgraded rather than started as clean-sheet designs. BTW, "kludge"
is in the eye of the beholder, and that eye may puff and turn black if the
original designer takes sufficient umbrage at his design being classified as
such.
This brings me to a point which I seldom if ever hear ID or ToE advocates
acknowledge: designs evolve. Let me repeat: designs evolve.
Human designers seldom have the luxury of starting a clean-sheet design.
Rather, due to time or resource constraints, or simply because they choose
to, human designers will adapt, co-opt and/or enhance existing designs
rather than create brand new ones. Now, we may say that a non-human
designer, the one we call God, isn't bound by some of these constraints. But
such an argument would result from assumptions we have about this God, none
of which can be validated through science, so far as I can tell. If you are
going to hold the ID proponent or creationist's feet to the fire of
falseability, make sure you dangle your own feet over the same fire when
argumentation carries you away. IOW, you are making a philosophical,
non-falsifiable argument if by "not from intelligent design" you really mean
"supernatural/divine design". Given freedom of speech, that is your
prerrogative, certainly, but don't give it the weight of a proof against ID.
--
øĪš°`°šĪø,,,,øĪš°`°šĪø,,,,øĪš°`°šĪø,,,,øĪš°`°šĪøĪš°`°šĪø,,,,øĪš
eNo
"If you can't go fast, go long."
øĪš°`°šĪø,,,,øĪš°`°šĪø,,,,øĪš°`°šĪø,,,,øĪš°`°šĪøĪš°`°šĪø,,,,øĪš
rich hammett
>>John Harshman wrote:
>>...
>>
>>> Tonight on "It's the Mind" we feature deja vu, that strange feeling you
>>> sometimes get that you've seen something before.
>>...
>>
>>Tonight on "It's the Mind" we feature deja vu, that strange feeling you
>>sometimes get that you've seen something before.
> Tonight on "It's the Mind" we feature deja vu, that strange feeling
> you sometimes get that you've seen something before.
I suddenly had the strange feeling that I'll never read another
post in this thread...
rich
--
-to reply, it's hot not warm
+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+
\ Rich Hammett http://home.hiwaay.net/~rhammett
/ "Better the pride that resides in a citizen of the world;
\ than the pride that divides
/ when a colorful rag is unfurled."
Mitchell Coffey
Followed by the previous week's "It's in the mind", when they featured
narapoia, that irrational conviction that you are persecuting
someone.
Mitchell Coffey
Noone Inparticular
John Wilkins wrote:
> John Harshman wrote:
> ...
>
> > Tonight on "It's the Mind" we feature deja vu, that strange feeling
you
> > sometimes get that you've seen something before.
> >
>
> ...
>
> Tonight on "It's the Mind" we feature deja vu, that strange feeling
you
> sometimes get that you've seen something before.
Tomorrow night on "It's the mind" we feature vuja de, that strange
feeling you sometimes get that you've not seen something before
Andrew Arensburger
> Andrew Arensburger wrote:
>> Not to be pedantic or anything, but that's called "jamais vu".
> I thought it was presque vu. I have a feeling that I've never seen
> anything like jamais vu before.
That sounds related to "t'as encore rien vu", the feeling that
you ain't seen nothin' yet.
--
Andrew Arensburger, Systems guy University of Maryland
arensb.no-...@umd.edu Office of Information Technology
Did you REALLY think I was serious?
rich hammett
> Followed by the previous week's "It's in the mind", when they featured
> narapoia, that irrational conviction that you are persecuting
> someone.
Is it narapoia if I really am out to get them?
John Harshman
It seems to me that you are saying that design is an untestable
hypothesis because there are no constraints on what a designer might do
or how he could operate. So what good is a design hypothesis,
scientifically?
John Wilkins
> Minä suojelen sinua kaikelta, mitä ikinä keksitkin sanoa, Mitchell Coffey:
>
>>On Fri, 20 May 2005 23:09:01 +1000, John Wilkins
>><j.wil...@uq.edu.au> wrote:
>
>
>>>John Harshman wrote:
>>>...
>>>
>>>
>>>>Tonight on "It's the Mind" we feature deja vu, that strange feeling you
>>>>sometimes get that you've seen something before.
>>>
>>>...
>>>
>>>Tonight on "It's the Mind" we feature deja vu, that strange feeling you
>>>sometimes get that you've seen something before.
>
>
>>Tonight on "It's the Mind" we feature deja vu, that strange feeling
>>you sometimes get that you've seen something before.
>
>
> I suddenly had the strange feeling that I'll never read another
> post in this thread...
>
> rich
>
Mark Isaak
>"Mark Isaak" <eci...@earthlinkNOSPAM.next> wrote in message
>news:sm8s815v86d5j5igd...@4ax.com...
>> >[...]
>> >We understood quite some time ago how to identify the start and stop
>> >codons that delineate a a gene.
>>
>> There is an exception to this that is not mentioned much, and which is
>> another nail in the coffin of intelligent design.
>>
>> The basic explanation of RNA translation is that there are 61 codons
>> which code for 20 amino acids, plus 3 stop codons. But one of the
>> stop codons (UGA) is not always a stop codon. Sometimes it codes for
>> a 21st amino acid, selenocysteine. Which it codes for depends on some
>> of the RNA downstream of codon, and there are at least a couple
>> different variations of the downstream RNA that can cause the
>> selenocystein interpretation. It has not been easy to tell when UGA
>> means stop and when UGA means selenocystein.
>>
>> There is plenty of redundancy among the codons to give selenocystine a
>> codon of its own. That is what we would expect of a deliberate
>> designer (or maybe one codon which always combines with other DNA to
>> produce alternate amino acids, leaving room for future enhancements).
>> The kludge of giving UGA a rare second function is the sort of thing
>> we expect from evolution, not from intelligent design.
>
>So, bottom line, you don't think designers ever implement dual-use
>functions?
Intelligent designers starting from scratch don't make them when there
are more efficient options available.
>I ask, because as a
>designer with occasional claims to intelligence, I do this often and see it
>in many of my colleagues' designs--especially those that are
>adapted/upgraded rather than started as clean-sheet designs. BTW, "kludge"
>is in the eye of the beholder, and that eye may puff and turn black if the
>original designer takes sufficient umbrage at his design being classified as
>such.
I agree. Some of the best evidence there is for life being designed
is that the design is amazingly crappy.
>This brings me to a point which I seldom if ever hear ID or ToE advocates
>acknowledge: designs evolve. Let me repeat: designs evolve.
Again I agree. That is a point I have made many times myself. If you
reject evolution, you reject design.
The point you seem to miss is that ID, as creationists such as Dembski
use the term, has nothing whatsoever to do with design. And when I
say "nothing whatsoever," I am not exaggerating. What the "design" of
ID means, besides a rejection of evolution, is magical creation. The
"intelligent" part, combined with the overt theology of its
proponents, means that the creation was supposed to be done by an
omnipotent god, which implies a god that knows what he is doing.
Life, however, gives lie to such suppositions.
Mark Isaak
Tonight on "It's the Mind" we feature paranoid schitzophrenia, that
strange suspicion that people are feeding irrational thoughts to your
brain over and over. Next week, we feature deja vu, that strange
feeling you sometimes get that you've seen something before.
--
George Evans
Shaw at non...@your.biz wrote on 5/19/05 8:37 PM:
<snip>
> So the ToE helped us identify those non coding segments regulatory
> function. So in this case our understanding of the ToE was neither
> incomplete nor was our application inaccurate. As a matter of fact this
> simple discovery should put an end to any rational open minded person
> having an objection to the ToE. Only because of the ToE did scientists
> have any reason to suspect anything unusual was going on with those non
> coding segments.
Here we have Ken Shaw admitting that the ToE puts an end to open mindedness.
Just as I suspected. :-)
George Evans
hers...@indiana.edu
As I am sure Ken would add, this favoring of the ToE by science will
only hold until there is some material evidence which requires a
different explanation or a modification of the current one.
In the particular example he used, it is and remains a fact that it was
an understanding of the theoretical consequences of the difference
between selection and drift over evolutionary timeframes from a common
ancestor that led scientists to identify noncoding sequences with
function. Let us know when or if you have a theory which would be
better at identifying noncoding sequences with function and the pattern
of differences that is observed. How does the theory of intelligent
design go about identifying these noncoding sequences with function?
How does it explain the observed pattern? What are the observable
consequences of an intelligent designer being involved? How does that
differ from the evolutionary expectation? Curious minds want to know.
> George Evans
George Evans
hers...@indiana.edu at hers...@indiana.edu wrote on 5/22/05 12:02 PM:
Still no sense of humor, Howard? But since you asked, I have been thinking
about all this "junk" DNA. Could it have something to do with the fact that
everything was bigger in the past? Maybe all genomes are deteriorating.
And then there is still the idea that unconserved regions, are variations of
genes or parts of genes that are ready to be called up if the organism faces
a new environmental challenge. Fetuses use a different hemoglobin en utero,
maybe there is a hemoglobin gene somewhere in all that junk that could be
used in a hyperbaric atmosphere.
George Evans
Ken Shaw
George Evans wrote:
> in article 1116788397.4...@o13g2000cwo.googlegroups.com,
> hers...@indiana.edu at hers...@indiana.edu wrote on 5/22/05 12:02 PM:
>
>>George Evans wrote:
>>
>>
>>>in article aYcje.794069$w62.2...@bgtnsc05-news.ops.worldnet.att.net, Ken
>>>Shaw at non...@your.biz wrote on 5/19/05 8:37 PM:
>>>
>>><snip>
>>>
>>>>So the ToE helped us identify those non coding segments regulatory function.
>>>>So in this case our understanding of the ToE was neither incomplete nor was
>>>>our application inaccurate. As a matter of fact this simple discovery should
>>>>put an end to any rational open minded person having an objection to the
>>>>ToE. Only because of the ToE did scientists have any reason to suspect
>>>>anything unusual was going on with those non coding segments.
>>>>
>>>
>>>Here we have Ken Shaw admitting that the ToE puts an end to open mindedness.
>>>Just as I suspected. :-)
Not put an end to open mindedness. Twisting and quote mining anyone's
words is dishonest.
>>
>>As I am sure Ken would add, this favoring of the ToE by science will
>>only hold until there is some material evidence which requires a
>>different explanation or a modification of the current one.
>>
>>In the particular example he used, it is and remains a fact that it was
>>an understanding of the theoretical consequences of the difference
>>between selection and drift over evolutionary timeframes from a common
>>ancestor that led scientists to identify noncoding sequences with
>>function. Let us know when or if you have a theory which would be
>>better at identifying noncoding sequences with function and the pattern
>>of differences that is observed. How does the theory of intelligent
>>design go about identifying these noncoding sequences with function?
>>How does it explain the observed pattern? What are the observable
>>consequences of an intelligent designer being involved? How does that
>>differ from the evolutionary expectation? Curious minds want to know.
>
>
> Still no sense of humor, Howard? But since you asked, I have been thinking
> about all this "junk" DNA. Could it have something to do with the fact that
> everything was bigger in the past? Maybe all genomes are deteriorating.
>
> And then there is still the idea that unconserved regions, are variations of
> genes or parts of genes that are ready to be called up if the organism faces
> a new environmental challenge. Fetuses use a different hemoglobin en utero,
> maybe there is a hemoglobin gene somewhere in all that junk that could be
> used in a hyperbaric atmosphere.
>
Genomes are not observed deteriorating between generations. Also
everything wasn't bigger in the past. The ancestors of modern elephants
and rhinos were the size of medium sized breed of dog.
Also noncoding "junk" DNA does not code for a protein. There may be
genes that produce proteins that don't do anything right now but without
any selective pressure they will tend to drift to a non functioning
state. This is observed in human's and other primates nonfunctional
Vitamin C synthesis.
Ken
George Evans
Shaw at non...@your.biz wrote on 5/22/05 4:23 PM:
> George Evans wrote:
>
>> in article 1116788397.4...@o13g2000cwo.googlegroups.com,
>> hers...@indiana.edu at hers...@indiana.edu wrote on 5/22/05 12:02 PM:
>>
>>> George Evans wrote:
>>>
>>>> in article aYcje.794069$w62.2...@bgtnsc05-news.ops.worldnet.att.net, Ken
>>>> Shaw at non...@your.biz wrote on 5/19/05 8:37 PM:
>>>>
>>>> <snip>
>>>>
>>>>> So the ToE helped us identify those non coding segments regulatory
>>>>> function. So in this case our understanding of the ToE was neither
>>>>> incomplete nor was our application inaccurate. As a matter of fact this
>>>>> simple discovery should put an end to any rational open minded person
>>>>> having an objection to the ToE. Only because of the ToE did scientists
>>>>> have any reason to suspect anything unusual was going on with those non
>>>>> coding segments.
>>>>
>>>> Here we have Ken Shaw admitting that the ToE puts an end to open
>>>> mindedness. Just as I suspected. :-)
>
> Not put an end to open mindedness. Twisting and quote mining anyone's
> words is dishonest.
See the smiley.
You mean putative ancestors, right. I know everything wasn't bigger, but
likewise, everything doesn't have the same proportion of junk DNA. Also,
genomes are observed deteriorating between generations as new genetic
diseases crop up.
> Also noncoding "junk" DNA does not code for a protein. There may be genes that
> produce proteins that don't do anything right now but without any selective
> pressure they will tend to drift to a non functioning state. This is observed
> in human's and other primates nonfunctional Vitamin C synthesis.
Bingo. We are prepared for the day when Vitamin C is no longer available.
George Evans
hers...@indiana.edu
Oh, I have it. I just sometimes choose not to express it. I also see
that you didn't answer the questions about how ID would be of any use
as a scientific theory.
> But since you asked, I have been thinking
> about all this "junk" DNA. Could it have something to do with the
fact that
> everything was bigger in the past? Maybe all genomes are
deteriorating.
Actually there is an argument that increasing the amount of genome DNA
(regardless of whether it has function or not) is one easy (in terms of
number of evolutionary steps required) way to increase the size of
cells. There is a feed-back loop that causes cells with large genomes
to be larger. For example, in plants triploids (often used in breeding
because it also forces one to keep buying seed) tend to have bigger
flowers (which is also selected for because it is desired by human
gardeners).
But essentially all mammals have roughly equivalent amounts of
DNA/genome and some amphibians and fish have more than this. Plants,
of course, are all over the map wrt amount of DNA/genome because of
polyploidy. Bacteria (and certain fungi) are actually the paragons of
efficiency and parsimony wrt having the minimal amount of noncoding
sequence. A large fraction of the non-coding DNA in humans and other
mammals actually involves repetitive sequences derived from various
transposons and retrotransposons rather than representing degenerate
sequences of pseudogenes. And these repetitive sequences differ from
species to species. That most mammals wind up with roughly the same
amount of DNA/genome may well indicate that there is an optimal level
of DNA/genome which differs significantly from the number of functional
genes the organism needs. I.e., any old "junk" will do.
> And then there is still the idea that unconserved regions, are
variations of
> genes or parts of genes that are ready to be called up if the
organism faces
> a new environmental challenge.
Can happen, but quite rarely. Only relatively recent duplicates of
genes generally need apply for such positions. New genes do not arise
from sequences which would require even tens of selectively neutral
changes. And, as I mentioned, a major part of the noncoding DNA is from
selfish transposon/retrotransposon species (some of these can, also
rarely, become part of a new regulatory sequence or lead to chimera
gene formation). In humans, it seems that the primary mechanism of
generating new functions is via new differential splicing of
pre-existing transcripts rather than even duplication and divergence.
But those last are clearly the most common ways of producing 'new'
proteins: Duplication and divergence (including chimeric duplication).
New differential splicing. Other mechanisms can occur, but are
relatively rarer. Starting from some maximally different sequence and
changing, in a selectively neutral way, until the new function arises
out of some utterly useless sequences appears to be nothing but a
creationist's fantasy strawman about how evolution works.
> Fetuses use a different hemoglobin en utero,
> maybe there is a hemoglobin gene somewhere in all that junk that
could be
> used in a hyperbaric atmosphere.
And the fetal hemoglobin (actually the beta globin component) is one of
several modified duplicates allowing specialization of hemoglobin to
specific developmental environments (including embryonic hemoglobin).
There is actually quite a bit known about the way hemoglobin evolved.
> George Evans
Tim Tyler
> http://www.godandscience.org/evolution/junkdna.html
>
> Any one know of citations debunking the claims made in this article?
That URL is self-debunking - you can judge it without looking any further.
--
__________
|im |yler http://timtyler.org/ t...@tt1lock.org Remove lock to reply.
Tim Tyler
> esw...@yahoo.com wrote:
> > I guess
> > to get through an experiment: remove the alleged junk DNA, inject the
> > clean DNA into a Zygote, carry it out to birth and see what you get. My
> > guess is we would quickly discover whether the junk was necessary or
> > not.
>
> That sounds very simple, but in fact it's beyond our current technology.
> However, nature has kindly carried out similar experiments. There are
> some vertebrates, for example, with genomes a tenth the size of the
> average mammal's (including humans). Fugu is one such. It has most of
> the same genes we do, but 90% of the non-coding DNA is missing. Yet
> fugus work just fine. I'm sure that some of the remainder is junk too,
> but it clearly demonstrates that most of the human genome is indeed junk.
A questionable premise there: that all mammals are roughly the same in
terms of their necessary genes.
IIRC, something very much like the above experiment has been done,
(with some pretty small and simple organisms). They managed to rip
out quite substantial fractions of the genome while still having
a viable organism at the end of it. That's not to say that what
went missing was junk - but it was obviously not critical material.
John Vreeland
<geor...@earthlink.net> wrote:
>> Also noncoding "junk" DNA does not code for a protein. There may be genes that
>> produce proteins that don't do anything right now but without any selective
>> pressure they will tend to drift to a non functioning state. This is observed
>> in human's and other primates nonfunctional Vitamin C synthesis.
>
>Bingo. We are prepared for the day when Vitamin C is no longer available.
>
>George Evans
Not likely. It's a bit too damaged for that. But Vitamin C is so
ubiquitous that we are not likely to run out of it either. Most of
the weeds in my lawn are loaded with it.
__
To be inerrant is to never know the truth.
John Vreeland - replace "eye-tripoli" with the appropriate tetragrammaton
John Harshman
> John Harshman <jharshman....@pacbell.net> wrote or quoted:
>
>>esw...@yahoo.com wrote:
>
>
>>>I guess
>>>to get through an experiment: remove the alleged junk DNA, inject the
>>>clean DNA into a Zygote, carry it out to birth and see what you get. My
>>>guess is we would quickly discover whether the junk was necessary or
>>>not.
>>
>>That sounds very simple, but in fact it's beyond our current technology.
>>However, nature has kindly carried out similar experiments. There are
>>some vertebrates, for example, with genomes a tenth the size of the
>>average mammal's (including humans). Fugu is one such. It has most of
>>the same genes we do, but 90% of the non-coding DNA is missing. Yet
>>fugus work just fine. I'm sure that some of the remainder is junk too,
>>but it clearly demonstrates that most of the human genome is indeed junk.
>
>
> A questionable premise there: that all mammals are roughly the same in
> terms of their necessary genes.
Why? Do you have any contrary evidence? Mice and humans, for example,
share something over 90% of their protein-coding genes. You could, I
suppose, claim that the differences are mostly in the "junk"; but on
what basis?
> IIRC, something very much like the above experiment has been done,
> (with some pretty small and simple organisms). They managed to rip
> out quite substantial fractions of the genome while still having
> a viable organism at the end of it. That's not to say that what
> went missing was junk - but it was obviously not critical material.
Yes, the problem with experiments like that is that one can always argue
that the missing material does have a function, just one too subtle to
be detected easily; maybe it's a function that is only needed once every
hundred generations. That's the beauty of looking at sequence
conservation, because it indexes long-term importance.
George Evans
hers...@indiana.edu at hers...@indiana.edu wrote on 5/23/05 8:01 AM:
Well, I am not an ID theorist, but I think that ID could have a great impact
on our understanding of the content and relative value of genetic
information. I wouldn't be surprised if a mathematical relationship between
energy expense and information content (per Dembski not Shannon) appears
soon for scrutiny. That area is wide open right now, and so far science has
almost nothing to say about it.
>> But since you asked, I have been thinking about all this "junk" DNA. Could it
>> have something to do with the fact that everything was bigger in the past?
>> Maybe all genomes are deteriorating.
>
> Actually there is an argument that increasing the amount of genome DNA
> (regardless of whether it has function or not) is one easy (in terms of number
> of evolutionary steps required) way to increase the size of cells. There is a
> feed-back loop that causes cells with large genomes to be larger. For
> example, in plants triploids (often used in breeding because it also forces
> one to keep buying seed) tend to have bigger flowers (which is also selected
> for because it is desired by human gardeners).
Also, I thought that polyploidy causes larger parts simple because there are
more copies of structural genes producing more structural elements.
> But essentially all mammals have roughly equivalent amounts of DNA/genome and
> some amphibians and fish have more than this. Plants, of course, are all over
> the map wrt amount of DNA/genome because of polyploidy. Bacteria (and certain
> fungi) are actually the paragons of efficiency and parsimony wrt having the
> minimal amount of noncoding sequence. A large fraction of the non-coding DNA
> in humans and other mammals actually involves repetitive sequences derived
> from various transposons and retrotransposons rather than representing
> degenerate sequences of pseudogenes. And these repetitive sequences differ
> from species to species. That most mammals wind up with roughly the same
> amount of DNA/genome may well indicate that there is an optimal level of
> DNA/genome which differs significantly from the number of functional genes the
> organism needs. I.e., any old "junk" will do.
It is the nature of these "various transposons" that bolsters my stored gene
hypothesis.
>> And then there is still the idea that unconserved regions, are variations of
>> genes or parts of genes that are ready to be called up if the organism faces
>> a new environmental challenge.
>>
> Can happen, but quite rarely. Only relatively recent duplicates of genes
> generally need apply for such positions. New genes do not arise from
> sequences which would require even tens of selectively neutral changes. And,
> as I mentioned, a major part of the noncoding DNA is from selfish
> transposon/retrotransposon species (some of these can, also rarely, become
> part of a new regulatory sequence or lead to chimera gene formation). In
> humans, it seems that the primary mechanism of generating new functions is via
> new differential splicing of pre-existing transcripts rather than even
> duplication and divergence. But those last are clearly the most common ways of
> producing 'new' proteins: Duplication and divergence (including chimeric
> duplication). New differential splicing. Other mechanisms can occur, but are
> relatively rarer. Starting from some maximally different sequence and
> changing, in a selectively neutral way, until the new function arises out of
> some utterly useless sequences appears to be nothing but a creationist's
> fantasy strawman about how evolution works.
Maybe it is a fantasy but it sure is intriguing. I'm thinking of a directed
mutation capability, kind of like "This enzyme isn't working so well, try
the next one up the chromosome." You have to admit this opens up some
interesting lines of thought.
>> Fetuses use a different hemoglobin en utero, maybe there is a hemoglobin gene
>> somewhere in all that junk that could be used in a hyperbaric atmosphere.
>>
> And the fetal hemoglobin (actually the beta globin component) is one of
> several modified duplicates allowing specialization of hemoglobin to specific
> developmental environments (including embryonic hemoglobin). There is actually
> quite a bit known about the way hemoglobin evolved.
This shows how hemoglobin has evolved or, alternatively, how it can be
altered.
George Evans
wizo...@hotmail.com
> There is plenty of redundancy among the codons to give selenocystine
a
> codon of its own. That is what we would expect of a deliberate
> designer (or maybe one codon which always combines with other DNA to
> produce alternate amino acids, leaving room for future enhancements).
> The kludge of giving UGA a rare second function is the sort of thing
> we expect from evolution, not from intelligent design.
>
times I have seen an otherwise seemingly intelligent and capable
programmer overload a particular symbol/encoding/value/name to mean
multiple things, when plenty of unused alternatives were available, is
testament to the ability of humans to make almost anything they do more
complicated than it needs to be. Worryingly, half the time the person
I have observed doing this has been yours truly.
Of course, I doubt too many ID'er would want to accuse their Designers
of being prone to very human sorts of irrational behaviour.
wizo...@hotmail.com
eNo wrote:
> If you are
> going to hold the ID proponent or creationist's feet to the fire of
> falseability, make sure you dangle your own feet over the same fire
when
> argumentation carries you away. IOW, you are making a philosophical,
> non-falsifiable argument if by "not from intelligent design" you
really mean
> "supernatural/divine design". Given freedom of speech, that is your
> prerrogative, certainly, but don't give it the weight of a proof
against ID.
>
because they work well, that we never see in nature. For instance,
co-opting a complete working component designed for contraption A and
using in contraption B that was designed more or less independently.
Also, when technology we design is not working as well as it might,
perhaps because during the design processs some decisions were made
that seemed good at the time but later turned out not to be, we have
the ability to start from scratch and see if we can come up with a
better way of solving the problem. So even if it were true that some
of the strange things we see in nature could still conceivably the
product of a less-than-perfect (but still intelligent) design process,
we would also expect to see corrections, applications of independent
design and evidence of occasional re-design from scratch (not
necessarily whole organisms, but at least major organs). We don't see
these things, therefore any claim that life on earth is intelligently
designed has to be able to at last give feasible explanations for why
there are so many things we see that are clearly not the product of
careful forethought and development from a plan, and basically nothing
that could only arise from these processes.
Ash
>
> esw...@yahoo.com wrote:
>
>
>>"Ken Shaw" <non...@your.biz> wrote in message
>>news:0I9je.793162$w62.2...@bgtnsc05-news.ops.worldnet.att.net...
>>
>>
>>>Not this again.
>>
>>
>>Sorry.
>>
>>
>>
>>>Some sections of DNA which do not code for proteins do appear to have
>>
>>
>>>regulatory functions. Do you know how to identify those sections?
>>
>>Find
>>
>>
>>>the ones highly conserved in the population. Scientists using a
>>>prediction of the ToE identified these sections of non coding DNA and
>>
>>
>>>discovered what they do. No IDist/creationist ideas were involved
>>
>>just
>>
>>
>>>the good old ToE.
>>
>>
>>I'm not really interested in taking this discussion into a ToE vs. ID
>>war. But this statement somewhat begs the question. Is it possible we
>>are declaring those portions of DNA ToE *didn't* predict as non-coding,
>>yet functional as dead/junk/whatever when if fact they aren't? Note
>>this wouldn't necessarily say ToE is wrong; it might be that our
>>understanding of ToE is incomplete and/or our application not entirely
>>accurate.
>>
>
>
> started getting sequenced it was discovered that lots of the base pairs
> on a chromosome didn't fall into a gene. At first it was assumed that
> these sections didn't do anything. The assumption was those stretches
> were the remnants of ancient virus insertions are various large scale
> duplication mutations that had drifted to a nonfunctional state. Some
> scientists noticed that some of these non coding sections were highly
> conserved. If these sections were truly junk then the ToE says those
> sections should not be conserved so scientists _using a prediction of
> the ToE_ investigated further to find out what was happening. It was
> then discovered that those highly conserved non coding segments had
> regulatory functions.
>
Of course, this is only valid if other parts of these non coding resions
are not conserved
Ken Shaw
Are you claiming otherwise?
Ken
hers...@indiana.edu
I, OTOH, would be shocked, shocked if such a relationship were found.
The 'energy expense' of duplicating a genome is largely sequence (and
thus information) independent. It does take more energy to break apart
the three H bonds of a G:C pair than the two of an A:T pair, but that
is about the only significant sequence difference I can think of. Can
you think of any reason why it would take more or less energy to
replicate a meaningless sequence containing a given proportion of A:T
to G:C than the same material that encodes proteins? If anything, it
takes more energy (aside from replication) to maintain the *useful*
bits, given that the useful bits are transcribed (and sometimes
translated) at higher frequency (but that is not always the case). But
even then, a single point mutation can produce a gene that is also
transcribed and translated into a useless protein. That change would
have no 'energy expense' consequences related to the replication of the
sequence or the production of protein product. The mutant protein
might, of course, have lethal consequences related to the ability of
the cell to extract energy from its environment, but that is a
different question.
What is it about these "various transposons" do you think bolsters any
sort of "stored gene" hypothesis. The transposon sequences are not
gene sequences. They are highly repetitive and the only 'gene
sequnces' that they seem to encode are (often defective) related to
transposition. They are not encoding cryptic betagalactosidases or
hemoglobins. Now, that doesn't mean that it is impossible for some or
a few of these transposons to be situated so as to be a regulatory
element. And the presence of repetitive and potentially mobile
transposable elements makes the sorts of duplications and chimera
formations that really are frequently involved in evolution more
doable. But the transposable elements themselves are not a very good
source of "stored genes". They are too repetitive and boring for that.
Not really. The assumption that there is a "next one [closely related
in sequence, but nonfunctional gene] up the chromosome" is largely
invalidated by empirical reality. The idea that new genes arise from
sequences distantly related in sequence to the functional sequence is a
fantasy strawman (I call it the Pitman fallacy for obvious reasons).
> >> Fetuses use a different hemoglobin en utero, maybe there is a
hemoglobin gene
> >> somewhere in all that junk that could be used in a hyperbaric
atmosphere.
> >>
> > And the fetal hemoglobin (actually the beta globin component) is
one of
> > several modified duplicates allowing specialization of hemoglobin
to specific
> > developmental environments (including embryonic hemoglobin). There
is actually
> > quite a bit known about the way hemoglobin evolved.
>
> This shows how hemoglobin has evolved or, alternatively, how it can
be
> altered.
No. The beta globin cluster in humans (and other apes) are clearly
derived by duplication and divergence rather than by altering
pre-existing transposon sequences. In fact, there is even a
non-functioning duplicate (pseudo beta1) and a pair of functionally
identical duplicates that differ by a single aa (gamma G and gamma A)
that provide real examples of putative intermediate states in the
duplication and divergence process.
The various thalassemias (especially Lepore, where the anti-Lepore --
which has 5 alpha globin genes -- has been found and is selectively
netural) show that unequal crossing-over events are a continuing and
major cause of the duplication/deletion events that generate the
duplications that get modified.
The alpha globin complex in humans has a zeta form (used in embryos), a
nonfunctioning pseudo zeta copy, two nonfunctioning pseudo alpha
copies, and two identical functioning alpha genes.
Other vertebrates have similar but not identical clusters (which, of
course, follow the nested hierarchy of the branching evolutionary
pathway). Unlike the human case, where the order of genes neatly
follows the order of utilization from embryonic to adult, that is not
the case in other organisms.
>
> George Evans
hers...@indiana.edu
wizo...@hotmail.com wrote:
> eNo wrote:
> > If you are
> > going to hold the ID proponent or creationist's feet to the fire of
> > falseability, make sure you dangle your own feet over the same fire
> when
> > argumentation carries you away. IOW, you are making a
philosophical,
> > non-falsifiable argument if by "not from intelligent design" you
> really mean
> > "supernatural/divine design". Given freedom of speech, that is your
> > prerrogative, certainly, but don't give it the weight of a proof
> against ID.
> >
> Perhaps, but there are methods of design that we do use ourselves
> because they work well, that we never see in nature. For instance,
> co-opting a complete working component designed for contraption A and
> using in contraption B that was designed more or less independently.
Well, it might depend on the types of copyright laws the gods have.
The reason for making different types of flight arms in bats, birds,
and pterodactyls (or tail propulsion systems in fish, ichthyosaurs, and
whales) rather than engage in direct borrowing might have to do with
the various gods not wanting to pay royalties to other gods. Somehow I
can't see ID theorists using this argument to explain the lack of
borrowing. ;-)
Mark Isaak
<geor...@earthlink.net> wrote:
>[...]
>Well, I am not an ID theorist, but I think that ID could have a great impact
>on our understanding of the content and relative value of genetic
>information. I wouldn't be surprised if a mathematical relationship between
>energy expense and information content (per Dembski not Shannon) appears
>soon for scrutiny. That area is wide open right now, and so far science has
>almost nothing to say about it.
You are correct that the area of genetic analysis is wide open right
now, but not that science has almost nothing to say about it. I am no
expert in the area, but I have seen enough to know that science is
doing a great deal of productive work there. I also know that the
productive work is based on evolution, not ID. In particular, lots of
analysis is done by comparing human genes with similar genes in mice,
fruit flies, or even yeast. Other analysis is done by looking at how
much areas of DNA change in evolutionary time. Dembskian
"information" cannot be of any help at all, because you cannot measure
it until after you already know what you wanted to know in the first
place, and more. Some bioinformatics gets into areas which, in a
vague sense, relate to design (such as DNA motifs that relate to
protein folding), but intelligent design theory has contributed
nothing to such areas, nor does it attempt to.
Ash
Ken Shaw
The regulatory non coding DNA segments were discovered because those
sections were conserved while the rest of the non coding DNA was not.
Seems pretty straight forward to me.
Ken
John Harshman
It should be noted that there are some conserved regions whose function,
if any, is unknown. But we assume they do have unknown functions, and
are not junk, precisely because they are conserved. So there are no
conserved non-coding regions that are considered junk.
George Evans
wizo...@hotmail.com at wizo...@hotmail.com wrote on 5/23/05 6:37 PM:
I've been doing some quick study on this strange subject. The way the
translation mechanism knows that UGA stop codon means Selenocysteine is by
the presence of an inserted segment, I think immediately after the UGA. Now
how does *that* happen by Darwinian mechanisms? This is a unique
manipulation of the coding method.
I'm thinking it is possibly a post-production modification. It's like DNA
all of the sudden contains [Editors notes]!
George Evans
George Evans
hers...@indiana.edu at hers...@indiana.edu wrote on 5/24/05 8:08 AM:
> George Evans wrote:
>
>> in article 1116860473.1...@f14g2000cwb.googlegroups.com,
>> hers...@indiana.edu at hers...@indiana.edu wrote on 5/23/05 8:01 AM:
>>
>>> George Evans wrote:
<snip>
True to form, you are once again stuck speaking as a hardware engineer--or
maybe I should say Xerox repairman. Yes, it costs the same to copy the
source code to OS X as it would to produce an equal number of pages of my
butt. However I am talking about Dembski information not Shannon
information, the house of cards and not the cards themselves. This is where
science is silent so far and you are hoping beyond hope that there is no
such information. But of course it's there.
Pardon me, but it doesn't sound like you really know much about what these
transposons do either. At the very least they rattle one of the two
Darwinian mechanisms--mutation. Suddenly, change looks a whole lot easier,
possibly because it's planned. Admit it, you don't know where to draw the
line between Darwinian-like random point mutations and designed
transpositions.
BTW-stockrooms and warehouses are usually boring.
Well then you just stay on your secure 3% island. Sean and I will journey
out onto the 97% of relatively uncharted waters.
>>>> Fetuses use a different hemoglobin en utero, maybe there is a hemoglobin
>>>> gene somewhere in all that junk that could be used in a hyperbaric
>>>> atmosphere.
>>>>
>>> And the fetal hemoglobin (actually the beta globin component) is one of
>>> several modified duplicates allowing specialization of hemoglobin to
>>> specific developmental environments (including embryonic hemoglobin). There
>>> is actually quite a bit known about the way hemoglobin evolved.
>>>
>> This shows how hemoglobin has evolved or, alternatively, how it can be
>> altered.
>>
> No. The beta globin cluster in humans (and other apes) are clearly derived by
> duplication and divergence rather than by altering pre-existing transposon
> sequences. In fact, there is even a non-functioning duplicate (pseudo beta1)
> and a pair of functionally identical duplicates that differ by a single aa
> (gamma G and gamma A) that provide real examples of putative intermediate
> states in the duplication and divergence process.
Has anyone tried to express these "non-functional" variants to determine
their physical properties compared to functional hemoglobin?
> The various thalassemias (especially Lepore, where the anti-Lepore -- which
> has 5 alpha globin genes -- has been found and is selectively netural) show
> that unequal crossing-over events are a continuing and major cause of the
> duplication/deletion events that generate the duplications that get modified.
>
> The alpha globin complex in humans has a zeta form (used in embryos), a
> nonfunctioning pseudo zeta copy, two nonfunctioning pseudo alpha copies, and
> two identical functioning alpha genes.
>
> Other vertebrates have similar but not identical clusters (which, of course,
> follow the nested hierarchy of the branching evolutionary pathway). Unlike
> the human case, where the order of genes neatly follows the order of
> utilization from embryonic to adult, that is not the case in other organisms.
Wow! That's not quite a 33 to 1 ratio, but if all functional genes have this
many modified "copies" on the shelf that could account for quite a bit of
all that junk.
George Evans
Tim Tyler
> Some of the best evidence there is for life being designed
> is that the design is amazingly crappy.
That's /usually/ presented as evidence that life evolved.
Tim Tyler
> Tim Tyler wrote:
> > John Harshman <jharshman....@pacbell.net> wrote or quoted:
> >>esw...@yahoo.com wrote:
> >>>I guess
> >>>to get through an experiment: remove the alleged junk DNA, inject the
> >>>clean DNA into a Zygote, carry it out to birth and see what you get. My
> >>>guess is we would quickly discover whether the junk was necessary or
> >>>not.
> >>
> >>That sounds very simple, but in fact it's beyond our current technology.
> >>However, nature has kindly carried out similar experiments. There are
> >>some vertebrates, for example, with genomes a tenth the size of the
> >>average mammal's (including humans). Fugu is one such. It has most of
> >>the same genes we do, but 90% of the non-coding DNA is missing. Yet
> >>fugus work just fine. I'm sure that some of the remainder is junk too,
> >>but it clearly demonstrates that most of the human genome is indeed junk.
> >
> > A questionable premise there: that all mammals are roughly the same in
> > terms of their necessary genes.
>
> Why? Do you have any contrary evidence? Mice and humans, for example,
> share something over 90% of their protein-coding genes. You could, I
> suppose, claim that the differences are mostly in the "junk"; but on
> what basis?
You claimed a clear demonstration that most of the human genome is junk.
The demonstration apparently depended on the premise that all mammals
genes that were unnecessary for survival in one species of mammal were
not relevant to survival in any other mammals.
I don't think that is established. Just because one mammal can at
least survive without 90% of the normal mammalian genome, it doesn't
follow that all mammals could compete equally well if 90% of their
genome was removed.
> > IIRC, something very much like the above experiment has been done,
> > (with some pretty small and simple organisms). They managed to rip
> > out quite substantial fractions of the genome while still having
> > a viable organism at the end of it. That's not to say that what
> > went missing was junk - but it was obviously not critical material.
>
> Yes, the problem with experiments like that is that one can always argue
> that the missing material does have a function, just one too subtle to
> be detected easily; maybe it's a function that is only needed once every
> hundred generations. That's the beauty of looking at sequence
> conservation, because it indexes long-term importance.
It indexes conserved genes.
Of course, genes for traits such as diseases resistance are not
necessarily conserved - and can be selected in such a way that
they are constantly changing.
Sequence conservation doesn't have too much to say about that.
George Evans
eci...@earthlinkNOSPAM.next wrote on 5/24/05 12:38 PM:
> On Tue, 24 May 2005 00:46:14 GMT, George Evans
> <geor...@earthlink.net> wrote:
>
>> [...]
>>
>> Well, I am not an ID theorist, but I think that ID could have a great impact
>> on our understanding of the content and relative value of genetic
>> information. I wouldn't be surprised if a mathematical relationship between
>> energy expense and information content (per Dembski not Shannon) appears soon
>> for scrutiny. That area is wide open right now, and so far science has almost
>> nothing to say about it.
>>
> You are correct that the area of genetic analysis is wide open right now, but
> not that science has almost nothing to say about it. I am no expert in the
> area, but I have seen enough to know that science is doing a great deal of
> productive work there. I also know that the productive work is based on
> evolution, not ID. In particular, lots of analysis is done by comparing human
> genes with similar genes in mice, fruit flies, or even yeast. Other analysis
> is done by looking at how much areas of DNA change in evolutionary time.
> Dembskian "information" cannot be of any help at all, because you cannot
> measure it until after you already know what you wanted to know in the first
> place, and more. Some bioinformatics gets into areas which, in a vague sense,
> relate to design (such as DNA motifs that relate to protein folding), but
> intelligent design theory has contributed nothing to such areas, nor does it
> attempt to.
I don't think the idea of nested hierarchies of homologous proteins is as
strong an argument as you think. As a general rule, the farther two
organisms are from each other in design and function, the greater will be
the design criterion for each of their parts but there is room for
exceptions. OTOH evolution would predict identical hierarchical structures
for all proteins because all the parts of a given organism branched at
exactly the same times. The empirical data, in my opinion, favors design.
George Evans
Raymond E. Griffith
geor...@earthlink.net wrote on 5/25/05 4:26 AM:
Sigh. Why is it that the "design" promoters and those who promote an
outright religious interpretation seemingly always have to LIE about what
evolution says or does?
George, it would be really good for you to know what you are talking about.
The fact is that you do not.
The chemistry of proteins demonstrates that proteins with different
components can still fold the same way in the active areas and perform the
same task. For example, we know that insulin is produced by almost every
organism, and while human insulin is *best* for humans, for a long time we
used swine insulin. It did the job.
Evolutionary science is not a denial of chemistry. Rather, evolutionary
science is built upon the observations of chemistry and other disciplines.
People like you try to make it appear that evolutionary science is just some
fantasy speculation. It isn't. The journals are full of evolutionary studies
based upon chemistry, biochemistry, genetics, etc.
As speciation occurs, there is a physical branching of the population. Yet
we know from genetic studies that not all parts of the genome mutate at the
same rate. There are some parts of the genome that are remarkably stable,
while other parts demonstrate a wide variability. It is not necessary for
most proteins to be identical to perform an identical purpose. As we have
easily demonstrated, proteins can vary significantly and still perform the
same purpose.
On the other hand, you have just produced an argument which *destroys* your
ID position. The evidence is completely against it.
You said: "As a general rule, the farther two organisms are from each other
in design and function, the greater will be the design criterion for each of
their parts but there is room for exceptions."
Pray tell, how do you even begin to *define* how far apart two organisms are
"in design" or "in function"?
What is an organism's "designed function" anyway? Are you introducing
Calvinistic predestination here?
Come on. Bring it forward. What definitions, standards, and measurements are
used to determine how far apart "two organisms are from each other in design
and function"? Or are you just blowing smoke? Do you get your religious
technobabble from Star Trek?
You are interested in design? Tell me about the "design" that allows for
Trisomy 21 or Trisomy 18? Come on, now! If "design" to produce a particular
"function" are what we see in genetics, then explain those. If you have an
Almighty Designer, a Perfect Intellect, One Who never makes mistakes, then
explain those variances. Explain why they even exist if each protein has a
"design criteria" for the species. Explain why they are created to suffer by
a loving God.
And explain, please, why you have to lie about science in order to make your
point. Don't liars go to the Lake of Fire and Brimstone, according to
Revelation? What did your Designer design your communication abilities to
do? Hmmm. I can see it now. "Designed to deceive".
You might want to really think about your future as you pursue the tactics
of lies and deceits in pressing your point. Think warm, warmer, hot, and
"where can I get a drop of water to soothe my torment?". God hates lying.
Regards,
Raymond E. Griffith
John Harshman
> John Harshman <jharshman....@pacbell.net> wrote or quoted:
>
>>Tim Tyler wrote:
>>
>>>John Harshman <jharshman....@pacbell.net> wrote or quoted:
>>>
>>>>esw...@yahoo.com wrote:
>
>
>>>>>I guess
>>>>>to get through an experiment: remove the alleged junk DNA, inject the
>>>>>clean DNA into a Zygote, carry it out to birth and see what you get. My
>>>>>guess is we would quickly discover whether the junk was necessary or
>>>>>not.
>>>>
>>>>That sounds very simple, but in fact it's beyond our current technology.
>>>>However, nature has kindly carried out similar experiments. There are
>>>>some vertebrates, for example, with genomes a tenth the size of the
>>>>average mammal's (including humans). Fugu is one such. It has most of
>>>>the same genes we do, but 90% of the non-coding DNA is missing. Yet
>>>>fugus work just fine. I'm sure that some of the remainder is junk too,
>>>>but it clearly demonstrates that most of the human genome is indeed junk.
>>>
>>>A questionable premise there: that all mammals are roughly the same in
>>>terms of their necessary genes.
>>
>>Why? Do you have any contrary evidence? Mice and humans, for example,
>>share something over 90% of their protein-coding genes. You could, I
>>suppose, claim that the differences are mostly in the "junk"; but on
>>what basis?
>
>
> You claimed a clear demonstration that most of the human genome is junk.
I think it's pretty clear.
> The demonstration apparently depended on the premise that all mammals
> genes that were unnecessary for survival in one species of mammal were
> not relevant to survival in any other mammals.
Not true. In fact it has nothing to do with genes. Genes make up only a
few percent of the genome.
> I don't think that is established. Just because one mammal can at
> least survive without 90% of the normal mammalian genome, it doesn't
> follow that all mammals could compete equally well if 90% of their
> genome was removed.
Feel free not to believe anything you like. But the evidence seems
pretty good to me. Vertebrates vary widely in the amount of "junk" they
have, and it's precisely that parts that are not conserved that are
varying. And I think it's a safe assumption that vertebrates all have
about the same quantity of functional need, absent any suggestion of a
reason why this shouldn't be true. (And by the way, fugu is a fish.)
Given your logic, why should we believe that the results of an
experiment on one individual should apply to other individuals of the
same species?
>>>IIRC, something very much like the above experiment has been done,
>>>(with some pretty small and simple organisms). They managed to rip
>>>out quite substantial fractions of the genome while still having
>>>a viable organism at the end of it. That's not to say that what
>>>went missing was junk - but it was obviously not critical material.
>>
>>Yes, the problem with experiments like that is that one can always argue
>>that the missing material does have a function, just one too subtle to
>>be detected easily; maybe it's a function that is only needed once every
>>hundred generations. That's the beauty of looking at sequence
>>conservation, because it indexes long-term importance.
>
> It indexes conserved genes.
>
> Of course, genes for traits such as diseases resistance are not
> necessarily conserved - and can be selected in such a way that
> they are constantly changing.
Yes, there are a few of those. They change at greater than the neutral
rate, and that stands out too.
> Sequence conservation doesn't have too much to say about that.
Yes it does, since change in those genes is actually accelerated. And
they are embedded in conserved sequences too -- only selected domains
have accelerated evolution. This has nothing to do with junk DNA.
hers...@indiana.edu
That is quite true. But what other form of information *that is
actually independently measureable* rather than a drawing of the bull's
eye after the arrow has stuck were you talking about?
> However I am talking about Dembski information not Shannon
> information, the house of cards and not the cards themselves.
I agree that Dembski information is a house of cards that has nothing
but _ex post facto_ teleological meaning. It is unmeasureable.
> This is where
> science is silent so far and you are hoping beyond hope that there is no
> such information. But of course it's there.
Actually it is you who is hoping that there actually is such a form of
information called Dembski information. There isn't.
No. I do know a modest amount about transposons. But even that modest
amount is much more than you know. Transposons usually don't *do*
anything (they are largely silenced, and many have become defective
pseudotransposons and are incapable of transposition anymore because of
the fact that they don't do anything). BTW, the P element of
Drosophila shows this silencing nicely and indicates how such events
can lead to reproductive isolation. Transposons are often neither
transcribed nor translated. Some may be transcribed but not
translated. They usually do not transpose. They are just there,
replicating along with the rest of the genome. But they certainly are
*not* a repository of spare genes (other than some involved in
transposition).
> At the very least they rattle one of the two
> Darwinian mechanisms--mutation.
No. Transposition *is* a rather common form of insertional mutation.
> Suddenly, change looks a whole lot easier,
> possibly because it's planned.
Transposition is not "planned". The transposing element may (or may
not, depending on the element) favor integration at a particular
sequence, but the sequence is small (often two nucleotides) and present
at literally millions of sites in the genome. Just like other
mutational events, transposition can produce a beneficial, neutral, or
detrimental effect depending upon the site it integrates into and
conditionally upon the environmnental constraints on the organism.
> Admit it, you don't know where to draw the
> line between Darwinian-like random point mutations and designed
> transpositions.
Transposition is not any more "designed" (wrt the relevant feature of
producing results that the cell needs) than random point mutations.
Transposition may favor integration at particular sequences, but
particular point mutations also are favored by surrounding features of
the sequence. Neither occurs in any teleological fashion according to
need.
> BTW-stockrooms and warehouses are usually boring.
Again. I will be explicit. Transposable elements have no sequence
similarity to the usual types of new sequences that would make them
useful as 'spare parts'. Your warehouse is filled with useless chads
when what your "junk" is 'spare parts' argument needs is that most of
the "junk" be readable ballots.
IOW, you will continue to argue against a fantasy strawman because you
know that is the only target you have an actual argument against. And
you will continue to lie and claim that *all* evolution involves
starting with some random maximally distal sequence and proceeds to
some teleological endpoint. Let me repeat. "Junk" DNA is NOT
(usually; nature will of course use whatever works so if there happens
to be some "junk" that, by chance, has a useful function, it will be
selected for) the source of new information in any *real* evolutionary
theory nor in any real organism.
> >>>> Fetuses use a different hemoglobin en utero, maybe there is a hemoglobin
> >>>> gene somewhere in all that junk that could be used in a hyperbaric
> >>>> atmosphere.
> >>>>
> >>> And the fetal hemoglobin (actually the beta globin component) is one of
> >>> several modified duplicates allowing specialization of hemoglobin to
> >>> specific developmental environments (including embryonic hemoglobin). There
> >>> is actually quite a bit known about the way hemoglobin evolved.
> >>>
> >> This shows how hemoglobin has evolved or, alternatively, how it can be
> >> altered.
> >>
> > No. The beta globin cluster in humans (and other apes) are clearly derived by
> > duplication and divergence rather than by altering pre-existing transposon
> > sequences. In fact, there is even a non-functioning duplicate (pseudo beta1)
> > and a pair of functionally identical duplicates that differ by a single aa
> > (gamma G and gamma A) that provide real examples of putative intermediate
> > states in the duplication and divergence process.
>
> Has anyone tried to express these "non-functional" variants to determine
> their physical properties compared to functional hemoglobin?
The "non-functional" variants in the globins typically have stop codons
and frameshifts that would prevent any mRNA transcript that is made
from producing a functional protein. Other pseudogenes (those
introduced by reverse transcriptase) often lack regulatory elements
needed for transcription or transmission out of the nucleus and don't
even get that far along the path to making a protein. The reason why
pseudogenes from such unequal crossover duplicates are nonfunctional is
that they have acquired mutations (or, because they are really only
partial sequences, never had the capacity to produce a product) that
prevent them from being transcribed or translated. Because they were
duplicates, there was (often, there are exceptions) little selective
pressure to retain their function.
> > The various thalassemias (especially Lepore, where the anti-Lepore -- which
> > has 5 alpha globin genes -- has been found and is selectively netural) show
> > that unequal crossing-over events are a continuing and major cause of the
> > duplication/deletion events that generate the duplications that get modified.
> >
> > The alpha globin complex in humans has a zeta form (used in embryos), a
> > nonfunctioning pseudo zeta copy, two nonfunctioning pseudo alpha copies, and
> > two identical functioning alpha genes.
> >
> > Other vertebrates have similar but not identical clusters (which, of course,
> > follow the nested hierarchy of the branching evolutionary pathway). Unlike
> > the human case, where the order of genes neatly follows the order of
> > utilization from embryonic to adult, that is not the case in other organisms.
>
> Wow! That's not quite a 33 to 1 ratio, but if all functional genes have this
> many modified "copies" on the shelf that could account for quite a bit of
> all that junk.
Note that the complex formed by a known mechanism of duplication
formation (unequal crossing over) which is a form of mutation.
Duplication and divergence (specialization of the duplicated forms to
produce a modified beta globin that, say, works better at the embryonic
stage and a second that works better at a later stage rather than a
single hemoglobin that suffices imperfectly at both stages). This is
what is commonly known as a *mechanism* in science. Specifically, it a
*mechanism* that does not involve producing the beta globin variants
out of thin air or out of transposon sequences or out of random
sequences of "junk" DNA as you seem to propose. Obviously some of the
failed duplicates (the pseudogenes) are or will become "junk" because
they are not under the constraint of selection and will continue to
accumulate mutations by neutral drift. Sean, of course, would not
regard this mechanism as evidence of "evolution" which he asserts
requires starting from some random sequence and wandering random
sequence space until it hits the predetermined target. It is so much
easier to attack a fantasy strawman mechanism than it is to attack a
real one.
> George Evans
Ken Shaw
Provide a way to measure Dembski information. A unit of measure would be
helpful as well.
Ken
TomS
<720le.249601$cg1....@bgtnsc04-news.ops.worldnet.att.net>, Ken Shaw stated..."
Is it an "extensive" or an "intensive" property?
An intensive property, I remind the readers, is one which is not
dependent upon the quantity of material. Such as temperature,
velocity, color.
While an extensive property is directly proportional to the amount
of material. Such as heat, momentum, weight.
If you have two objects each with property X, then the combination
also has property X if it is intensive, while it has 2X if the property
is extensive.
That is a handy, elementary way of beginning to describe a property.
Perhaps you remember something like that from freshman chemistry.
--
---Tom S. <http://talkreason.org/articles/chickegg.cfm>
"Can you even assert this, Lucullus, that there is some force, united I supposed
with providence and design, that has moulded or, to use your word, fabricated a
human being? What sort of workmanship is that? where was it applied? when? why?
how?" Cicero, Academica Priora II (Lucullus) xxvii.87
hers...@indiana.edu
[snip]
Wrt Dembski information, which has more information, a copy of the
source code to OS X or a copy of your irreducibly complex living butt
(replicated a certain number of times)?
r norman
>"On Wed, 25 May 2005 14:34:43 GMT, in article
><720le.249601$cg1....@bgtnsc04-news.ops.worldnet.att.net>, Ken Shaw stated..."
>>
< snip previous discussion of Dembski "information" >
>>Provide a way to measure Dembski information. A unit of measure would be
>>helpful as well.
>
> Is it an "extensive" or an "intensive" property?
>
> An intensive property, I remind the readers, is one which is not
>dependent upon the quantity of material. Such as temperature,
>velocity, color.
>
> While an extensive property is directly proportional to the amount
>of material. Such as heat, momentum, weight.
>
> If you have two objects each with property X, then the combination
>also has property X if it is intensive, while it has 2X if the property
>is extensive.
>
> That is a handy, elementary way of beginning to describe a property.
>Perhaps you remember something like that from freshman chemistry.
In addition, intensive times extensive is work or energy. More
properly, the integral of an intensive variable (corresponding to a
"force" term) with respect to an extensive variable (corresponding to
a "distance" term) is work done (energy change involved) in making the
change in the extensive term.
Information in the classical sense corresponds closely with entropy
which is an extensive term associated with temperature as the
corresponding intensive term. Statistical thermodynamics treats
entropy as a the logarithm of the volume (more accurately, the
"measure") of a region in a phase space. This is identical to the
negative of the classical Shannon information measure, hence
information as "negentropy". Does Dembski information have any
similar thermodynamic relevance? There are all sorts of conceptual
measures you can define and call "information". But if they have no
relation to physics or physical chemistry, then they are not really
relevant in helping us understand the way the world works.
Mark Isaak
>Mark Isaak <eci...@earthlinknospam.next> wrote or quoted:
>
>> Some of the best evidence there is for life being designed
>> is that the design is amazingly crappy.
>
>That's /usually/ presented as evidence that life evolved.
Like I said, without evolution, you don't have design.
Mark Isaak
<geor...@earthlink.net> wrote:
>in article 1116898646.1...@g44g2000cwa.googlegroups.com,
>wizo...@hotmail.com at wizo...@hotmail.com wrote on 5/23/05 6:37 PM:
>
>> Mark Isaak wrote:
>>> There is plenty of redundancy among the codons to give selenocystine
>> a
>>> codon of its own. That is what we would expect of a deliberate
>>> designer (or maybe one codon which always combines with other DNA to
>>> produce alternate amino acids, leaving room for future enhancements).
>>> The kludge of giving UGA a rare second function is the sort of thing
>>> we expect from evolution, not from intelligent design.
>>>
>> You my friend are clearly not a computer programmer! The number of
>> times I have seen an otherwise seemingly intelligent and capable
>> programmer overload a particular symbol/encoding/value/name to mean
>> multiple things, when plenty of unused alternatives were available, is
>> testament to the ability of humans to make almost anything they do more
>> complicated than it needs to be. Worryingly, half the time the person
>> I have observed doing this has been yours truly.
>>
>> Of course, I doubt too many ID'er would want to accuse their Designers
>> of being prone to very human sorts of irrational behaviour.
>
>I've been doing some quick study on this strange subject. The way the
>translation mechanism knows that UGA stop codon means Selenocysteine is by
>the presence of an inserted segment, I think immediately after the UGA.
No, the pattern is AUGA__AA__GA, where the first "A" is just before
the UGA in question, "__" stands for a variable number of variable
bases (but bases which form a helix and a terminal loop in the RNA),
and the "AA" may be replaced with "CC". The trailing part of this
pattern may or may not go past the coding section of the RNA.
>Now how does *that* happen by Darwinian mechanisms?
Gradually. The first selenocystein was probably advantageous but not
essential. The pattern which triggered the first selenocystein could
have been the pattern that just happened to be there, where a mutant
enzyme happened to react to it. If you cannot think of a gradual
sequence which plausibly could lead to such a mechanism, you simply
are not trying. (Not that I would blame you for not trying, since
part of it would require learning a lot of biochemistry.)
>This is a unique manipulation of the coding method.
>I'm thinking it is possibly a post-production modification. It's like DNA
>all of the sudden contains [Editors notes]!
There are all kinds of post-production modifications, from the
selenocystein one which barely qualifies as "post-", to modifications
that affect how long before mRNA gets degraded. Another interesting
one from a design standpoint is a set of enzymes that replace one
amino acid of an mRNA with another, although none of those enzymes
would be necessary if the DNA coded for the second amino acid to begin
with. And, of course, there are all kinds of pre-production
modifications, too. It all screams design by unintelligent evolution.
Mark Isaak
<geor...@earthlink.net> wrote:
I don't understand what you are saying. What does "farther in design"
mean? What does "greater design criterion" mean?
And how do you explain two organisms which are virtually identical in
their function but entirely different in form? (I am thinking
especially of certain hummingbirds and sphinx moths which both feed on
nectar as they hover before flowers.)
>OTOH evolution would predict identical hierarchical structures
>for all proteins because all the parts of a given organism branched at
>exactly the same times.
Evolution does not say that all proteins evolved at exactly the same
rates, or that random chance would not sometimes obscure true
relationships. In fact, it does not even say that all parts of an
organism branched at the same time. It is possible to get gene
duplications within a species, so that gene A of species X is more
closely related to gene B of species X than to gene A from species Y.
Or vice versa. Determining hierarchies is not trivial, but it can be
done, and it has never yet favored design.
> The empirical data, in my opinion, favors design.
Only because human design processes share so much with evolution.
Mainly, they start with existing designs and alter them, and they rely
on trial and error. But there are significant differences, too, which
rule out design as an explanation.
Mark Isaak
<rgri...@ctc.net> wrote:
>You might want to really think about your future as you pursue the tactics
>of lies and deceits in pressing your point. Think warm, warmer, hot, and
>"where can I get a drop of water to soothe my torment?". God hates lying.
Not the God of intelligent design. Intelligent design requires that
God be responsible for innumerable miseries in the world; in fact, it
requires that He deliberately created those miseries. Given the fact
that the intelligent design God is evil, it should not be surprising
if the intelligent design God loves lying.
r norman
<eci...@earthlinkNOSPAM.next> wrote:
>On Wed, 25 May 2005 08:19:15 -0400, "Raymond E. Griffith"
><rgri...@ctc.net> wrote:
>
>>You might want to really think about your future as you pursue the tactics
>>of lies and deceits in pressing your point. Think warm, warmer, hot, and
>>"where can I get a drop of water to soothe my torment?". God hates lying.
>
>Not the God of intelligent design. Intelligent design requires that
>God be responsible for innumerable miseries in the world; in fact, it
>requires that He deliberately created those miseries. Given the fact
>that the intelligent design God is evil, it should not be surprising
>if the intelligent design God loves lying.
Of course, if you were _truly_ worthy, you wouldn't be subject to
miseries! All those innocent children probably really weren't
baptized properly, so they deserved what they got, too!
Tim Tyler
Obviously - but your supporting argument was of the form: if one
mammal can survive without 90% of its DNA, the equivalant DNA
in other mammals can have no adaptive function.
*You* might find that convincing - but I don't see any reason why
*others* should follow you in that line of reasoning.
> Given your logic, why should we believe that the results of an
> experiment on one individual should apply to other individuals of the
> same species?
Obviously, that is going to depend on the species and experiment:
If the experiment is on fingernail patterns or eye colour, there's
typically little basis for such a belief.
If the experiment is on genitals, there's often a 50% chance of
the result not applying.
On the other hand, if the experiment involves the on number of
legs, there may be a firmer basis for the belief.
> >>Yes, the problem with experiments like that is that one can always argue
> >>that the missing material does have a function, just one too subtle to
> >>be detected easily; maybe it's a function that is only needed once every
> >>hundred generations. That's the beauty of looking at sequence
> >>conservation, because it indexes long-term importance.
> >
> > It indexes conserved genes.
> >
> > Of course, genes for traits such as diseases resistance are not
> > necessarily conserved - and can be selected in such a way that
> > they are constantly changing.
>
> Yes, there are a few of those. They change at greater than the neutral
> rate, and that stands out too.
So: some selected genes change faster then neutral genes - and other
selected genes change slower than neutral genes. Maybe some also
change at about the same speed as neutral genes.
> > Sequence conservation doesn't have too much to say about that.
>
> Yes it does, since change in those genes is actually accelerated. And
> they are embedded in conserved sequences too -- only selected domains
> have accelerated evolution. This has nothing to do with junk DNA.
The topic arose because you suggested that only conserved sequences
were likely to be important in the long term.
That is surely false - since selection for diseases resistance traits
can favour novelty, the not-before seen. Only looking at conserved
sequences would result in an underestimation of the volume of DNA
which is subjected to selection.
Also, the role of DNA as a spacer should not be neglected. Just because
a sequence is variable that doesn't mean it serves no purpose. A DNA
sequence has other properties besides the details of the order of the
base pairs on it - in particular it has a length.
Several of the proposed functions of junk DNA involve this notion -
that the DNA affects linkage patterns - that it acts as a sink
for intracellular mutagens - that it allows space for expansion
at the end of coding regions - that it allows gene duplication
without changing chromosome size - that it harbours LINEs and
SINEs - which act as types of highly non-random mutagen - and
so on.
Consequently to argue from a variable sequence to non-functionality,
represents a logical flaw - since a stretch of DNA has heritable
properties which do not depend on its sequence data.
Tim Tyler
> On Wed, 25 May 2005 07:41:02 GMT, Tim Tyler <t...@tt1lock.org> wrote:
> >Mark Isaak <eci...@earthlinknospam.next> wrote or quoted:
> >> Some of the best evidence there is for life being designed
> >> is that the design is amazingly crappy.
> >
> >That's /usually/ presented as evidence that life evolved.
>
> Like I said, without evolution, you don't have design.
So what?
Crappiness is not good evidence for design over evolution - since
both design and evolution can produce poor quality results.
Crappiness may count at evidence against an omnipotent designer,
who is /supposed/ to have created man in his image, though.
John Harshman
And you might find that unconvincing, but why? It seems to be an appeal
to ignorance: we don't know everything, therefore we shouldn't draw any
conclusions from the evidence we do have. Would you agree that the tiny
genome of fugu (which is a fish, not a mammal, by the way) is in fact
evidence, whether conclusive or not, in favor of junk being junk?
>>Given your logic, why should we believe that the results of an
>>experiment on one individual should apply to other individuals of the
>>same species?
>
> Obviously, that is going to depend on the species and experiment:
>
> If the experiment is on fingernail patterns or eye colour, there's
> typically little basis for such a belief.
>
> If the experiment is on genitals, there's often a 50% chance of
> the result not applying.
>
> On the other hand, if the experiment involves the on number of
> legs, there may be a firmer basis for the belief.
Why? Do we have to come to you for decisions on this sort of thing, or
is there a rule we can follow?
>>>>Yes, the problem with experiments like that is that one can always argue
>>>>that the missing material does have a function, just one too subtle to
>>>>be detected easily; maybe it's a function that is only needed once every
>>>>hundred generations. That's the beauty of looking at sequence
>>>>conservation, because it indexes long-term importance.
>>>
>>>It indexes conserved genes.
>>>
>>>Of course, genes for traits such as diseases resistance are not
>>>necessarily conserved - and can be selected in such a way that
>>>they are constantly changing.
>>
>>Yes, there are a few of those. They change at greater than the neutral
>>rate, and that stands out too.
>
> So: some selected genes change faster then neutral genes - and other
> selected genes change slower than neutral genes. Maybe some also
> change at about the same speed as neutral genes.
Why would that happen? The reason some genes are slow is that they
perform a function for which a particular sequence is better than those
near to them. The reason some genes are fast is that their function
actively selects for differences. What would cause sequences to be
selected for evolution at a neutral rate? And what leads you to believe
that the bulk of our DNA could possibly be made up of such sequences?
>>>Sequence conservation doesn't have too much to say about that.
>>
>>Yes it does, since change in those genes is actually accelerated. And
>>they are embedded in conserved sequences too -- only selected domains
>>have accelerated evolution. This has nothing to do with junk DNA.
>
> The topic arose because you suggested that only conserved sequences
> were likely to be important in the long term.
>
> That is surely false - since selection for diseases resistance traits
> can favour novelty, the not-before seen. Only looking at conserved
> sequences would result in an underestimation of the volume of DNA
> which is subjected to selection.
True to a very minor degree. The number of these fast-evolving sequences
is quite small, and again they are embedded within conserved sequences,
and also are conserved in some other ways -- they maintain open reading
frames, for example -- that neutrally evolving sequences are not.
> Also, the role of DNA as a spacer should not be neglected. Just because
> a sequence is variable that doesn't mean it serves no purpose. A DNA
> sequence has other properties besides the details of the order of the
> base pairs on it - in particular it has a length.
True. Some DNA may be important merely as a spacer, and other DNA may be
selected merely because it makes a cell bigger. But these are doubtful
exceptions. There are no hidden functions there to delight the
creationist, and that's what this argument is really about.
> Several of the proposed functions of junk DNA involve this notion -
> that the DNA affects linkage patterns - that it acts as a sink
> for intracellular mutagens - that it allows space for expansion
> at the end of coding regions - that it allows gene duplication
> without changing chromosome size - that it harbours LINEs and
> SINEs - which act as types of highly non-random mutagen - and
> so on.
Some of these ideas are silly, if you ask me. And they all founder on
the extreme variability in genome size, unless you can think of a reason
why these factors should all differ so greatly among vertebrates.
> Consequently to argue from a variable sequence to non-functionality,
> represents a logical flaw - since a stretch of DNA has heritable
> properties which do not depend on its sequence data.
Agreed, to a point. There are some cases in which DNA is just a
place-holder. However, I think the great variability in genome size does
argue that most of the neutrally evolving DNA does indeed fill no
function. Why should mammals require so much more of these bulk
functions than fugu, and so much less than frogs? There's just no
sensible, functional explanation for that.
Mark Isaak
>Mark Isaak <eci...@earthlinknospam.next> wrote or quoted:
>> On Wed, 25 May 2005 07:41:02 GMT, Tim Tyler <t...@tt1lock.org> wrote:
>> >Mark Isaak <eci...@earthlinknospam.next> wrote or quoted:
>
>> >> Some of the best evidence there is for life being designed
>> >> is that the design is amazingly crappy.
>> >
>> >That's /usually/ presented as evidence that life evolved.
>>
>> Like I said, without evolution, you don't have design.
>
>So what?
>
>Crappiness is not good evidence for design over evolution - since
>both design and evolution can produce poor quality results.
>
>Crappiness may count at evidence against an omnipotent designer,
>who is /supposed/ to have created man in his image, though.
Yes, you are right. Crappiness could result from either, so is
evidence for neither. I should have written of "compatibility with"
rather than "evidence for."
But remember the general quality of evidence for design in nature.
"Some of the best" evidence for design includes anything that is not
actually evidence *against* design.
hers...@indiana.edu
Rather, the argument is that the DNA equivalent to the missing DNA has
no obvious significant adaptive function. To have an adaptive function
means that it must fill a need. Since the fugu performs the same basic
functions as, say, the zebra fish, that does rather argue that the type
of missing DNA in fugu that is present in the zebra fish is not highly
significant wrt function.
And, of course, there is also the matter of major deletions (especially
in chromosomes that don't have many coding genes, like the Y) that have
minimal effects indicating that a great deal of DNA in other organisms
is not highly significant.
> *You* might find that convincing - but I don't see any reason why
> *others* should follow you in that line of reasoning.
>
> > Given your logic, why should we believe that the results of an
> > experiment on one individual should apply to other individuals of the
> > same species?
>
> Obviously, that is going to depend on the species and experiment:
>
> If the experiment is on fingernail patterns or eye colour, there's
> typically little basis for such a belief.
>
> If the experiment is on genitals, there's often a 50% chance of
> the result not applying.
>
> On the other hand, if the experiment involves the on number of
> legs, there may be a firmer basis for the belief.
>
> > >>Yes, the problem with experiments like that is that one can always argue
> > >>that the missing material does have a function, just one too subtle to
> > >>be detected easily; maybe it's a function that is only needed once every
> > >>hundred generations. That's the beauty of looking at sequence
> > >>conservation, because it indexes long-term importance.
> > >
> > > It indexes conserved genes.
And what, pray tell, distinguishes a conserved sequence from a
non-conserved on other than that the conserved ones have selective
utility? We know that pure chance will lead to changes at roughly a
give rate in the absence of selection. It is significant difference
from that rate due to chance alone that determines conservation.
> > > Of course, genes for traits such as diseases resistance are not
> > > necessarily conserved - and can be selected in such a way that
> > > they are constantly changing.
> >
> > Yes, there are a few of those. They change at greater than the neutral
> > rate, and that stands out too.
>
> So: some selected genes change faster then neutral genes - and other
> selected genes change slower than neutral genes. Maybe some also
> change at about the same speed as neutral genes.
That is so silly you should look at it again.
Some sequences change *significantly* faster than selectively neutral
genes. That is because these sequences are under strong selective
pressure favoring the changes. This is typically a rare phenomenon,
but happens, for example, in frequency-dependent selection where rare
alleles are always selectively favored. An example would be
self-sterility alleles in certain plants.
Other sequences change *significantly* less than would be expected from
neutral drift alone. These are conserved sequences. They are
conserved precisely because they perform selectively useful features
and already are fairly well optimized.
Sequences that don't change *significantly* faster than the
expectations of neutral drift, and *significance* in this case means
the x% range for changes that would be expected by chance alone. If,
for example, 50% of genes were allele a and 50% were allele b, both
selectively neutral, one would not expect the next generation to have
exactly 50% of each, but would expect the variance to be relatively
small depending on population size. 95% of the time, the next
generation will be, for a certain population size, between, say, 50.5%
a and 49.5% a. Since chance has no memory, the *expectation* of the
next generation will be whatever ratio there is in the current
generation. That is the cause of neutral drift. But sequences that
don't change *significantly* faster than neutral drift are *by
definition* selectively neutral. Note that neutrality is dependent
upon the frequency of alleles in the current population and population
size only.
The above does assume that selective conditions are constant. That is
not always, of course, a correct assumption. That is, selection or
neutrality is *always* contingent upon environmental conditions.
> > > Sequence conservation doesn't have too much to say about that.
> >
> > Yes it does, since change in those genes is actually accelerated. And
> > they are embedded in conserved sequences too -- only selected domains
> > have accelerated evolution. This has nothing to do with junk DNA.
>
> The topic arose because you suggested that only conserved sequences
> were likely to be important in the long term.
> That is surely false - since selection for diseases resistance traits
> can favour novelty, the not-before seen. Only looking at conserved
> sequences would result in an underestimation of the volume of DNA
> which is subjected to selection.
Disease resistance does not usually result in significant change in an
otherwise conserved sequence. Resistance to streptomycin, for example,
is due to a single aa alteration of a ribosomal protein. The rest of
the protein is as conserved as any other protein. Conservation does
not mean the protein remains completely unchanged. It means the rate
of change is slower and constrained to parts of the protein that are
less actively engaged in function. The case of the self-sterile
alleles in plants would be a partial exception to the rule. The rule
is that conservation of sequence is an excellent clue to functional
utility. Sequences that change *faster* than neutrality while
retaining function are rare as hen's teeth if not non-existent. I
doubt that even the self-sterility alleles would meet that criteria, as
they have conserved areas in addition to the areas of more rapid
evolutionary selective change.
>
> Also, the role of DNA as a spacer should not be neglected. Just because
> a sequence is variable that doesn't mean it serves no purpose. A DNA
> sequence has other properties besides the details of the order of the
> base pairs on it - in particular it has a length.
I.e., a need for bulk can be filled by otherwise utterly useless
sequences. It can be filled by "junk" and serve the function of just
being there. And lo, that does seem to be the case. 90+% of the human
genome is filled by "junk" that serves no purpose other than being
there.
Moreover, it is quite clear that not only is this DNA's 'utility'
independent of sequence, it is also largely independent or not highly
dependent on the length of the sequence, since it can often be deleted
or expanded without any detectable consequence. Not only is its
sequence not particularly important; its length is also not
particularly important to whatever 'function' you want to apply to it.
> Several of the proposed functions of junk DNA involve this notion -
> that the DNA affects linkage patterns - that it acts as a sink
> for intracellular mutagens - that it allows space for expansion
> at the end of coding regions - that it allows gene duplication
> without changing chromosome size - that it harbours LINEs and
> SINEs - which act as types of highly non-random mutagen - and
> so on.
That doesn't make such sequence-independent DNA any less "junk". These
bulk features only require the presence of some DNA. It does not
require the presence of any specific sequence (LINEs and SINEs
excepted, but they are not there for the benefit of the organism, but
have a more selfish origin). "Junk" DNA serves no purpose but 'being
there'. That means that 90+% of our DNA is there for no purpose but
being there and, possibly, some bulk effect. Only 3% is coding
sequence important to function (and, of course, even much of that is
subject to quasi-neutral drift). The remaining 7% includes regulatory
sequences (conserved), centromeric and telomeric (and other structural
features) sequences (conserved), siRNAs and other RNA-only coding
sequences (conserved). Sequences that have *specific* useful functions
are largely conserved sequences.
> Consequently to argue from a variable sequence to non-functionality,
> represents a logical flaw - since a stretch of DNA has heritable
> properties which do not depend on its sequence data.
Of course. Junk DNA replicates just like functional (sequence vital)
DNA. SFW? The sequence of junk DNA, unlike sequence functional DNA,
drifts like selectively neutral sequences (including changes in
length). Selectively important DNA, OTOH, usually have a significantly
conserved sequence. Rarely (mostly in frequency dependent selection),
it will change more rapidly than by drift.
George Evans
eci...@earthlinkNOSPAM.next wrote on 5/25/05 11:39 AM:
I know a lot of Biochemistry, that's why I am perplexed. It looks like at
least three separate, quite involved, and neutral mutations need to happen
at the same time in order to even incorporate a selenocysteine in a protein.
A new tRNA would be needed, the ribosome would have to "learn" the new code
in order to not allow the leading AUG to be translated, and the mRNA would
have to be modified. Any suggestions? Wait, I know........Gradually.
<snip>
George Evans
John Harshman
> Tim Tyler wrote:
[snip]
> Sequences that don't change *significantly* faster than the
> expectations of neutral drift, and *significance* in this case means
> the x% range for changes that would be expected by chance alone. If,
> for example, 50% of genes were allele a and 50% were allele b, both
> selectively neutral, one would not expect the next generation to have
> exactly 50% of each, but would expect the variance to be relatively
> small depending on population size. 95% of the time, the next
> generation will be, for a certain population size, between, say, 50.5%
> a and 49.5% a. Since chance has no memory, the *expectation* of the
> next generation will be whatever ratio there is in the current
> generation. That is the cause of neutral drift. But sequences that
> don't change *significantly* faster than neutral drift are *by
> definition* selectively neutral.
I beg to quibble on this point, twice. First, significance is a function
of sample size and of the sensitivity of the test, not of the neutrality
or lack thereof of the sequence/site itself. Signifigance may determine
our ability to tell whether a sequence/site is evolving neutrally, but
lack of significance can't determine whether a site is actually evolving
neutrally. Second, the definition of neutrality has nothing to do with
rate, and everything to do with lack of selection. Consider a sequence
in which p sites are completely conserved, and q sites are evolving at
the maximum selectable rate. We can adjust p and q so that the sequence
as a whole evolves at any rate we like, including the neutral rate.
That's a contrived example, but in fact it is indeed possible for
selection to operate so as to simulate a neutral rate of evolution,
though there would most likely be other ways to tell that it wasn't
evolving neutrally.
> Note that neutrality is dependent
> upon the frequency of alleles in the current population and population
> size only.
You mean the probability of neutral fixation here, presumably.
Neutrality itself is dependent on the absence of selection, period.
[snip]
>>Also, the role of DNA as a spacer should not be neglected. Just because
>>a sequence is variable that doesn't mean it serves no purpose. A DNA
>>sequence has other properties besides the details of the order of the
>>base pairs on it - in particular it has a length.
>
>
> I.e., a need for bulk can be filled by otherwise utterly useless
> sequences. It can be filled by "junk" and serve the function of just
> being there. And lo, that does seem to be the case. 90+% of the human
> genome is filled by "junk" that serves no purpose other than being
> there.
My bet is that most of the junk isn't even filling a bulk purpose;
that's a little bit harder to show, but if it were, would the DNA
content of vertebrate cells vary as much as it does?
[snip]
George Evans
hers...@indiana.edu at hers...@indiana.edu wrote on 5/25/05 7:30 AM:
>
> George Evans wrote:
>
>> in article 1116947284.8...@g43g2000cwa.googlegroups.com,
>> hers...@indiana.edu at hers...@indiana.edu wrote on 5/24/05 8:08 AM:
>>
>>> George Evans wrote:
<snip>
>>> I, OTOH, would be shocked, shocked if such a relationship were found. The
>>> 'energy expense' of duplicating a genome is largely sequence (and thus
>>> information) independent. It does take more energy to break apart the three
>>> H bonds of a G:C pair than the two of an A:T pair, but that is about the
>>> only significant sequence difference I can think of. Can you think of any
>>> reason why it would take more or less energy to replicate a meaningless
>>> sequence containing a given proportion of A:T to G:C than the same material
>>> that encodes proteins? If anything, it takes more energy (aside from
>>> replication) to maintain the *useful* bits, given that the useful bits are
>>> transcribed (and sometimes translated) at higher frequency (but that is not
>>> always the case). But even then, a single point mutation can produce a gene
>>> that is also transcribed and translated into a useless protein. That change
>>> would have no 'energy expense' consequences related to the replication of
>>> the sequence or the production of protein product. The mutant protein
>>> might, of course, have lethal consequences related to the ability of the
>>> cell to extract energy from its environment, but that is a different
>>> question.
>>>
>> True to form, you are once again stuck speaking as a hardware engineer--or
>> maybe I should say Xerox repairman. Yes, it costs the same to copy the source
>> code to OS X as it would to produce an equal number of pages of my butt.
>>
> That is quite true. But what other form of information *that is actually
> independently measureable* rather than a drawing of the bull's eye after the
> arrow has stuck were you talking about?
The kind of information that you hardware engineers can only sit and marvel
at.
>> However I am talking about Dembski information not Shannon information, the
>> house of cards and not the cards themselves.
>>
> I agree that Dembski information is a house of cards that has nothing but _ex
> post facto_ teleological meaning. It is unmeasureable.
But it's there so just learn to appreciate it intuitively for now.
>> This is where science is silent so far and you are hoping beyond hope that
>> there is no such information. But of course it's there.
>>
> Actually it is you who is hoping that there actually is such a form of
> information called Dembski information. There isn't.
I'm sorry you have to look so ignorant.
<snip>
>>> What is it about these "various transposons" do you think bolsters any sort
>>> of "stored gene" hypothesis. The transposon sequences are not gene
>>> sequences. They are highly repetitive and the only 'gene sequnces' that they
>>> seem to encode are (often defective) related to transposition. They are not
>>> encoding cryptic betagalactosidases or hemoglobins. Now, that doesn't mean
>>> that it is impossible for some or a few of these transposons to be situated
>>> so as to be >>> a regulatory element. And the presence of repetitive and
>>> potentially mobile transposable elements makes the sorts of duplications and
>>> chimera formations that really are frequently involved in evolution more
>>> doable. But the transposable elements themselves are not a very good source
>>> of "stored genes". They are too repetitive and boring for that.
>>>
>> Pardon me, but it doesn't sound like you really know much about what these
>> transposons do either.
>>
> No. I do know a modest amount about transposons. But even that modest amount
> is much more than you know. Transposons usually don't *do* anything (they are
> largely silenced, and many have become defective pseudotransposons and are
> incapable of transposition anymore because of the fact that they don't do
> anything). BTW, the P element of Drosophila shows this silencing nicely and
> indicates how such events can lead to reproductive isolation. Transposons are
> often neither transcribed nor translated. Some may be transcribed but not
> translated. They usually do not transpose. They are just there, replicating
> along with the rest of the genome. But they certainly are *not* a repository
> of spare genes (other than some involved in transposition).
You don't know that. And it is impossible to maintain that position in light
of the fact that the movement of transposons into and out of genes is
responsible for known phenotypic changes, for example the different colored
kernels of Indian Corn.
>> At the very least they rattle one of the two Darwinian mechanisms--mutation.
>>
> No. Transposition *is* a rather common form of insertional mutation.
But that's not the slow, minute change that Darwin predicted. And if it
amounts to taking a part off the shelf, it is a stretch to call it a
mutation at all.
>> Suddenly, change looks a whole lot easier, possibly because it's planned.
>>
> Transposition is not "planned". The transposing element may (or may not,
> depending on the element) favor integration at a particular sequence, but the
> sequence is small (often two nucleotides) and present at literally millions of
> sites in the genome. Just like other mutational events, transposition can
> produce a beneficial, neutral, or detrimental effect depending upon the site
> it integrates into and conditionally upon the environmnental constraints on
> the organism.
I don't know. If I were in research I would be writing a grant proposal to
search genomes for areas that matched introns of active genes. Also, keep in
mind that just because something is planned doesn't mean it can't go haywire
now and then.
>> Admit it, you don't know where to draw the line between Darwinian-like random
>> point mutations and designed transpositions.
>>
> Transposition is not any more "designed" (wrt the relevant feature of
> producing results that the cell needs) than random point mutations.
> Transposition may favor integration at particular sequences, but particular
> point mutations also are favored by surrounding features of the sequence.
> Neither occurs in any teleological fashion according to need.
>
>> BTW-stockrooms and warehouses are usually boring.
>>
> Again. I will be explicit. Transposable elements have no sequence similarity
> to the usual types of new sequences that would make them useful as 'spare
> parts'. Your warehouse is filled with useless chads when what your "junk" is
> 'spare parts' argument needs is that most of the "junk" be readable ballots.
Please be as explicit as possible about your hypothetical views.
<snip>
>>>> Maybe it is a fantasy but it sure is intriguing. I'm thinking of a directed
>>>> mutation capability, kind of like "This enzyme isn't working so well, try
>>>> the next one up the chromosome." You have to admit this opens up some
>>>> interesting lines of thought.
>>>>
>>> Not really. The assumption that there is a "next one [closely related in
>>> sequence, but nonfunctional gene] up the chromosome" is largely invalidated
>>> by empirical reality. The idea that new genes arise from sequences
>>> distantly related in sequence to the functional sequence is a fantasy
>>> strawman (I call it the Pitman fallacy for obvious reasons).
>>>
>> Well then you just stay on your secure 3% island. Sean and I will journey out
>> onto the 97% of relatively uncharted waters.
>>
> IOW, you will continue to argue against a fantasy strawman because you know
> that is the only target you have an actual argument against. And you will
> continue to lie and claim that *all* evolution involves starting with some
> random maximally distal sequence and proceeds to some teleological endpoint.
> Let me repeat. "Junk" DNA is NOT (usually; nature will of course use whatever
> works so if there happens to be some "junk" that, by chance, has a useful
> function, it will be selected for) the source of new information in any *real*
> evolutionary theory nor in any real organism.
And let me repeat. You DO NOT know that, you are guessing.
<snip>
I have been reading your discussions with Sean for a while now and am
prepared to answer this. Sean does not require starting from a random
sequence, his model starts from a *functional* island. His "target" is
predetermined only in the sense of being another functional island, not in
the sense of being unique in space. Now are these two false
characterizations fantasy strawmen or are they real ones?
George Evans
George Evans
Shaw at non...@your.biz wrote on 5/25/05 7:34 AM:
>
> George Evans wrote:
>
>> in article 1116947284.8...@g43g2000cwa.googlegroups.com,
>> hers...@indiana.edu at hers...@indiana.edu wrote on 5/24/05 8:08 AM:
>>
>>> George Evans wrote:
<snip>
Well, I think this is difficult because the the measure is going to be in
terms of what a gene is does and how valuable that is to the cell. It's like
trying to figure how much a cell would pay for a gene on the open market.
But being able to measure a quantity is not the be and and end all of
existence. We found ways to measure heat and it doesn't exist. We can't
measure the information content of a computer program but the programmer
would object to the idea that it didn't exist.
George Evans
hers...@indiana.edu
Still not capable of describing Dembski information in any meaningful
public way, are you? Dembski information, like beauty, is in the eye
of the beholder and only in the eye of the beholder.
> >> However I am talking about Dembski information not Shannon information, the
> >> house of cards and not the cards themselves.
> >>
> > I agree that Dembski information is a house of cards that has nothing but _ex
> > post facto_ teleological meaning. It is unmeasureable.
>
> But it's there so just learn to appreciate it intuitively for now.
>
> >> This is where science is silent so far and you are hoping beyond hope that
> >> there is no such information. But of course it's there.
> >>
> > Actually it is you who is hoping that there actually is such a form of
> > information called Dembski information. There isn't.
>
> I'm sorry you have to look so ignorant.
Still not capable of describing Dembski information in any meaningful
public way, are you? Dembski information, like beauty, is in the eye
of the beholder and only in the eye of the beholder.
Is that why you don't reply with, "No. Dembski information is
measureable by ..."?
Yes, I do indeed know that. Transposons make up the *repetitive*
sequences found in genomes. 'Repetitive' in this sense means that they
all have similar sequences (some now being pseudotransposons because of
mutation). The features that make them transposable elements precludes
their being a varied source of "stored genes".
> And it is impossible to maintain that position in light
> of the fact that the movement of transposons into and out of genes is
> responsible for known phenotypic changes, for example the different colored
> kernels of Indian Corn.
Do you know how the movement of transposons (out of in this particular
case) cause the change in phenotype? It is rather simple. When
inserted, the largish transposon (inside an intron) means that a
particular gene will be transcribed, but the transcript will not be
spliced properly. When the transposon pops out (in a specific tissue
in which it the transposase activity is activated), leaving behind a
small duplicate (which would cause mistranslation in a coding sequence)
the restored rough size (a few added nucleotides are irrelevant in an
intron) of the intron allows proper splicing and translation. The
transposon is not carrying in or taking out any "stored gene" sequence.
It is acting as a regulated transposable element. Causing a somatic
mutant phenotype (the color) when it pops out in a specific tissue. It
also caused a mutation when it inserted into the intron, inactivating a
gene that caused colored kernals.
> >> At the very least they rattle one of the two Darwinian mechanisms--mutation.
> >>
> > No. Transposition *is* a rather common form of insertional mutation.
>
> But that's not the slow, minute change that Darwin predicted.
A transposition event is different wrt rate of change than a point
mutation. It may at a rate which is more (or less) frequent than point
mutations, but transpostions do not cause directed teleological
mutations any better than point mutations or frameshifts or deletions
or chromosomal rearrangements. The effect of transposition is
determined by where it inserts. That occasional organisms have
domesticated certain of their transposable elements (MAT locus in
yeast) doesn't mean that transposon
> And if it
> amounts to taking a part off the shelf, it is a stretch to call it a
> mutation at all.
It isn't taking any part off the shelf other than the transposon
itself. Where do you get this bizarre idea that transposons contain
all these various "hidden gene sequences". They are *repetitive*
elements.
> >> Suddenly, change looks a whole lot easier, possibly because it's planned.
> >>
> > Transposition is not "planned". The transposing element may (or may not,
> > depending on the element) favor integration at a particular sequence, but the
> > sequence is small (often two nucleotides) and present at literally millions of
> > sites in the genome. Just like other mutational events, transposition can
> > produce a beneficial, neutral, or detrimental effect depending upon the site
> > it integrates into and conditionally upon the environmnental constraints on
> > the organism.
>
> I don't know. If I were in research I would be writing a grant proposal to
> search genomes for areas that matched introns of active genes.
Been done. Most of the sequence in introns is selectively neutral and
changes at the rate of neutral drift over evolutionary time frames. The
parts that are conserved are typically the small sequences that specify
splice points.
> Also, keep in
> mind that just because something is planned doesn't mean it can't go haywire
> now and then.
And your evidence for planning is the somatic (not germ line) changes
in Indian corn?
> >> Admit it, you don't know where to draw the line between Darwinian-like random
> >> point mutations and designed transpositions.
> >>
> > Transposition is not any more "designed" (wrt the relevant feature of
> > producing results that the cell needs) than random point mutations.
> > Transposition may favor integration at particular sequences, but particular
> > point mutations also are favored by surrounding features of the sequence.
> > Neither occurs in any teleological fashion according to need.
> >
> >> BTW-stockrooms and warehouses are usually boring.
> >>
> > Again. I will be explicit. Transposable elements have no sequence similarity
> > to the usual types of new sequences that would make them useful as 'spare
> > parts'. Your warehouse is filled with useless chads when what your "junk" is
> > 'spare parts' argument needs is that most of the "junk" be readable ballots.
>
> Please be as explicit as possible about your hypothetical views.
I wasn't talking about hypothetical views. I was stating what the
evidence from transposon research tells us. Transposons are typically
repetitive elements and cannot serve as the source of any hypothetical
"spare enzymatic genes". That is based on actual sequencing of actual
transposons.
> <snip>
>
> >>>> Maybe it is a fantasy but it sure is intriguing. I'm thinking of a directed
> >>>> mutation capability, kind of like "This enzyme isn't working so well, try
> >>>> the next one up the chromosome." You have to admit this opens up some
> >>>> interesting lines of thought.
> >>>>
> >>> Not really. The assumption that there is a "next one [closely related in
> >>> sequence, but nonfunctional gene] up the chromosome" is largely invalidated
> >>> by empirical reality. The idea that new genes arise from sequences
> >>> distantly related in sequence to the functional sequence is a fantasy
> >>> strawman (I call it the Pitman fallacy for obvious reasons).
> >>>
> >> Well then you just stay on your secure 3% island. Sean and I will journey out
> >> onto the 97% of relatively uncharted waters.
> >>
> > IOW, you will continue to argue against a fantasy strawman because you know
> > that is the only target you have an actual argument against. And you will
> > continue to lie and claim that *all* evolution involves starting with some
> > random maximally distal sequence and proceeds to some teleological endpoint.
> > Let me repeat. "Junk" DNA is NOT (usually; nature will of course use whatever
> > works so if there happens to be some "junk" that, by chance, has a useful
> > function, it will be selected for) the source of new information in any *real*
> > evolutionary theory nor in any real organism.
>
> And let me repeat. You DO NOT know that, you are guessing.
Do you honestly think that transposon sequences are an unknown that can
hide all your hypothetical "spare parts genes"? Or is that simply your
ignorance speaking? Again, transposon sequences are known. Take Alu
sequences for example. Alu sequences are highly repetitive and the Alu
transposon is largely a domesticated transposon, with most of the
sequences remaining stable. When one does move, it is as likely to
cause a deleterious change as any other mutation. That doesn't
preclude it from occasionally producing a beneficial change. It is
acting just like a G to A missense mutational change.
Sean specifically starts from *anywhere* in *total* random sequence
space (actually his unstated mathematical assumption is that the
starting point protein is different in every single sequence site from
the end result because he assumes that every single one of his 'fairly
specified aa residues' did not exist in the starting sequence). His
model most certainly does not start from a *functional* island unless
one assumes that that island is maximally different from the end
protein by the total number of 'fairly specified aa residues'. And
most importantly, his model *specifically* does *not* start from the
pre-existing *functional* island that is most similar in sequence to
the desired result, as any evolutionary model would; it starts (he
says, but the math says most distant) with some random sequence in
total sequence space. He also makes the false assumption that *rare*
functional islands are *evenly* distributed in sequence space in order
to maximize the gaps between them. I have never argued that he was
talking about a single sequence. He is talking about a teleological
goal or function which can be filled by a small number (relative to
total sequence space) of sequences.
And the fact remains that transposons are simply not magical entities
carrying "spare genes" designed at some unspecified time by some
unspecified entity for some unspecified, but designed, purpose. They
are uniquely unqualified for that role because they are boringly
repetitive.
> George Evans
George Evans
hers...@indiana.edu at hers...@indiana.edu wrote on 5/25/05 8:45 AM:
>
> George Evans wrote:
<snip>
>> True to form, you are once again stuck speaking as a hardware engineer--or
>> maybe I should say Xerox repairman. Yes, it costs the same to copy the
>> source code to OS X as it would to produce an equal number of pages of my
>> butt. However I am talking about Dembski information not Shannon
>> information, the house of cards and not the cards themselves. This is where
>> science is silent so far and you are hoping beyond hope that there is no
>> such information. But of course it's there.
>>
> [snip]
>
> Wrt Dembski information, which has more information, a copy of the
> source code to OS X or a copy of your irreducibly complex living butt
> (replicated a certain number of times)?
That's easy. The copy of OS X contains all the information of OS X, whereas
the amazing complexity of my butt is more than just skin deep.
George Evans
George Evans
eci...@earthlinkNOSPAM.next wrote on 5/25/05 2:16 PM:
Sorry, my last sentence was mangled somehow. Here is the second draft. As a
general rule, the farther two organisms are from each other in form and
function, the greater will be the difference in design criterion for each of
their parts but there is room for exceptions.
>> OTOH evolution would predict identical hierarchical structures for all
>> proteins because all the parts of a given organism branched at exactly the
>> same times.
>>
> Evolution does not say that all proteins evolved at exactly the same rates, or
> that random chance would not sometimes obscure true relationships. In fact,
> it does not even say that all parts of an organism branched at the same time.
> It is possible to get gene duplications within a species, so that gene A of
> species X is more closely related to gene B of species X than to gene A from
> species Y. Or vice versa. Determining hierarchies is not trivial, but it can
> be done, and it has never yet favored design.
I can see that it is complicated. I was picturing proteins and other parts
that are present on both branches of a split. All these must physically part
ways at the same time. Secondly, you say that not all proteins evolved at
the same rate, but isn't that the basis of relative ages of branch points?
Isn't it based on standard rates of mutation?
<snip>
George Evans
George Evans
rgri...@ctc.net wrote on 5/25/05 5:19 AM:
> in article BEB984B6.6924%geor...@earthlink.net, George Evans at
> geor...@earthlink.net wrote on 5/25/05 4:26 AM:
<snip>
>> I don't think the idea of nested hierarchies of homologous proteins is as
>> strong an argument as you think. As a general rule, the farther two organisms
>> are from each other in design and function, the greater will be the design
>> criterion for each of their parts but there is room for exceptions. OTOH
>> evolution would predict identical hierarchical structures for all proteins
>> because all the parts of a given organism branched at exactly the same times.
>> The empirical data, in my opinion, favors design.
>>
> Sigh. Why is it that the "design" promoters and those who promote an outright
> religious interpretation seemingly always have to LIE about what evolution
> says or does?
Apparently I just am not aware that I was lying!
> George, it would be really good for you to know what you are talking about.
> The fact is that you do not.
>
> The chemistry of proteins demonstrates that proteins with different components
> can still fold the same way in the active areas and perform the same task. For
> example, we know that insulin is produced by almost every organism, and while
> human insulin is *best* for humans, for a long time we used swine insulin. It
> did the job.
>
> Evolutionary science is not a denial of chemistry. Rather, evolutionary
> science is built upon the observations of chemistry and other disciplines.
> People like you try to make it appear that evolutionary science is just some
> fantasy speculation. It isn't. The journals are full of evolutionary studies
> based upon chemistry, biochemistry, genetics, etc.
>
> As speciation occurs, there is a physical branching of the population. Yet we
> know from genetic studies that not all parts of the genome mutate at the same
> rate. There are some parts of the genome that are remarkably stable, while
> other parts demonstrate a wide variability. It is not necessary for most
> proteins to be identical to perform an identical purpose. As we have easily
> demonstrated, proteins can vary significantly and still perform the same
> purpose.
This is certainly true but at least in "recently" branched organisms each
particular gene should be in approximately the same position. Although the
different types of genes might mutate at different rates, individual gene
types should give the same relative branching patterns. IOW the hemoglobin
tree should be identical to the insulin tree, etc.
> On the other hand, you have just produced an argument which *destroys* your ID
> position. The evidence is completely against it.
>
> You said: "As a general rule, the farther two organisms are from each other in
> design and function, the greater will be the design criterion for each of
> their parts but there is room for exceptions."
>
> Pray tell, how do you even begin to *define* how far apart two organisms are
> "in design" or "in function"?
>
> What is an organism's "designed function" anyway? Are you introducing
> Calvinistic predestination here?
>
> Come on. Bring it forward. What definitions, standards, and measurements are
> used to determine how far apart "two organisms are from each other in design
> and function"? Or are you just blowing smoke? Do you get your religious
> technobabble from Star Trek?
I'm kind of partial to Zoology and Botany. Have you heard of these?
> You are interested in design? Tell me about the "design" that allows for
> Trisomy 21 or Trisomy 18? Come on, now! If "design" to produce a particular
> "function" are what we see in genetics, then explain those. If you have an
> Almighty Designer, a Perfect Intellect, One Who never makes mistakes, then
> explain those variances. Explain why they even exist if each protein has a
> "design criteria" for the species. Explain why they are created to suffer by a
> loving God.
Here's where you guys always lie about our position. You seem to always,
conveniently forget there is an enemy afoot.
> And explain, please, why you have to lie about science in order to make your
> point. Don't liars go to the Lake of Fire and Brimstone, according to
> Revelation? What did your Designer design your communication abilities to do?
> Hmmm. I can see it now. "Designed to deceive".
I can only be lying if I know what I'm saying is untrue. I feel safe, do
you?
> You might want to really think about your future as you pursue the tactics of
> lies and deceits in pressing your point. Think warm, warmer, hot, and "where
> can I get a drop of water to soothe my torment?". God hates lying.
Are you throwing a tantrum? It sounds like you're stomping your feet and
beating your head against the wall. Are you OK?
George Evans
Tim Tyler
> Tim Tyler wrote:
> > John Harshman <jharshman....@pacbell.net> wrote or quoted:
> >>Tim Tyler wrote:
> >>>John Harshman <jharshman....@pacbell.net> wrote or quoted:
> >>>>Tim Tyler wrote:
> >>>>>John Harshman <jharshman....@pacbell.net> wrote or quoted:
[...]
> >>>>>>However, nature has kindly carried out similar experiments. There are
> >>>>>>some vertebrates, for example, with genomes a tenth the size of the
> >>>>>>average mammal's (including humans). Fugu is one such. It has most of
> >>>>>>the same genes we do, but 90% of the non-coding DNA is missing. Yet
> >>>>>>fugus work just fine. I'm sure that some of the remainder is junk too,
> >>>>>>but it clearly demonstrates that most of the human genome is indeed junk.
> >>>>>
> >>>>>A questionable premise there: that all mammals are roughly the same in
> >>>>>terms of their necessary genes.
> >>>>
> >>>>Why? Do you have any contrary evidence? Mice and humans, for example,
> >>>>share something over 90% of their protein-coding genes. You could, I
> >>>>suppose, claim that the differences are mostly in the "junk"; but on
> >>>>what basis?
> >>>
> >>>You claimed a clear demonstration that most of the human genome is junk.
> >>
> >>I think it's pretty clear.
> >
> > Obviously - but your supporting argument was of the form: if one
> > mammal can survive without 90% of its DNA, the equivalant DNA
> > in other mammals can have no adaptive function.
> >
> > *You* might find that convincing - but I don't see any reason why
> > *others* should follow you in that line of reasoning.
>
> And you might find that unconvincing, but why? [...]
Because it does not have the correct form of a logical argument.
> Would you agree that the tiny genome of fugu (which is a fish, not a
> mammal, by the way) is in fact evidence, whether conclusive or not, in
> favor of junk being junk?
I don't know much about the specific case of fugu, aside from the
fact that it has a small genome, which proves very little - besides
the fact that such creatures can be viable.
> >>Given your logic, why should we believe that the results of an
> >>experiment on one individual should apply to other individuals of the
> >>same species?
> >
> > Obviously, that is going to depend on the species and experiment:
> >
> > If the experiment is on fingernail patterns or eye colour, there's
> > typically little basis for such a belief.
> >
> > If the experiment is on genitals, there's often a 50% chance of
> > the result not applying.
> >
> > On the other hand, if the experiment involves the on number of
> > legs, there may be a firmer basis for the belief.
>
> Why? Do we have to come to you for decisions on this sort of thing, or
> is there a rule we can follow?
There are reasons for thinking that an experiment will or won't apply
to other members of the same species. There are lots of approaches
to the issue, involving things like drawing on experience of similar
traits or similar species. However, this seems to be going off at
a bit of a tangent to the subject under discussion.
> >>>>Yes, the problem with experiments like that is that one can always argue
> >>>>that the missing material does have a function, just one too subtle to
> >>>>be detected easily; maybe it's a function that is only needed once every
> >>>>hundred generations. That's the beauty of looking at sequence
> >>>>conservation, because it indexes long-term importance.
> >>>
> >>>It indexes conserved genes.
> >>>
> >>>Of course, genes for traits such as diseases resistance are not
> >>>necessarily conserved - and can be selected in such a way that
> >>>they are constantly changing.
> >>
> >>Yes, there are a few of those. They change at greater than the neutral
> >>rate, and that stands out too.
> >
> > So: some selected genes change faster then neutral genes - and other
> > selected genes change slower than neutral genes. Maybe some also
> > change at about the same speed as neutral genes.
>
> Why would that happen? The reason some genes are slow is that they
> perform a function for which a particular sequence is better than those
> near to them. The reason some genes are fast is that their function
> actively selects for differences. What would cause sequences to be
> selected for evolution at a neutral rate?
Selection based on infrequent events - such as plagues originating from
inter-species infections.
> And what leads you to believe that the bulk of our DNA could possibly
> be made up of such sequences?
What leads you to attribute this unlikely view to me?
> >>>Sequence conservation doesn't have too much to say about that.
> >>
> >>Yes it does, since change in those genes is actually accelerated. And
> >>they are embedded in conserved sequences too -- only selected domains
> >>have accelerated evolution. This has nothing to do with junk DNA.
> >
> > The topic arose because you suggested that only conserved sequences
> > were likely to be important in the long term.
> >
> > That is surely false - since selection for diseases resistance traits
> > can favour novelty, the not-before seen. Only looking at conserved
> > sequences would result in an underestimation of the volume of DNA
> > which is subjected to selection.
>
> True to a very minor degree. The number of these fast-evolving sequences
> is quite small, and again they are embedded within conserved sequences,
> and also are conserved in some other ways -- they maintain open reading
> frames, for example -- that neutrally evolving sequences are not.
>
> > Also, the role of DNA as a spacer should not be neglected. Just because
> > a sequence is variable that doesn't mean it serves no purpose. A DNA
> > sequence has other properties besides the details of the order of the
> > base pairs on it - in particular it has a length.
>
> True. Some DNA may be important merely as a spacer, and other DNA may be
> selected merely because it makes a cell bigger. But these are doubtful
> exceptions. There are no hidden functions there to delight the
> creationist, and that's what this argument is really about.
Ah. I'm not discussing creationism. That seems like it would be
a waste of time.
There *does* seem to be the view that the idea that junk DNA really
is junk must be defended at all costs - since the creationsts are
saying it can't /really/ be junk, and their enterpise badly needs
demolishing, so their ability to indoctrinate children is diminished.
However, that isn't a scientific approach. The scientist should look at
the evidence, without a prior political agenda.
> > Several of the proposed functions of junk DNA involve this notion -
> > that the DNA affects linkage patterns - that it acts as a sink
> > for intracellular mutagens - that it allows space for expansion
> > at the end of coding regions - that it allows gene duplication
> > without changing chromosome size - that it harbours LINEs and
> > SINEs - which act as types of highly non-random mutagen - and
> > so on.
>
> Some of these ideas are silly, if you ask me. And they all founder on
> the extreme variability in genome size, unless you can think of a reason
> why these factors should all differ so greatly among vertebrates.
It seems clearly experimentally demonstrated that selection can act
to reduce the junk DNA in organisms.
Vertebrates may differ in the extent which they have been subject to such
selection pressures, in the relatively recent past.
> > Consequently to argue from a variable sequence to non-functionality,
> > represents a logical flaw - since a stretch of DNA has heritable
> > properties which do not depend on its sequence data.
>
> Agreed, to a point. There are some cases in which DNA is just a
> place-holder. However, I think the great variability in genome size does
> argue that most of the neutrally evolving DNA does indeed fill no
> function. Why should mammals require so much more of these bulk
> functions than fugu, and so much less than frogs? There's just no
> sensible, functional explanation for that.
The variability of the volume of junk DNA suggests it is not very
important. It doesn't prove it though - since it could also vary
under selection pressures not yet fully understood.
Also, neutrality is a matter of degree. Very little is likely
to be absoultely neutral - and in large populations, even very
small selection pressures can produce significant long term
results. Junk DNA may not be *vitally* important - but it could
still be significant enough to contribute to species traits -
such as evolvability.
Tim Tyler
My comments were directed towards the argument as quoted above.
You are presenting a different argument.
> To have an adaptive function means that it must fill a need. Since the
> fugu performs the same basic functions as, say, the zebra fish, that
> does rather argue that the type of missing DNA in fugu that is present
> in the zebra fish is not highly significant wrt function.
Are the fugu and the zebra fish *really* functionally equivalent?
Are they under the same selection pressures? What parasites
do the they have to combat? Isn't the Fugu from Japan? Japan
is an island ecosystem, surrounded on all sides by deep water.
Are you sure this has not influenced the Fugu's predators or
diet?
It seems without demonstrating these sorts of things, the argument
that the Zebra fish gets no benefit from its extra genes doesn't
stand up.
> And, of course, there is also the matter of major deletions (especially
> in chromosomes that don't have many coding genes, like the Y) that have
> minimal effects indicating that a great deal of DNA in other organisms
> is not highly significant.
I think we can agree that most non-coding DNA is not highly significant.
However I wouldn't describe everything which is not highly significant
using the term "junk".
"Junk" implies something has negligible significance - and non-coding
DNA may be something which is inappropraite to describe using such a term.
> > > >>Yes, the problem with experiments like that is that one can always argue
> > > >>that the missing material does have a function, just one too subtle to
> > > >>be detected easily; maybe it's a function that is only needed once every
> > > >>hundred generations. That's the beauty of looking at sequence
> > > >>conservation, because it indexes long-term importance.
> > > >
> > > > It indexes conserved genes.
>
> And what, pray tell, distinguishes a conserved sequence from a
> non-conserved on other than that the conserved ones have selective
> utility?
Questionable premise: that fact doesn't distinguish conserved sequence
from a non-conserved sequences - because non-conserved sequences can have
selective utility.
> We know that pure chance will lead to changes at roughly a
> give rate in the absence of selection. It is significant difference
> from that rate due to chance alone that determines conservation.
The term "conservation" is usually used to mean that something stays the
same.
AFAICS, you are trying to redefine the term. Do you have a precedent
for your proposed redefinition?
> definition* selectively neutral. [...]
I am talking about sequences that change at the same long-term *rate*
as neutral ones - but are the subject of selection - as can be seen
by examining the spatio-temporal pattern of how these genes across the
entire population.
It is not true that sequences which change at the same overall rate
as neutral genes over an extended period of time are neutral by
definition.
Genes change at a wide range of rates. Some change slowly, some
change quickly - and others change at every rate you can imagine
in between. The original idea that only the slow-changing genes
are the object of selection is not correct.
> > > > Sequence conservation doesn't have too much to say about that.
> > >
> > > Yes it does, since change in those genes is actually accelerated. And
> > > they are embedded in conserved sequences too -- only selected domains
> > > have accelerated evolution. This has nothing to do with junk DNA.
> >
> > The topic arose because you suggested that only conserved sequences
> > were likely to be important in the long term.
>
> > That is surely false - since selection for diseases resistance traits
> > can favour novelty, the not-before seen. Only looking at conserved
> > sequences would result in an underestimation of the volume of DNA
> > which is subjected to selection.
>
> Disease resistance does not usually result in significant change in an
> otherwise conserved sequence.
Indeed not.
> The rule is that conservation of sequence is an excellent clue to
> functional utility. Sequences that change *faster* than neutrality while
> retaining function are rare as hen's teeth if not non-existent.
Didn't you just a moment ago claim:
``Some sequences change *significantly* faster than selectively neutral
genes. That is because these sequences are under strong selective
pressure favoring the changes.''
...?
IMO, *that* was correct - and what you are now saying is not.
The *usual* function in question with these sorts of changes
is resisting some pathogen or other.
> > Also, the role of DNA as a spacer should not be neglected. Just because
> > a sequence is variable that doesn't mean it serves no purpose. A DNA
> > sequence has other properties besides the details of the order of the
> > base pairs on it - in particular it has a length.
>
> I.e., a need for bulk can be filled by otherwise utterly useless
> sequences. It can be filled by "junk" and serve the function of just
> being there. And lo, that does seem to be the case. 90+% of the human
> genome is filled by "junk" that serves no purpose other than being
> there.
>
> Moreover, it is quite clear that not only is this DNA's 'utility'
> independent of sequence, it is also largely independent or not highly
> dependent on the length of the sequence, since it can often be deleted
> or expanded without any detectable consequence. [...]
...but then attempts to detect it have usually been pretty feeble.
> > Several of the proposed functions of junk DNA involve this notion -
> > that the DNA affects linkage patterns - that it acts as a sink
> > for intracellular mutagens - that it allows space for expansion
> > at the end of coding regions - that it allows gene duplication
> > without changing chromosome size - that it harbours LINEs and
> > SINEs - which act as types of highly non-random mutagen - and
> > so on.
>
> That doesn't make such sequence-independent DNA any less "junk".
IMO, "junk" implies near-complete lack of function. Something acting as a
spacer would at least have *some* function.
> These bulk features only require the presence of some DNA. It does
> not require the presence of any specific sequence (LINEs and SINEs
> excepted, but they are not there for the benefit of the organism, but
> have a more selfish origin).
As mutagens, they are probably deleterious to the organism. However they
may conceivably benefit the species. LINEs and SINEs do behave selfishly
- but that may not be their only role.
> "Junk" DNA serves no purpose but 'being there'. That means that 90+%
> of our DNA is there for no purpose but being there and, possibly, some
> bulk effect. [...]
If your premise that "junk" DNA serves no purpose is accepted, that
follows - otherwise not. You are just assuming (or asserting) what you
are trying to prove here.
> > Consequently to argue from a variable sequence to non-functionality,
> > represents a logical flaw - since a stretch of DNA has heritable
> > properties which do not depend on its sequence data.
>
> Of course. Junk DNA replicates just like functional (sequence vital)
> DNA. SFW?
That is not what I meant. What I meant was that junk DNA's length
is inherited - to to argue that because it has a variable sequence
it is not functional ignores the possibility that it may function
as a spacer.
> The sequence of junk DNA, unlike sequence functional DNA,
> drifts like selectively neutral sequences (including changes in
> length).
We know that is not true in general - since in some organisms
junk DNA is selected against - sometimes powerfully so -
resulting in changes in length being subjected to selection
and behaving highly non-randomly.
Also, most *changes* in length are nowhere near neutral:
Instead, they are strongly deleterious - since they often
result in the organism carrying them being unable to recombine
its genes with other members of the species.
As a result, to claim that changes in length of non-coding
sequences are similar to neutral changes doesn't make
much sense - since they are typically *much* less likely
to spread than neutral changes are.
Tim Tyler
> Well, I am not an ID theorist, but I think that ID could have a great impact
> on our understanding of the content and relative value of genetic
> information. I wouldn't be surprised if a mathematical relationship between
> energy expense and information content (per Dembski not Shannon) appears
> soon for scrutiny. That area is wide open right now, and so far science has
> almost nothing to say about it.
Energy expense - on what? Information content - of what?
Bigger creatures have larger genomes (more information) and take
more energy to reproduce. Is that what you mean?
John Harshman
I don't really see the problem here, unless you assume that we don't
know anything about how animals work. As far as we can tell, all
vertebrates do most of the same things in terms of proteins expressed,
and in terms of developmental and physiological processes. There is no
reason to suppose that any given vertebrate "needs" much more DNA than
any other. I think we have good reason to suppose that they all have
roughly the same size of useful genome.
You, on the other hand, must be driven to postulate that humans (and
most teleosts, for that matter) need a much larger genome than does
fugu. You can assume so if you like, but it would be good if you had
some basis for that. Sure, it's logically conceivable and can never be
completely contradicted by evidence, since the extra functions could be
so subtle we could never detect them. But science doesn't work by
formal, logical proofs, and can't afford to.
>>>>Given your logic, why should we believe that the results of an
>>>>experiment on one individual should apply to other individuals of the
>>>>same species?
>>>
>>>Obviously, that is going to depend on the species and experiment:
>>>
>>>If the experiment is on fingernail patterns or eye colour, there's
>>>typically little basis for such a belief.
>>>
>>>If the experiment is on genitals, there's often a 50% chance of
>>>the result not applying.
>>>
>>>On the other hand, if the experiment involves the on number of
>>>legs, there may be a firmer basis for the belief.
>>
>>Why? Do we have to come to you for decisions on this sort of thing, or
>>is there a rule we can follow?
>
> There are reasons for thinking that an experiment will or won't apply
> to other members of the same species. There are lots of approaches
> to the issue, involving things like drawing on experience of similar
> traits or similar species. However, this seems to be going off at
> a bit of a tangent to the subject under discussion.
So what are the reasons for thinking that the fugu genome can't tell us
anything about the genomes of other species?
>>>>>>Yes, the problem with experiments like that is that one can always argue
>>>>>>that the missing material does have a function, just one too subtle to
>>>>>>be detected easily; maybe it's a function that is only needed once every
>>>>>>hundred generations. That's the beauty of looking at sequence
>>>>>>conservation, because it indexes long-term importance.
>>>>>
>>>>>It indexes conserved genes.
>>>>>
>>>>>Of course, genes for traits such as diseases resistance are not
>>>>>necessarily conserved - and can be selected in such a way that
>>>>>they are constantly changing.
>>>>
>>>>Yes, there are a few of those. They change at greater than the neutral
>>>>rate, and that stands out too.
>>>
>>>So: some selected genes change faster then neutral genes - and other
>>>selected genes change slower than neutral genes. Maybe some also
>>>change at about the same speed as neutral genes.
>>
>>Why would that happen? The reason some genes are slow is that they
>>perform a function for which a particular sequence is better than those
>>near to them. The reason some genes are fast is that their function
>>actively selects for differences. What would cause sequences to be
>>selected for evolution at a neutral rate?
>
> Selection based on infrequent events - such as plagues originating from
> inter-species infections.
I agree that it's logically possible for selection to cause change at
the neutral rate. But again, if you have a huge number of sequences
evolving at the neutral rate, what are the odds that any large
proportion of them are under selection that just happens (out of all the
rates that are possible) to mimic neutral evolution?
>>And what leads you to believe that the bulk of our DNA could possibly
>>be made up of such sequences?
>
> What leads you to attribute this unlikely view to me?
You are trying to cast doubt on the idea that most of our DNA is junk,
and that evolving at the neutral rate is good evidence that a sequence
is evolving neutrally. If the bulk of the sequences evolving at the
neutral rate are indeed neutral, you have no point and have been wasting
our time.
>>>>>Sequence conservation doesn't have too much to say about that.
>>>>
>>>>Yes it does, since change in those genes is actually accelerated. And
>>>>they are embedded in conserved sequences too -- only selected domains
>>>>have accelerated evolution. This has nothing to do with junk DNA.
>>>
>>>The topic arose because you suggested that only conserved sequences
>>>were likely to be important in the long term.
>>>
>>>That is surely false - since selection for diseases resistance traits
>>>can favour novelty, the not-before seen. Only looking at conserved
>>>sequences would result in an underestimation of the volume of DNA
>>>which is subjected to selection.
>>
>>True to a very minor degree. The number of these fast-evolving sequences
>>is quite small, and again they are embedded within conserved sequences,
>>and also are conserved in some other ways -- they maintain open reading
>>frames, for example -- that neutrally evolving sequences are not.
>>
>>
>>>Also, the role of DNA as a spacer should not be neglected. Just because
>>>a sequence is variable that doesn't mean it serves no purpose. A DNA
>>>sequence has other properties besides the details of the order of the
>>>base pairs on it - in particular it has a length.
>>
>>True. Some DNA may be important merely as a spacer, and other DNA may be
>>selected merely because it makes a cell bigger. But these are doubtful
>>exceptions. There are no hidden functions there to delight the
>>creationist, and that's what this argument is really about.
>
> Ah. I'm not discussing creationism. That seems like it would be
> a waste of time.
No? That's the main purpose of this group. At any rate, the argument
from variability in DNA content would also apply to the claim that most
of the junk is spacers and "useful bulk".
> There *does* seem to be the view that the idea that junk DNA really
> is junk must be defended at all costs - since the creationsts are
> saying it can't /really/ be junk, and their enterpise badly needs
> demolishing, so their ability to indoctrinate children is diminished.
>
> However, that isn't a scientific approach. The scientist should look at
> the evidence, without a prior political agenda.
I see no such view, and no such agenda.
>>>Several of the proposed functions of junk DNA involve this notion -
>>>that the DNA affects linkage patterns - that it acts as a sink
>>>for intracellular mutagens - that it allows space for expansion
>>>at the end of coding regions - that it allows gene duplication
>>>without changing chromosome size - that it harbours LINEs and
>>>SINEs - which act as types of highly non-random mutagen - and
>>>so on.
>>
>>Some of these ideas are silly, if you ask me. And they all founder on
>>the extreme variability in genome size, unless you can think of a reason
>>why these factors should all differ so greatly among vertebrates.
>
> It seems clearly experimentally demonstrated that selection can act
> to reduce the junk DNA in organisms.
>
> Vertebrates may differ in the extent which they have been subject to such
> selection pressures, in the relatively recent past.
Well, of course selection can reduce junk. There is a cost of
replication, after all. But so what? This can happen if it's really
junk. In fact, it will happen much more easily if it's junk. That's no
argument.
>>>Consequently to argue from a variable sequence to non-functionality,
>>>represents a logical flaw - since a stretch of DNA has heritable
>>>properties which do not depend on its sequence data.
>>
>>Agreed, to a point. There are some cases in which DNA is just a
>>place-holder. However, I think the great variability in genome size does
>>argue that most of the neutrally evolving DNA does indeed fill no
>>function. Why should mammals require so much more of these bulk
>>functions than fugu, and so much less than frogs? There's just no
>>sensible, functional explanation for that.
>
> The variability of the volume of junk DNA suggests it is not very
> important. It doesn't prove it though - since it could also vary
> under selection pressures not yet fully understood.
There is no such thing as proof in science. Junk could always have a
function that's too subtle to detect. This is "function of the gaps".
> Also, neutrality is a matter of degree. Very little is likely
> to be absoultely neutral - and in large populations, even very
> small selection pressures can produce significant long term
> results. Junk DNA may not be *vitally* important - but it could
> still be significant enough to contribute to species traits -
> such as evolvability.
Always conceivable. But we're a long way from the idea that junk DNA has
hidden functions here, which is where we started out.
Ken Shaw
Presupposition of conclusion. You cannot assume a gene is designed until
you provide a way to determine that fact. Dembski information must be a
way of determining this fact in an objective not subjective manner if it
is to even attempt to be science rather than propaganda.
Even more generally ID must provide an objective methodology for
identifying intelligently designed objects. As a trivial test such a
test should correctly sort a beaver dam and an earthen man made dam.
> But being able to measure a quantity is not the be and and end all of
> existence. We found ways to measure heat and it doesn't exist.
Heat doesn't exist? The amount of kinetic energy contained in a material
doesn't exist?
We can't
> measure the information content of a computer program but the programmer
> would object to the idea that it didn't exist.
>
Actually the amount of information in a computer program is measurable.
Several different methods are used. Lines of code, number of
subroutines, number of branch points and number of symbols used are all
used as metrics of information contained in a program.
Ken
Steve Schaffner
> George Evans wrote:
> > in article 720le.249601$cg1....@bgtnsc04-news.ops.worldnet.att.net, Ken
> > Shaw at non...@your.biz wrote on 5/25/05 7:34 AM:
> > But being able to measure a quantity is not the be and and end all of
> > existence. We found ways to measure heat and it doesn't exist.
>
> Heat doesn't exist? The amount of kinetic energy contained in a material
> doesn't exist?
That's the internal energy, not the heat. Heat is the energy
transferred between bodies at different temperatures. (I hope I
got that right -- thermal physics was never my thing.)
Whether heat "exists" or not strikes me a meaningless question. It's
a well-defined and measurable attribute of physical systems,
characteristics it seems not to share with "Dembski information".
--
Steve Schaffner s...@broad.mit.edu
Immediate assurance is an excellent sign of probable lack of
insight into the topic. Josiah Royce
Mark Isaak
<geor...@earthlink.net> wrote:
The new tRNA could have been a late addition. As I recall, many of
the selenocysteins can be replaced with cystein and still function,
albeit not as efficiently. The first modified stop codon might have
been to add cystein, not selenocystein.
The leading AUG would not be translated in any case, since that A is
the trailing base of the previous triplet. What is needed is
something to keep things going even though UGA usually means stop.
The mRNA need not have been modified. The "something" in the previous
paragraph could have used the pattern that just happened to be there,
as I said in my previous post.
hers...@indiana.edu
Pretty much. Differences in size and shape, certainly. But wrt number
of coding genes or functional products I doubt that there is more than
a 5% differnce (about the difference between mouse and man).
> Are they under the same selection pressures? What parasites
> do the they have to combat? Isn't the Fugu from Japan? Japan
> is an island ecosystem, surrounded on all sides by deep water.
> Are you sure this has not influenced the Fugu's predators or
> diet?
>
> It seems without demonstrating these sorts of things, the argument
> that the Zebra fish gets no benefit from its extra genes doesn't
> stand up.
We aren't talking about extra *genes* that code for extra *protein
products* or even extra *RNA products*. We are talking about extra DNA
that doesn't code for anything. The DNA we are discussing is
non-coding sequence. Any function it has has to be consistent with the
fact that it is non-coding.
> > And, of course, there is also the matter of major deletions (especially
> > in chromosomes that don't have many coding genes, like the Y) that have
> > minimal effects indicating that a great deal of DNA in other organisms
> > is not highly significant.
>
> I think we can agree that most non-coding DNA is not highly significant.
>
> However I wouldn't describe everything which is not highly significant
> using the term "junk".
When you have a function of even minor significance, let us know. The
absence of sequence conservation tells us that most (but not all) of
the non-coding sequence in vertebrates is of negligible significance
wrt *any* function related to sequence. That rules out any coding
function, any regulatory function, any specific structural function
(centromere, telomere). All that is left is insignificant bulk
functions that really are negligible in importance, given that there is
not even a strong relationship with bulk. There are two Hyla species
(tiny frogs). These differ by one being a tetraploid and the other a
diploid. The *only* way to distinguish between them morphologically is
by their mating calls (and, of course, a chromosome count).
> "Junk" implies something has negligible significance - and non-coding
> DNA may be something which is inappropraite to describe using such a term.
Any function unrelated to sequence is pretty much of negligible
significance; of no more importance than the amount of starch (also a
polymer of sugars) in a cell. DNA, absent sequence specificity, is of
little more importance to the cell than starch, and of less utility,
since it cannot be used for energy storage.
> > > > >>Yes, the problem with experiments like that is that one can always argue
> > > > >>that the missing material does have a function, just one too subtle to
> > > > >>be detected easily; maybe it's a function that is only needed once every
> > > > >>hundred generations. That's the beauty of looking at sequence
> > > > >>conservation, because it indexes long-term importance.
> > > > >
> > > > > It indexes conserved genes.
> >
> > And what, pray tell, distinguishes a conserved sequence from a
> > non-conserved on other than that the conserved ones have selective
> > utility?
>
> Questionable premise: that fact doesn't distinguish conserved sequence
> from a non-conserved sequences - because non-conserved sequences can have
> selective utility.
>
> > We know that pure chance will lead to changes at roughly a
> > give rate in the absence of selection. It is significant difference
> > from that rate due to chance alone that determines conservation.
>
> The term "conservation" is usually used to mean that something stays the
> same.
In terms of sequence, "conservation" is a quantitative feature, not an
absolute qualitative one. The rate of sequence change is important.
For example, histone 4B is more highly conserved over evolutionary time
in aa sequence than cytochrome c, which in turn is more highly
conserved than hemoglobin, which is more highly conserved than
fibrinogen peptide (which, since its only purpose is to be cleaved off
to activate fibrinogen is almost completely free to change by random
drift; i.e, is almost completely selectively neutral). The rate of
change is related to how free the aa's of a protein are to change.
Some aa's in a protein are irrelevant to function, others are more so.
The most highly conserved aa's are those involved in the active site of
enzymes (a small number, usually) and those involved in proper folding.
Others are constrained to, say, only those that easily work in alpha
helices or beta sheets.
> AFAICS, you are trying to redefine the term. Do you have a precedent
> for your proposed redefinition?
Yes. Sequences differ in the degree of conservation, from highly
conserved to selectively neutral to (more rarely) highly unconserved
(usually cases like the sequences involved in recognition sites in
self-sterility alleles -- frequency dependent selection sites).
You would have to have a strange sequence indeed to manage this. It
would have to be composed of regions undergoing significantly faster
than neutral rates of change and other regious undergoing significantly
slower than neutral rates of change. Again, sequences that undergo
*faster* than normal rates of change are rare (frequency-dependent
selection) and are usually localized rather than randomly distributed
in a sequence.
> It is not true that sequences which change at the same overall rate
> as neutral genes over an extended period of time are neutral by
> definition.
As an operational definition, they *are* selectively neutral over that
time frame. I agree that this could be an artifact if the sequence
underwent both faster than neutral *and* slower than neutral rates of
change that just happened to balance out. But if a sequence (aside
from the hybid sequence containing both faster than normal change and
slower than normal change subparts described above) is changing at a
*constant* rate indistinguishable from the rate of neutral drift, how
could selection be involved unless that sequence has either a much
higher or lower mutation rate than other sequences (which would really
mean that *its* rate of neutral drift differs from the average
sequence's rate of neutral drift)? If the sequence also has a
specified rate of mutation and there is no detectable difference in
the rate of change than that expected by neutral drift it is
selectively neutral.
> Genes change at a wide range of rates. Some change slowly, some
> change quickly - and others change at every rate you can imagine
> in between. The original idea that only the slow-changing genes
> are the object of selection is not correct.
I am not saying that. *Genes* do indeed change at a wide range of
rates. Histone changes more slowly than cytochrome c. Cytochrome c
changes more slowly than hemoglobin. Hemoglobin changes more slowly
than fibrinogen peptide. But *genes* (coding sequences, regulatory
sequences, specific structural sequences) almost always (I have
mentioned the rare exceptions as being regions under
frequency-dependent selection, but it could also include a gene when
there is a discrepancy between current sequence and optimal sequence in
a particular environment, also rare at any given time point) change at
a rate which is *slower than* the rate of change of neutral drift.
> > > > > Sequence conservation doesn't have too much to say about that.
> > > >
> > > > Yes it does, since change in those genes is actually accelerated. And
> > > > they are embedded in conserved sequences too -- only selected domains
> > > > have accelerated evolution. This has nothing to do with junk DNA.
> > >
> > > The topic arose because you suggested that only conserved sequences
> > > were likely to be important in the long term.
> >
> > > That is surely false - since selection for diseases resistance traits
> > > can favour novelty, the not-before seen. Only looking at conserved
> > > sequences would result in an underestimation of the volume of DNA
> > > which is subjected to selection.
> >
> > Disease resistance does not usually result in significant change in an
> > otherwise conserved sequence.
>
> Indeed not.
>
> > The rule is that conservation of sequence is an excellent clue to
> > functional utility. Sequences that change *faster* than neutrality while
> > retaining function are rare as hen's teeth if not non-existent.
>
> Didn't you just a moment ago claim:
>
> ``Some sequences change *significantly* faster than selectively neutral
> genes. That is because these sequences are under strong selective
> pressure favoring the changes.''
Yes. Leave off the "if not non-existent". Frequency-depedent
sequences are rare. So are genes that are sub-optimal for current
environment.
>
> ...?
>
> IMO, *that* was correct - and what you are now saying is not.
My description of these sites as being rare is also correct. For most
*coding sequences* (or regulatory or structural), conservation (rates
of change slower than that of neutral drift) is the norm.
> The *usual* function in question with these sorts of changes
> is resisting some pathogen or other.
Only if the pathogen is "new". And even so, the *rest* of the protein
is still highly conserved. One rapid aa change out of 1000 will be
insignificant over several million years compared to the more highly
conserved sites needed for retaining protein function. The *usual*
observable case involves frequency-dependent selection.
> > > Also, the role of DNA as a spacer should not be neglected. Just because
> > > a sequence is variable that doesn't mean it serves no purpose. A DNA
> > > sequence has other properties besides the details of the order of the
> > > base pairs on it - in particular it has a length.
> >
> > I.e., a need for bulk can be filled by otherwise utterly useless
> > sequences. It can be filled by "junk" and serve the function of just
> > being there. And lo, that does seem to be the case. 90+% of the human
> > genome is filled by "junk" that serves no purpose other than being
> > there.
> >
> > Moreover, it is quite clear that not only is this DNA's 'utility'
> > independent of sequence, it is also largely independent or not highly
> > dependent on the length of the sequence, since it can often be deleted
> > or expanded without any detectable consequence. [...]
>
> ...but then attempts to detect it have usually been pretty feeble.
Remember that you are talking about a currently unknown and unspecified
effect of 'bulk' that *may* exist. You are saying that mere amount of
DNA *might* do something, but you don't know or have any idea what that
something is nor how to test it. What tests we do have, indicating
that length of intron sequences, the number of SINES and LINES and
other repetitive elements, etc., are pretty flexible and can accomodate
a wide range of amount of "junk" DNA present only as spacers.
> > > Several of the proposed functions of junk DNA involve this notion -
> > > that the DNA affects linkage patterns - that it acts as a sink
> > > for intracellular mutagens - that it allows space for expansion
> > > at the end of coding regions - that it allows gene duplication
> > > without changing chromosome size - that it harbours LINEs and
> > > SINEs - which act as types of highly non-random mutagen - and
> > > so on.
> >
> > That doesn't make such sequence-independent DNA any less "junk".
>
> IMO, "junk" implies near-complete lack of function. Something acting as a
> spacer would at least have *some* function.
Only if the *length* of that spacer were crucial. If the length can
vary widely, then the amount of spacer is pretty much irrelevant.
> > These bulk features only require the presence of some DNA. It does
> > not require the presence of any specific sequence (LINEs and SINEs
> > excepted, but they are not there for the benefit of the organism, but
> > have a more selfish origin).
>
> As mutagens, they are probably deleterious to the organism. However they
> may conceivably benefit the species. LINEs and SINEs do behave selfishly
> - but that may not be their only role.
Evolution often co-opts any rare event that works to the benefit of the
organism. That includes co-opting specific LINEs and SINEs that have
landed at specific sites by random chance.
> > "Junk" DNA serves no purpose but 'being there'. That means that 90+%
> > of our DNA is there for no purpose but being there and, possibly, some
> > bulk effect. [...]
>
> If your premise that "junk" DNA serves no purpose is accepted, that
> follows - otherwise not. You are just assuming (or asserting) what you
> are trying to prove here.
I am saying that you have not presented a single specific *function*
that the vast majority of non-coding DNA in a genome can play. How can
one argue against the statement that "It might be doing something. I
don't know what it could be doing or how it could be doing it. But it
might be doing something." I can point out, from the evidence, that
whatever it "could be doing" is not related to sequence and is not
strongly related to length or number (in the case of SINEs and LINEs)
of DNA present (see fugu). What other property are you proposing that
this DNA use to exert its currently unspecified function? I am
perfectly willing to change the terminology from "junk" to whatever
function you claim (and can support from evidence) for this DNA. But
you haven't done that.
> > > Consequently to argue from a variable sequence to non-functionality,
> > > represents a logical flaw - since a stretch of DNA has heritable
> > > properties which do not depend on its sequence data.
> >
> > Of course. Junk DNA replicates just like functional (sequence vital)
> > DNA. SFW?
>
> That is not what I meant. What I meant was that junk DNA's length
> is inherited - to to argue that because it has a variable sequence
> it is not functional ignores the possibility that it may function
> as a spacer.
>
> > The sequence of junk DNA, unlike sequence functional DNA,
> > drifts like selectively neutral sequences (including changes in
> > length).
>
> We know that is not true in general - since in some organisms
> junk DNA is selected against - sometimes powerfully so -
> resulting in changes in length being subjected to selection
> and behaving highly non-randomly.
Organisms that are environments where rapid replication is required for
survival (largely unicellular) select in favor of parsimony in their
genome. That does not mean that in organisms where other selective
factors are more important that larger, less parsimonious genome have
positive *selective* value.
> Also, most *changes* in length are nowhere near neutral:
>
> Instead, they are strongly deleterious - since they often
> result in the organism carrying them being unable to recombine
> its genes with other members of the species.
Evidence? The example I gave was the variable length of the Y. What
example of a deletion that has little phenotypic effect because, say,
it removes only intergene sequences results in an organism unable to
recombine its genes with other members of the species?
> As a result, to claim that changes in length of non-coding
> sequences are similar to neutral changes doesn't make
> much sense - since they are typically *much* less likely
> to spread than neutral changes are.
The size of vertebrate (and human) genomes wrt expansion and
contraction is actually quite flexible at a certain scale of size
changes. That is why, for example, one actually has a DNA fingerprint.
These are due to selectively neutral expansions and contractions of
DNA sequences due to unequal crossing over. Because the number of
repeats is selectively neutral there are often multiple alleles that
are more or less frequent in the population. Enough so that we have
these pretty darn unique combinations (unique enough to make for great
TV crime shows).
George Evans
eci...@earthlinkNOSPAM.next wrote on 5/27/05 11:20 AM:
It doesn't matter if a Selenium or a Sulfur is dangling out at the other
end. Either way it requires a new tRNA to relate the cysteine to UGA.
> The leading AUG would not be translated in any case, since that A is
> the trailing base of the previous triplet. What is needed is
> something to keep things going even though UGA usually means stop.
Does that mean a selenocysteine can only follow a codon ending in A?
> The mRNA need not have been modified. The "something" in the previous
> paragraph could have used the pattern that just happened to be there,
> as I said in my previous post.
OK, possibly the mRNA could be the same, but what would recognize the
"something". Either the new tRNA has a highly abnormal mRNA binding end and
just butted in, in which case that would seem to be fatal to code downstream
(I understand some proteins have selenocysteine at the front end), or the
ribosome would have to be modified to recognize it.
George Evans
Tim Tyler
> Tim Tyler wrote:
> > John Harshman <jharshman....@pacbell.net> wrote or quoted:
> >>Tim Tyler wrote:
> >>>John Harshman <jharshman....@pacbell.net> wrote or quoted:
> >>>>Tim Tyler wrote:
> >>>>>John Harshman <jharshman....@pacbell.net> wrote or quoted:
> >>>>>>Tim Tyler wrote:
> >>>>>>>John Harshman <jharshman....@pacbell.net> wrote or quoted:
> >>>>>>>>However, nature has kindly carried out similar experiments. There are
The extra functions don't have to be particularly subtle - they just
have to be unimportant enough for an organism to remain viable after
they have been removed.
You could remove the genes for eye colour and hair colour from me
and my descendants would probably be able to at least survive -
but it doesn't follow that those traits are neutral or that they are
not the subject of selection.
> >>>Obviously, that is going to depend on the species and experiment:
> >>>
> >>>If the experiment is on fingernail patterns or eye colour, there's
> >>>typically little basis for such a belief.
> >>>
> >>>If the experiment is on genitals, there's often a 50% chance of
> >>>the result not applying.
> >>>
> >>>On the other hand, if the experiment involves the on number of
> >>>legs, there may be a firmer basis for the belief.
> >>
> >>Why? Do we have to come to you for decisions on this sort of thing, or
> >>is there a rule we can follow?
> >
> > There are reasons for thinking that an experiment will or won't apply
> > to other members of the same species. There are lots of approaches
> > to the issue, involving things like drawing on experience of similar
> > traits or similar species. However, this seems to be going off at
> > a bit of a tangent to the subject under discussion.
>
> So what are the reasons for thinking that the fugu genome can't tell us
> anything about the genomes of other species?
Firstly, what is your reason for concluding I think anything of the sort?
To clarify, I *don't* think that.
> >>>>>>That's the beauty of looking at sequence
> >>>>>>conservation, because it indexes long-term importance.
> >>>>>
> >>>>>It indexes conserved genes.
> >>>>>
> >>>>>Of course, genes for traits such as diseases resistance are not
> >>>>>necessarily conserved - and can be selected in such a way that
> >>>>>they are constantly changing.
> >>>>
> >>>>Yes, there are a few of those. They change at greater than the neutral
> >>>>rate, and that stands out too.
> >>>
> >>>So: some selected genes change faster then neutral genes - and other
> >>>selected genes change slower than neutral genes. Maybe some also
> >>>change at about the same speed as neutral genes.
> >>
> >>Why would that happen? The reason some genes are slow is that they
> >>perform a function for which a particular sequence is better than those
> >>near to them. The reason some genes are fast is that their function
> >>actively selects for differences. What would cause sequences to be
> >>selected for evolution at a neutral rate?
> >
> > Selection based on infrequent events - such as plagues originating from
> > inter-species infections.
>
> I agree that it's logically possible for selection to cause change at
> the neutral rate. But again, if you have a huge number of sequences
> evolving at the neutral rate, what are the odds that any large
> proportion of them are under selection that just happens (out of all the
> rates that are possible) to mimic neutral evolution?
Very likely low.
> >>And what leads you to believe that the bulk of our DNA could possibly
> >>be made up of such sequences?
> >
> > What leads you to attribute this unlikely view to me?
>
> You are trying to cast doubt on the idea that most of our DNA is junk,
> and that evolving at the neutral rate is good evidence that a sequence
> is evolving neutrally. [...]
What I was originally trying to cast doubt on was the notion that
sequence conservation indexes long-term importance.
I agree that most sequences that are evolving on average at the overall
neutral rate are indeed likely to be neutral. I don't agree that /all/
of them will be, though.
> >>>Also, the role of DNA as a spacer should not be neglected. Just because
> >>>a sequence is variable that doesn't mean it serves no purpose. A DNA
> >>>sequence has other properties besides the details of the order of the
> >>>base pairs on it - in particular it has a length.
> >>
> >>True. Some DNA may be important merely as a spacer, and other DNA may be
> >>selected merely because it makes a cell bigger. But these are doubtful
> >>exceptions. There are no hidden functions there to delight the
> >>creationist, and that's what this argument is really about.
> >
> > Ah. I'm not discussing creationism. That seems like it would be
> > a waste of time.
>
> No? That's the main purpose of this group.
I thought this group was for discussion of origins.
> >>>Several of the proposed functions of junk DNA involve this notion -
> >>>that the DNA affects linkage patterns - that it acts as a sink
> >>>for intracellular mutagens - that it allows space for expansion
> >>>at the end of coding regions - that it allows gene duplication
> >>>without changing chromosome size - that it harbours LINEs and
> >>>SINEs - which act as types of highly non-random mutagen - and
> >>>so on.
> >>
> >>Some of these ideas are silly, if you ask me. And they all founder on
> >>the extreme variability in genome size, unless you can think of a reason
> >>why these factors should all differ so greatly among vertebrates.
> >
> > It seems clearly experimentally demonstrated that selection can act
> > to reduce the junk DNA in organisms.
> >
> > Vertebrates may differ in the extent which they have been subject to such
> > selection pressures, in the relatively recent past.
>
> Well, of course selection can reduce junk. There is a cost of
> replication, after all. But so what? This can happen if it's really
> junk. In fact, it will happen much more easily if it's junk. That's no
> argument.
You asked for a reason why vertebrates should differ so much in the volume
of junk DNA - if it serves some useful purpose.
My answer to that was that they may differ in the extent to which they
have been subject to selection to eliminate the junk. It's easy to
imagine how hard times, or fierce competition, or dietary shortages -
or any number of other factors - might sometimes produce selection
that penalises those with large genomes.
> >>>Consequently to argue from a variable sequence to non-functionality,
> >>>represents a logical flaw - since a stretch of DNA has heritable
> >>>properties which do not depend on its sequence data.
> >>
> >>Agreed, to a point. There are some cases in which DNA is just a
> >>place-holder. However, I think the great variability in genome size does
> >>argue that most of the neutrally evolving DNA does indeed fill no
> >>function. Why should mammals require so much more of these bulk
> >>functions than fugu, and so much less than frogs? There's just no
> >>sensible, functional explanation for that.
> >
> > The variability of the volume of junk DNA suggests it is not very
> > important. It doesn't prove it though - since it could also vary
> > under selection pressures not yet fully understood.
>
> There is no such thing as proof in science. Junk could always have a
> function that's too subtle to detect. This is "function of the gaps".
So, until more comprehensive evidence on the issue comes in, should we
say that non-coding DNA has no well-established function, or should we
label it as junk - and deny it has any function at all?
It's not as though the evidence in favour of junk DNA being useless is
even very good.
Have you come across the Cavalier-Smith, "skeletal DNA" hypothesis?
This notes that genome size is strongly correlated with cell size.
That's an obvious clue that something other than simple random forces
is involved - and has suggested various possible adaptive functions
of the supposedly 'junk' DNA - e.g.:
``According to the skeletal DNA hypothesis, then, more noncoding DNA is
necessary for larger cells -- perhaps by more widely spacing the protein
and RNA-coding genes, transcription can occur more rapidly, allowing the
production of more proteins necessary for the larger cell.''
- http://wiki.cotch.net/index.php/Junk_DNA
Tim Tyler
> Tim Tyler wrote:
> > hers...@indiana.edu wrote or quoted:
> > > Tim Tyler wrote:
> > > > John Harshman <jharshman....@pacbell.net> wrote or quoted:
> > > > > Tim Tyler wrote:
> > > > > > John Harshman <jharshman....@pacbell.net> wrote or quoted:
> > > > > >>Tim Tyler wrote:
> > > > > >>>John Harshman <jharshman....@pacbell.net> wrote or quoted:
> > > > > > You claimed a clear demonstration that most of the human genome is junk.
> > > > >
> > > > > I think it's pretty clear.
> > > >
> > > > Obviously - but your supporting argument was of the form: if one
> > > > mammal can survive without 90% of its DNA, the equivalant DNA
> > > > in other mammals can have no adaptive function.
> > >
> > > Rather, the argument is that the DNA equivalent to the missing DNA has
> > > no obvious significant adaptive function.
> >
> > My comments were directed towards the argument as quoted above.
> >
> > You are presenting a different argument.
> >
> > > To have an adaptive function means that it must fill a need. Since the
> > > fugu performs the same basic functions as, say, the zebra fish, that
> > > does rather argue that the type of missing DNA in fugu that is present
> > > in the zebra fish is not highly significant wrt function.
> >
> > Are the fugu and the zebra fish *really* functionally equivalent?
>
> Pretty much. Differences in size and shape, certainly. But wrt number
> of coding genes or functional products I doubt that there is more than
> a 5% differnce (about the difference between mouse and man).
I'm not convinced that they are "functionally equivalent".
You made no effort to argue that they are under the same selection
pressures, or have the same pathogens or predators. They might
look roughly the same, but be in what are effectively wildly
different environments.
> > Are they under the same selection pressures? What parasites
> > do the they have to combat? Isn't the Fugu from Japan? Japan
> > is an island ecosystem, surrounded on all sides by deep water.
> > Are you sure this has not influenced the Fugu's predators or
> > diet?
> >
> > It seems without demonstrating these sorts of things, the argument
> > that the Zebra fish gets no benefit from its extra genes doesn't
> > stand up.
>
> We aren't talking about extra *genes* that code for extra *protein
> products* or even extra *RNA products*. We are talking about extra DNA
> that doesn't code for anything. The DNA we are discussing is
> non-coding sequence. Any function it has has to be consistent with the
> fact that it is non-coding.
Absolutely. I tend to use the term "gene" in the Dawkins/William sense -
not the molecular biology sense - and so intended no implication that
genes code for protein fragments.
> > > And, of course, there is also the matter of major deletions (especially
> > > in chromosomes that don't have many coding genes, like the Y) that have
> > > minimal effects indicating that a great deal of DNA in other organisms
> > > is not highly significant.
> >
> > I think we can agree that most non-coding DNA is not highly significant.
> >
> > However I wouldn't describe everything which is not highly significant
> > using the term "junk".
>
> When you have a function of even minor significance, let us know.
Junk DNA has a significant effect on cell size - and it's not hard to
imagine increased cell size being adaptive - some of the time.
> The absence of sequence conservation tells us that most (but not all)
> of the non-coding sequence in vertebrates is of negligible significance
> wrt *any* function related to sequence.
I thought we had previously agreed that sequence conservation and
being the subject of selection were not the same thing. Sequence
conservation is a shaky metric to use when looking for selective
function.
> That rules out any coding function, any regulatory function, any
> specific structural function (centromere, telomere).
Nope - those are all still on the table as possible roles for
non-coding regions - at least under some circumstances.
> All that is left is insignificant bulk functions that really are
> negligible in importance, given that there is not even a strong
> relationship with bulk.
Non-coding DNA volume is pretty strongly correlated with genome size - and
genome size is pretty strongly correlated with cell size. What are you
saying there is not a strong relationship between again?
> There are two Hyla species (tiny frogs). These differ by one being a
> tetraploid and the other a diploid. The *only* way to distinguish
> between them morphologically is by their mating calls (and, of course,
> a chromosome count).
That's a bit different. Those organisms presumably have the same
proportion of coding DNA - just a different number of chromosomes.
What they indicate is that the cost of reproducing those extra
chromosomes is bearable, and not enough to obliterate them.
We already know that in spades from polyploid plants.
It seems quite possible that the benefits from being able to
duplicate and modify a few sequences, outweigh the costs of
all the extra DNA copying involved in cases like these.
> > "Junk" implies something has negligible significance - and non-coding
> > DNA may be something which is inappropraite to describe using such a term.
>
> Any function unrelated to sequence is pretty much of negligible
> significance; of no more importance than the amount of starch (also a
> polymer of sugars) in a cell. DNA, absent sequence specificity, is of
> little more importance to the cell than starch, and of less utility,
> since it cannot be used for energy storage.
This sounds like speculation on your part.
So, to clarify, you are claiming that there's biological literature
supporting your use of the term "conservation" to mean something like
"changing at anything other than the normal rate".
Please be more specific - where can I see some examples of this sort
of usage of the term "conservation" from someone other than you
The selection in question could be temporal, rather than varing along the
genome.
If a gene sequence is selectied to be conserved most of the time,
but is periodically selected to be different intermittently, then
its overall rate of change could match the rate of neutral evolution.
Intermittent events happen in nature. Plagues are probably those most
likely to cause selection for novelty when they strike.
> > It is not true that sequences which change at the same overall rate
> > as neutral genes over an extended period of time are neutral by
> > definition.
>
> As an operational definition, they *are* selectively neutral over that
> time frame. I agree that this could be an artifact if the sequence
> underwent both faster than neutral *and* slower than neutral rates of
> change that just happened to balance out. But if a sequence (aside
> from the hybid sequence containing both faster than normal change and
> slower than normal change subparts described above) is changing at a
> *constant* rate indistinguishable from the rate of neutral drift, how
> could selection be involved unless that sequence has either a much
> higher or lower mutation rate than other sequences (which would really
> mean that *its* rate of neutral drift differs from the average
> sequence's rate of neutral drift)? [...]
I don't know.
The example I was thinking of was subject to stabilising selection most of
the time - and selection for novelty on rare occasions.
Look at such a sequence on a long timescale and it might appear neutral -
but if examining it on a shorter timescale it would appear to be
under the influence of selection.
> > > > Also, the role of DNA as a spacer should not be neglected. Just because
> > > > a sequence is variable that doesn't mean it serves no purpose. A DNA
> > > > sequence has other properties besides the details of the order of the
> > > > base pairs on it - in particular it has a length.
> > >
> > > I.e., a need for bulk can be filled by otherwise utterly useless
> > > sequences. It can be filled by "junk" and serve the function of just
> > > being there. And lo, that does seem to be the case. 90+% of the human
> > > genome is filled by "junk" that serves no purpose other than being
> > > there.
> > >
> > > Moreover, it is quite clear that not only is this DNA's 'utility'
> > > independent of sequence, it is also largely independent or not highly
> > > dependent on the length of the sequence, since it can often be deleted
> > > or expanded without any detectable consequence. [...]
> >
> > ...but then attempts to detect it have usually been pretty feeble.
>
> Remember that you are talking about a currently unknown and unspecified
> effect of 'bulk' that *may* exist. You are saying that mere amount of
> DNA *might* do something, but you don't know or have any idea what that
> something is nor how to test it.
I do have a number of ideas on that subject, though I may not have
gone into much depth about them on this thread.
What I meant above is that attempts to identify side effects of
genetic changes are very often limited by funding. If an organism
has the same number of kids, fertility is rearded as unaffected -
and the organism is labelled as not detectably different.
Issues such as whether a gene conveying resistance to an infrequent
plague has accidentally been deleted are rarely addressed in this
sort of study.
> > > > Several of the proposed functions of junk DNA involve this notion -
> > > > that the DNA affects linkage patterns - that it acts as a sink
> > > > for intracellular mutagens - that it allows space for expansion
> > > > at the end of coding regions - that it allows gene duplication
> > > > without changing chromosome size - that it harbours LINEs and
> > > > SINEs - which act as types of highly non-random mutagen - and
> > > > so on.
> > >
> > > That doesn't make such sequence-independent DNA any less "junk".
> >
> > IMO, "junk" implies near-complete lack of function. Something acting as a
> > spacer would at least have *some* function.
>
> Only if the *length* of that spacer were crucial. If the length can
> vary widely, then the amount of spacer is pretty much irrelevant.
The junk DNA hypothesis suggests spacing is irrelevant. The skeletal
DNA hypothesis suggests it is important. Either way, the amount of
DNA spacing elements certainly do not vary anywhere near randomly -
and they occur overwhelmingly more frequently in larger organisms.
> > > These bulk features only require the presence of some DNA. It does
> > > not require the presence of any specific sequence (LINEs and SINEs
> > > excepted, but they are not there for the benefit of the organism, but
> > > have a more selfish origin).
> >
> > As mutagens, they are probably deleterious to the organism. However they
> > may conceivably benefit the species. LINEs and SINEs do behave selfishly
> > - but that may not be their only role.
>
> Evolution often co-opts any rare event that works to the benefit of the
> organism. That includes co-opting specific LINEs and SINEs that have
> landed at specific sites by random chance.
Indeed. What I mean is something like:
LINEs and SINEs may have been preferred by evolution over some other
self-replicating germ-line parasites - not through being better at
reproducing themselves within genomes - but because they had fewer
deleterious effects on the organisms that carried them. It that case,
they might be regarded as serving the adaptive function of competing
for resources with those more harmful germ-line parasites.
> > > "Junk" DNA serves no purpose but 'being there'. That means that 90+%
> > > of our DNA is there for no purpose but being there and, possibly, some
> > > bulk effect. [...]
> >
> > If your premise that "junk" DNA serves no purpose is accepted, that
> > follows - otherwise not. You are just assuming (or asserting) what you
> > are trying to prove here.
>
> I am saying that you have not presented a single specific *function*
> that the vast majority of non-coding DNA in a genome can play. How can
> one argue against the statement that "It might be doing something. I
> don't know what it could be doing or how it could be doing it. But it
> might be doing something." I can point out, from the evidence, that
> whatever it "could be doing" is not related to sequence and is not
> strongly related to length or number (in the case of SINEs and LINEs)
> of DNA present (see fugu).
IMO, those are both substantial over-statements.
Non-coding DNA could be doing things dependent on its sequence information
provided those things are not terribly important.
It could also be doing things that depend on its size. The case there
is stronger - since size so obviously affects linkage, affects cell
size, and has a number of other effects.
> What other property are you proposing that this DNA use to exert its
> currently unspecified function?
No other property: sequence information and size.
> > > > Consequently to argue from a variable sequence to non-functionality,
> > > > represents a logical flaw - since a stretch of DNA has heritable
> > > > properties which do not depend on its sequence data.
> > >
> > > Of course. Junk DNA replicates just like functional (sequence vital)
> > > DNA. SFW?
> >
> > That is not what I meant. What I meant was that junk DNA's length
> > is inherited - to to argue that because it has a variable sequence
> > it is not functional ignores the possibility that it may function
> > as a spacer.
> >
> > > The sequence of junk DNA, unlike sequence functional DNA,
> > > drifts like selectively neutral sequences (including changes in
> > > length).
> >
> > We know that is not true in general - since in some organisms
> > junk DNA is selected against - sometimes powerfully so -
> > resulting in changes in length being subjected to selection
> > and behaving highly non-randomly.
>
> Organisms that are environments where rapid replication is required for
> survival (largely unicellular) select in favor of parsimony in their
> genome. That does not mean that in organisms where other selective
> factors are more important that larger, less parsimonious genome have
> positive *selective* value.
It doesn't - but it *does* indicate that there's a difference in
nature between non-coding DNA and neutral changes - and thus that
changes in DNA length are often not neutral.
> > Also, most *changes* in length are nowhere near neutral:
> >
> > Instead, they are strongly deleterious - since they often
> > result in the organism carrying them being unable to recombine
> > its genes with other members of the species.
>
> Evidence? [...]
I don't know what proportion of changes in length cause this -
but changes in DNA lengths within chromosomes can lead to
increased probability of mismatch during meiosis. If that happens,
the result is often not viable - and is likely to miscarry.
> > As a result, to claim that changes in length of non-coding
> > sequences are similar to neutral changes doesn't make
> > much sense - since they are typically *much* less likely
> > to spread than neutral changes are.
>
> The size of vertebrate (and human) genomes wrt expansion and
> contraction is actually quite flexible at a certain scale of
> size changes.
*Small* changes can be adjusted for during meiosis. *Larger* changes
cannot. The result is a substantial degree of selection before
birth maintaining the status quo - and resisting changes in genome
size. That is a big part of the reason why humans all have roughly
the same genome size.
> That is why, for example, one actually has a DNA fingerprint.
> These are due to selectively neutral expansions and contractions of
> DNA sequences due to unequal crossing over. Because the number of
> repeats is selectively neutral there are often multiple alleles that
> are more or less frequent in the population. Enough so that we have
> these pretty darn unique combinations (unique enough to make for great
> TV crime shows).
SNPs are more common than indels and frameshift mutations - and
would be quite enough alone to give us a unique genetic ID.
Mark Isaak
>> > Are the fugu and the zebra fish *really* functionally equivalent?
>>
>> Pretty much. Differences in size and shape, certainly. But wrt number
>> of coding genes or functional products I doubt that there is more than
>> a 5% differnce (about the difference between mouse and man).
>
>I'm not convinced that they are "functionally equivalent".
>
>You made no effort to argue that they are under the same selection
>pressures, or have the same pathogens or predators. They might
>look roughly the same, but be in what are effectively wildly
>different environments.
As I recall, there was another fish in the same genus as fugu which
had three times the fugu's genome size. I think I saw this before the
fugu was reclassified as Takifugu, so I don't know if they are still
in the same genus, but they would still be closely related.
Another point I have not seen brought up (perhaps just because I don't
read all of the posts) is that some organisms have mechanisms to get
rid of excess DNA. That sort of implies that some DNA is excess. (I
know nothing of these mechanisms except their existence, so I will
shut up now.)
Mark Isaak
<geor...@earthlink.net> wrote:
Or the loss of an old tRNA since then.
>> The leading AUG would not be translated in any case, since that A is
>> the trailing base of the previous triplet. What is needed is
>> something to keep things going even though UGA usually means stop.
>
>Does that mean a selenocysteine can only follow a codon ending in A?
Apparently. I don't know enough about the mechanism to know how that
first A fits in, just that it is given as part of the requirement.
>> The mRNA need not have been modified. The "something" in the previous
>> paragraph could have used the pattern that just happened to be there,
>> as I said in my previous post.
>
>OK, possibly the mRNA could be the same, but what would recognize the
>"something". Either the new tRNA has a highly abnormal mRNA binding end and
>just butted in, in which case that would seem to be fatal to code downstream
>(I understand some proteins have selenocysteine at the front end), or the
>ribosome would have to be modified to recognize it.
The occurrence of "AA__GA" in the downstream region is not a very
stringent constraint. Remember that genes have a lot of wiggle room,
in the third base of many codons and often in some amino acids not
being important for the function of the final protein. There are
likely other subtler constraints, too, but the same principle holds
for them.
Always remember, if you want to convince us that a particular scenario
did not happen, your job is not to convince us that it is hard to
imagine how it happened. That would be a comment only about people's
imagination, not on anything relevant to the scenario. Your job is
not even to prove that it could not have happened. That would be an
impossible job, since it would require you to consider an infinite
number of pathways. Your job is to make predictions whose outcomes
would differ depending on whether it happened or not, and then look at
the outcomes. Coincidentally, that is exactly the same job of a
person who proposes the scenario with an intent to convince people it
happened.
John Harshman
OK. Now let's suppose that we have a population in which a mutant arises
that has lost some huge amount of the genome. If the lost material is
the subject of selection, will that mutant genotype increase in
frequency in the population, or will it not? Or to put it another way,
what's so special about the environment of fugu that their ancestral
population was able to drop most of their genome, even though (in your
theory) it should be functional and selected?
>>>>>Obviously, that is going to depend on the species and experiment:
>>>>>
>>>>>If the experiment is on fingernail patterns or eye colour, there's
>>>>>typically little basis for such a belief.
>>>>>
>>>>>If the experiment is on genitals, there's often a 50% chance of
>>>>>the result not applying.
>>>>>
>>>>>On the other hand, if the experiment involves the on number of
>>>>>legs, there may be a firmer basis for the belief.
>>>>
>>>>Why? Do we have to come to you for decisions on this sort of thing, or
>>>>is there a rule we can follow?
>>>
>>>There are reasons for thinking that an experiment will or won't apply
>>>to other members of the same species. There are lots of approaches
>>>to the issue, involving things like drawing on experience of similar
>>>traits or similar species. However, this seems to be going off at
>>>a bit of a tangent to the subject under discussion.
>>
>>So what are the reasons for thinking that the fugu genome can't tell us
>>anything about the genomes of other species?
>
> Firstly, what is your reason for concluding I think anything of the sort?
>
> To clarify, I *don't* think that.
Good. Then you agree that the small size of the fugu genome does indeed
suggest that most of the human genome is junk. Right?
>>>>>>>>That's the beauty of looking at sequence
>>>>>>>>conservation, because it indexes long-term importance.
>>>>>>>
>>>>>>>It indexes conserved genes.
>>>>>>>
>>>>>>>Of course, genes for traits such as diseases resistance are not
>>>>>>>necessarily conserved - and can be selected in such a way that
>>>>>>>they are constantly changing.
>>>>>>
>>>>>>Yes, there are a few of those. They change at greater than the neutral
>>>>>>rate, and that stands out too.
>>>>>
>>>>>So: some selected genes change faster then neutral genes - and other
>>>>>selected genes change slower than neutral genes. Maybe some also
>>>>>change at about the same speed as neutral genes.
>>>>
>>>>Why would that happen? The reason some genes are slow is that they
>>>>perform a function for which a particular sequence is better than those
>>>>near to them. The reason some genes are fast is that their function
>>>>actively selects for differences. What would cause sequences to be
>>>>selected for evolution at a neutral rate?
>>>
>>>Selection based on infrequent events - such as plagues originating from
>>>inter-species infections.
>>
>>I agree that it's logically possible for selection to cause change at
>>the neutral rate. But again, if you have a huge number of sequences
>>evolving at the neutral rate, what are the odds that any large
>>proportion of them are under selection that just happens (out of all the
>>rates that are possible) to mimic neutral evolution?
>
> Very likely low.
And therefore the objection you raised to considering the "junk" to be
evolving neutrally is bogus, right?
>>>>And what leads you to believe that the bulk of our DNA could possibly
>>>>be made up of such sequences?
>>>
>>>What leads you to attribute this unlikely view to me?
>>
>>You are trying to cast doubt on the idea that most of our DNA is junk,
>>and that evolving at the neutral rate is good evidence that a sequence
>>is evolving neutrally. [...]
>
> What I was originally trying to cast doubt on was the notion that
> sequence conservation indexes long-term importance.
>
> I agree that most sequences that are evolving on average at the overall
> neutral rate are indeed likely to be neutral. I don't agree that /all/
> of them will be, though.
Doesn't matter, as long as most of them are. Focus.
>>>>>Also, the role of DNA as a spacer should not be neglected. Just because
>>>>>a sequence is variable that doesn't mean it serves no purpose. A DNA
>>>>>sequence has other properties besides the details of the order of the
>>>>>base pairs on it - in particular it has a length.
>>>>
>>>>True. Some DNA may be important merely as a spacer, and other DNA may be
>>>>selected merely because it makes a cell bigger. But these are doubtful
>>>>exceptions. There are no hidden functions there to delight the
>>>>creationist, and that's what this argument is really about.
>>>
>>>Ah. I'm not discussing creationism. That seems like it would be
>>>a waste of time.
>>
>>No? That's the main purpose of this group.
>
> I thought this group was for discussion of origins.
Codeword for creationism. Real discussion of "origins", a term used more
or less only by creationists, happens on groups like sci.bio.evolution.
So you're saying that there is a balance between the usefulness of the
junk and the cost of producing it. Fine. But we don't need the junk to
be useful in order to get a balance; all we need is that junk would
increase in the absence of selection. And this usefulness of junk is
entirely hypothetical.
>>>>>Consequently to argue from a variable sequence to non-functionality,
>>>>>represents a logical flaw - since a stretch of DNA has heritable
>>>>>properties which do not depend on its sequence data.
>>>>
>>>>Agreed, to a point. There are some cases in which DNA is just a
>>>>place-holder. However, I think the great variability in genome size does
>>>>argue that most of the neutrally evolving DNA does indeed fill no
>>>>function. Why should mammals require so much more of these bulk
>>>>functions than fugu, and so much less than frogs? There's just no
>>>>sensible, functional explanation for that.
>>>
>>>The variability of the volume of junk DNA suggests it is not very
>>>important. It doesn't prove it though - since it could also vary
>>>under selection pressures not yet fully understood.
>>
>>There is no such thing as proof in science. Junk could always have a
>>function that's too subtle to detect. This is "function of the gaps".
>
> So, until more comprehensive evidence on the issue comes in, should we
> say that non-coding DNA has no well-established function, or should we
> label it as junk - and deny it has any function at all?
Under your logic, there is no possible combination of evidence that
would lead us to conclude that the junk was indeed junk. There will
always be the possibility of a use that we don't know of yet, until such
time as we know everything there is to know about everything. Right now,
junk is the way to bet, and that's all science ever does.
> It's not as though the evidence in favour of junk DNA being useless is
> even very good.
>
> Have you come across the Cavalier-Smith, "skeletal DNA" hypothesis?
>
> This notes that genome size is strongly correlated with cell size.
Yes.
> That's an obvious clue that something other than simple random forces
> is involved - and has suggested various possible adaptive functions
> of the supposedly 'junk' DNA - e.g.:
>
> ``According to the skeletal DNA hypothesis, then, more noncoding DNA is
> necessary for larger cells -- perhaps by more widely spacing the protein
> and RNA-coding genes, transcription can occur more rapidly, allowing the
> production of more proteins necessary for the larger cell.''
>
> - http://wiki.cotch.net/index.php/Junk_DNA
I'd be interested to know how strong this correlation really is within
vertebrates. Do fugu have smaller cells than zebrafish? At any rate,
such a bulk function still leaves it as junk, for almost all practical
purposes.
hers...@indiana.edu
Tim Tyler wrote:
> John Harshman <jharshman....@pacbell.net> wrote or quoted:
> > Tim Tyler wrote:
> > > John Harshman <jharshman....@pacbell.net> wrote or quoted:
[snip]
> > > It seems clearly experimentally demonstrated that selection can act
> > > to reduce the junk DNA in organisms.
> > >
> > > Vertebrates may differ in the extent which they have been subject to such
> > > selection pressures, in the relatively recent past.
> >
> > Well, of course selection can reduce junk. There is a cost of
> > replication, after all. But so what? This can happen if it's really
> > junk. In fact, it will happen much more easily if it's junk. That's no
> > argument.
>
> You asked for a reason why vertebrates should differ so much in the volume
> of junk DNA - if it serves some useful purpose.
>
> My answer to that was that they may differ in the extent to which they
> have been subject to selection to eliminate the junk.
And this is specifically saying that the DNA in question *is* junk with
no real useful purpose. It certainly is not providing the "junk" with
any specific useful purpose. It is saying that it is dispensible.
> It's easy to
> imagine how hard times, or fierce competition, or dietary shortages -
> or any number of other factors - might sometimes produce selection
> that penalises those with large genomes.
Specifically, small parsimonious genomes are seen more or less
consistently in *unicellular* organisms that rely on rapid replication
to outgrow any threats or limited transitory resources.
[snip]
> > There is no such thing as proof in science. Junk could always have a
> > function that's too subtle to detect. This is "function of the gaps".
>
> So, until more comprehensive evidence on the issue comes in, should we
> say that non-coding DNA has no well-established function, or should we
> label it as junk - and deny it has any function at all?
It has no sequence-dependent function. That much is clear. It's
extensivity-related functions (functions related to how much of it
there is) are unclear and clearly quite flexible by about an order of
magnitude (the difference between fugu and other vertebrates). That
relative lack of need for as much DNA as is present is supported by
other smaller scale experiments (both in nature and artificial).
hers...@indiana.edu
The logical argument is of the form that fugu (which is a fish) is not
only viable, but performs essentially every important, vital, or useful
function that any other fish (and most vertebrates) does. It is not
poorly viable or some sort of weakling species compared to other fish.
So your problem is to find some *function* for the DNA that is missing
in fugu but present in other vertebrates. That means you have to
propose some sort of *important* or *vital* or *useful* function that
this DNA performs in other vertebrates that is NOT being performed in
fugu because that DNA is missing in this species. I can't think of any
such function. Can you? If you can, you certainly haven't stated it.
You are proposing that the DNA that is missing in fugu but present in
other species has some function on the basis of what? A wish that it
have some function?
> > Would you agree that the tiny genome of fugu (which is a fish, not a
> > mammal, by the way) is in fact evidence, whether conclusive or not, in
> > favor of junk being junk?
>
> I don't know much about the specific case of fugu, aside from the
> fact that it has a small genome, which proves very little - besides
> the fact that such creatures can be viable.
Not only viable, but just as viable as any other fish. Fugu is not
some sort of primitive weakling fish barely able to move or function or
missing whole categories of functional coding sequences. It is a
perfectly normal fish as well adapted and functional as any other
species that has 3-5 times as much DNA. So, given that fugu is not
some sort of recognizably abnormal species from any morphological,
biochemical, or physiological perspective, why would anyone claim that
the missing DNA must be there to perform some important function. The
function that creationists would like it to perform, namely being
designed spare parts, is explicitly contradicted by the fact that the
missing DNA in fugu is unconserved (wrt sequence) DNA in species that
retain it. If there is any reason why this DNA is retained in other
species, it is not because it has any detectable important effect on
behavior, physiology, development, or function.
> > >>Given your logic, why should we believe that the results of an
> > >>experiment on one individual should apply to other individuals of the
> > >>same species?
> > >
> > > Obviously, that is going to depend on the species and experiment:
> > >
> > > If the experiment is on fingernail patterns or eye colour, there's
> > > typically little basis for such a belief.
> > >
> > > If the experiment is on genitals, there's often a 50% chance of
> > > the result not applying.
> > >
> > > On the other hand, if the experiment involves the on number of
> > > legs, there may be a firmer basis for the belief.
> >
> > Why? Do we have to come to you for decisions on this sort of thing, or
> > is there a rule we can follow?
>
> There are reasons for thinking that an experiment will or won't apply
> to other members of the same species. There are lots of approaches
> to the issue, involving things like drawing on experience of similar
> traits or similar species. However, this seems to be going off at
> a bit of a tangent to the subject under discussion.
Yes. And all of those other experiments also say that the DNA in
question (the DNA of the type missing from fugu) plays little or no
*important* (defined in selective terms of reproductive success) role
in physiology, selective advantage or disadvantage, morphology, or
development. Fugu is simply a clear natural experiment in the effect
of *removing* the so-called "junk" DNA because the common ancestors of
fugu species had more DNA than fugu does.
>
> > >>>>Yes, the problem with experiments like that is that one can always argue
> > >>>>that the missing material does have a function, just one too subtle to
> > >>>>be detected easily; maybe it's a function that is only needed once every
> > >>>>hundred generations. That's the beauty of looking at sequence
> > >>>>conservation, because it indexes long-term importance.
> > >>>
> > >>>It indexes conserved genes.
> > >>>
> > >>>Of course, genes for traits such as diseases resistance are not
> > >>>necessarily conserved - and can be selected in such a way that
> > >>>they are constantly changing.
> > >>
> > >>Yes, there are a few of those. They change at greater than the neutral
> > >>rate, and that stands out too.
> > >
> > > So: some selected genes change faster then neutral genes - and other
> > > selected genes change slower than neutral genes. Maybe some also
> > > change at about the same speed as neutral genes.
Genes, coding sequences that retain the original function, almost
*always* (and perhaps even always, if you average over the entire
sequence of a gene) change at a slower rate (averaged over sufficiently
long time frames; change can be episodic) than the rate of change for
selectively neutral sequences. It may seem startling to hear that; but
it is true. Most change over time is selectively neutral change. When
a gene changes function, it may undergo a rapid change. But all
cytochrome c's for example, change at slower rate than fibrinogen
peptide *because* certain parts of the sequence are more or less
important to function.
> > Why would that happen? The reason some genes are slow is that they
> > perform a function for which a particular sequence is better than those
> > near to them. The reason some genes are fast is that their function
> > actively selects for differences. What would cause sequences to be
> > selected for evolution at a neutral rate?
>
> Selection based on infrequent events - such as plagues originating from
> inter-species infections.
Selection for such features may be fast at the one or two aa residues
important for the modified (resistant) features, but change will remain
slower than drift at aa residues responsible for the proteins basic
function. The net effect, averaged over the entire gene (coding)
sequence will be change slower than drift.
> > And what leads you to believe that the bulk of our DNA could possibly
> > be made up of such sequences?
>
> What leads you to attribute this unlikely view to me?
>
> > >>>Sequence conservation doesn't have too much to say about that.
> > >>
> > >>Yes it does, since change in those genes is actually accelerated.
But only at the sites that are crucial for modified function. At sites
important for basic function, there will still be conservation. At
other sites in the same protein, there will likely be simple drift,
since the aa's at those sites are not important. Averaged over a
protein's *entire* sequence, the net effect is almost always (if not
always) slower change than would occur by drift alone. That doesn't
mean that the sequence will not change *at all*. It will, by drift
and, more rarely, by selection. Different proteins will change at
different rates depending upon how many of its aa residues are
important for function and how they are important for function. But,
once a protein is optimized by selection, change (over the entire
sequence) will almost always be slower than if all the sequence were
selectively neutral.
I call it junk because it seems to be largely dispensible without
significant consequence wrt organismic (selective) function. And I
flatly reject, on the basis of much available evidence, that this DNA
looks like it was designed for some important function like being
'spare' genes or 'future' genes.
> However, that isn't a scientific approach. The scientist should look at
> the evidence, without a prior political agenda.
When you propose a specific function for this DNA that depends upon
some property of DNA that is important and unique to DNA (like
sequence) rather than on properties like extent that can vary over
several multiples of difference with little effect, you will have my
rapt attention. Until then, I have to go with the evidence that says
this DNA doesn't do much if anything important and is largely
dispensible.
> > > Several of the proposed functions of junk DNA involve this notion -
> > > that the DNA affects linkage patterns - that it acts as a sink
> > > for intracellular mutagens - that it allows space for expansion
> > > at the end of coding regions - that it allows gene duplication
> > > without changing chromosome size - that it harbours LINEs and
> > > SINEs - which act as types of highly non-random mutagen - and
> > > so on.
> >
> > Some of these ideas are silly, if you ask me. And they all founder on
> > the extreme variability in genome size, unless you can think of a reason
> > why these factors should all differ so greatly among vertebrates.
>
> It seems clearly experimentally demonstrated that selection can act
> to reduce the junk DNA in organisms.
Which is what happened in the case of fugu. With no detectable ill
effects.
> Vertebrates may differ in the extent which they have been subject to such
> selection pressures, in the relatively recent past.
Of course. And I am sure that there is probably a point beyond which
too much DNA/genome would be a drag on survival (reproductive success).
But that point does not have to mean that the DNA needed to reach it
must all have functional utility. [And the evidence indicates that a
lot of it is pretty unnecessary.]
> > > Consequently to argue from a variable sequence to non-functionality,
> > > represents a logical flaw - since a stretch of DNA has heritable
> > > properties which do not depend on its sequence data.
> >
> > Agreed, to a point. There are some cases in which DNA is just a
> > place-holder. However, I think the great variability in genome size does
> > argue that most of the neutrally evolving DNA does indeed fill no
> > function. Why should mammals require so much more of these bulk
> > functions than fugu, and so much less than frogs? There's just no
> > sensible, functional explanation for that.
>
> The variability of the volume of junk DNA suggests it is not very
> important. It doesn't prove it though - since it could also vary
> under selection pressures not yet fully understood.
When you have some argument other than "there might possibly be a
function we don't know about", let us know.
>
> Also, neutrality is a matter of degree. Very little is likely
> to be absoultely neutral - and in large populations, even very
> small selection pressures can produce significant long term
> results.
Selective pressures that are so small as to be overwhelmed by pure
chance fluctuations (in real populations) are effectively neutral and
can be ignored. Pure chance (aka neutrality) is more important in
these cases.
> Junk DNA may not be *vitally* important - but it could
> still be significant enough to contribute to species traits -
> such as evolvability.
The presence of transposable and repetitive elements certainly can lead
to rearrangements, deletions, insertions, chimeric gene formation, etc.
These types of mutations are part of the fuel of evolution (which
obviously includes much more than just point mutations). That doesn't
mean that they are there for that function and certainly doesn't give
that DNA any physiological, developmental, or other function during the
life of the organism.
George Evans
news:1117169623.4...@f14g2000cwb.googlegroups.com...
>
> George Evans wrote:
>
>> in article 1117031431....@o13g2000cwo.googlegroups.com,
>> hers...@indiana.edu at hers...@indiana.edu wrote on 5/25/05 7:30 AM:
>> >
>> > George Evans wrote:
<snip>
>> >> True to form, you are once again stuck speaking as a hardware
>> >> engineer--or
>> >> maybe I should say Xerox repairman. Yes, it costs the same to copy the
>> >> source
>> >> code to OS X as it would to produce an equal number of pages of my
>> >> butt.
>> >>
>> > That is quite true. But what other form of information *that is
>> > actually
>> > independently measureable* rather than a drawing of the bull's eye
>> > after the
>> > arrow has stuck were you talking about?
>>
>> The kind of information that you hardware engineers can only sit and
>> marvel
>> at.
>
> Still not capable of describing Dembski information in any meaningful
> public way, are you? Dembski information, like beauty, is in the eye
> of the beholder and only in the eye of the beholder.
Well, we are getting somewhere at least. You think Dembski information is
like beauty. :-)
<snip>
You said it yourself. These are not a repository of spare genes *other than
some* involved in transposition. Admit it, you haven't checked them all.
These transposons really bear a striking resemblance to what would be
predicted for a repository.
>> And it is impossible to maintain that position in light
>> of the fact that the movement of transposons into and out of genes is
>> responsible for known phenotypic changes, for example the different
>> colored
>> kernels of Indian Corn.
>
> Do you know how the movement of transposons (out of in this particular
> case) cause the change in phenotype? It is rather simple. When
> inserted, the largish transposon (inside an intron) means that a
> particular gene will be transcribed, but the transcript will not be
> spliced properly. When the transposon pops out (in a specific tissue
> in which it the transposase activity is activated), leaving behind a
> small duplicate (which would cause mistranslation in a coding sequence)
> the restored rough size (a few added nucleotides are irrelevant in an
> intron) of the intron allows proper splicing and translation. The
> transposon is not carrying in or taking out any "stored gene" sequence.
> It is acting as a regulated transposable element. Causing a somatic
> mutant phenotype (the color) when it pops out in a specific tissue. It
> also caused a mutation when it inserted into the intron, inactivating a
> gene that caused colored kernals.
That's simple? More like a briar patch. Try again.
>> >> At the very least they rattle one of the two Darwinian
>> >> mechanisms--mutation.
>> >>
>> > No. Transposition *is* a rather common form of insertional mutation.
>>
>> But that's not the slow, minute change that Darwin predicted.
>
> A transposition event is different wrt rate of change than a point
> mutation. It may at a rate which is more (or less) frequent than point
> mutations, but transpostions do not cause directed teleological
> mutations any better than point mutations or frameshifts or deletions
> or chromosomal rearrangements. The effect of transposition is
> determined by where it inserts. That occasional organisms have
> domesticated certain of their transposable elements (MAT locus in
> yeast) doesn't mean that transposon
Working with relatively conservative mechanisms like mutation and natural
selection, what would be the selectable improvement in a system that cuts
and pastes chunks of DNA willy-nilly? Whichever came first, cutting or
pasting, how would an organism in which it started survive? When my kids
were little and I was working on a paper I didn't mind them occasionally
pushing a random key here and there, but I sure wasn't going to teach them
how to cut and paste!
>> And if it
>> amounts to taking a part off the shelf, it is a stretch to call it a
>> mutation at all.
>
> It isn't taking any part off the shelf other than the transposon
> itself. Where do you get this bizarre idea that transposons contain
> all these various "hidden gene sequences". They are *repetitive*
> elements.
Repetitive with variations sounds like it could have something to do with a
built in ability to vary and adapt. Clearly, some of these transposons carry
genetic information and are not junk.
>> >> Suddenly, change looks a whole lot easier, possibly because it's
>> >> planned.
>> >>
>> > Transposition is not "planned". The transposing element may (or may
>> > not,
>> > depending on the element) favor integration at a particular sequence,
>> > but the
>> > sequence is small (often two nucleotides) and present at literally
>> > millions of
>> > sites in the genome. Just like other mutational events, transposition
>> > can
>> > produce a beneficial, neutral, or detrimental effect depending upon the
>> > site
>> > it integrates into and conditionally upon the environmnental
>> > constraints on
>> > the organism.
>>
>> I don't know. If I were in research I would be writing a grant proposal
>> to
>> search genomes for areas that matched introns of active genes.
>
> Been done. Most of the sequence in introns is selectively neutral and
> changes at the rate of neutral drift over evolutionary time frames. The
> parts that are conserved are typically the small sequences that specify
> splice points.
My mistake, I specifically meant those splice point sequences.
>> Also, keep in
>> mind that just because something is planned doesn't mean it can't go
>> haywire
>> now and then.
>
> And your evidence for planning is the somatic (not germ line) changes
> in Indian corn?
No, my evidence for planning is the cell itself.
There are tons of these things. Certainly not enough study has been done to
support the negative assertion you are making.
<snip>
> Do you honestly think that transposon sequences are an unknown that can
> hide all your hypothetical "spare parts genes"? Or is that simply your
> ignorance speaking? Again, transposon sequences are known. Take Alu
> sequences for example. Alu sequences are highly repetitive and the Alu
> transposon is largely a domesticated transposon, with most of the
> sequences remaining stable. When one does move, it is as likely to
> cause a deleterious change as any other mutation. That doesn't
> preclude it from occasionally producing a beneficial change. It is
> acting just like a G to A missense mutational change.
Yes, all transposon sequences are "known" because the whole genome has been
sequenced. Have you been through the whole thing with a fine tooth comb?
Some transposons have been studied thoroughly and some have been found to
carry useful genetic material. That's where I'm getting this "bizarre" idea.
<snip>
George Evans
George Evans
"Steve Schaffner" <s...@darwin.broad.mit.edu> wrote in message
news:ydlpsvc...@darwin.broad.mit.edu...
>
> Ken Shaw <non...@your.biz> writes:
>
>> George Evans wrote:
>>
>> > in article 720le.249601$cg1....@bgtnsc04-news.ops.worldnet.att.net,
>> > Ken
>> > Shaw at non...@your.biz wrote on 5/25/05 7:34 AM:
>
>> > But being able to measure a quantity is not the be and and end all of
>> > existence. We found ways to measure heat and it doesn't exist.
>>
>> Heat doesn't exist? The amount of kinetic energy contained in a material
>> doesn't exist?
>
> That's the internal energy, not the heat. Heat is the energy
> transferred between bodies at different temperatures. (I hope I
> got that right -- thermal physics was never my thing.)
You got it. Heat is a leftover quantity from when it was viewed as a fluid
flowing from one thing to another. Now we understand it completely in terms
of kinetics of atoms and molecules. Energy is transferred by collision or
vibration.
> Whether heat "exists" or not strikes me a meaningless question. It's
> a well-defined and measurable attribute of physical systems,
> characteristics it seems not to share with "Dembski information".
It just shows that being able to measure something isn't proof of existence.
George Evans