Possible vs. Likely
Seanpit
> > Again, you confuse what is possible with what is likely . . .
>
> And you think it "likely" that there is only one possible "gap"
> involved in going from your "hypothetical unnamed undescribed"
> starting point to the final teleologic "system" you name?
You simply can't stop using the word "possible". You just did it
again here. Anything is possible. There are many "possible" gap
distances. Which of these possibilities is most likely without
knowing the answer ahead of time? That's the question here.
You simply assume that the minimum possible gap distance is likely
without actually doing any statistical analysis to support this
assumption - nor have you presented any actual demonstration or direct
observational evidence. All you really have are bald assertions and
just-so stories. That's not science.
> > It
> > isn't enough to present what is possible Howard. You have to actually
> > show that what you're presenting is even remotely likely in a given
> > span of time . . .
>
> Yes. Which is exactly what the evidence shows for humans and
> chimpanzees.
Name a unique functional difference between humans and chimps that
isn't just quantitative but qualitative . . . Then, once you have
done this, show the minimum number of genetic differences needed to
produce this novel functional difference.
The problem here, of course is that no one knows anything about such
functional differences between humans and chimps - at least not
adequately at this point. That is why you use this example all the
time. You're conveniently hiding behind a lack of information. Try
dealing with examples that we know more about - like subcellular
systems.
You're argument is not based on any form of statistical analysis
whatsoever when it comes to known differences in levels of functional
complexity. You're argument is based entirely on what you know could
happen but have no idea how likely it is to happen. That's not
science Howard. That's wishful thinking.
< snip >
> > You
> > never even think about what is
> > likely - only about what is possible.
> > That's not science Howard.
>
> Your entire argument is equivalent to claiming that it was almost
> impossible for Barack Obama to be elected president of the U.S. in
> 2008 because the likely probability of any individual being elected
> president is one over the number of people that meet the legal
> requirements (the size of total sequence space that meets the minimum
> functional and structural requirements for being president). That is
> exactly the argument your math presents, only substituting "total
> sequence space that meets the minimum sequence requirements for some
> named function that already exists"). It is an ahistorical argument
> based on a false premise.
Someone within the population is guaranteed to win the presidency
ahead of time within a certain period of time. Finding a target
within sequence space is not guaranteed to happen in a given span of
time for a given population. The locations of the targets are
unknown. The search algorithm is completely random. The odds of
finding a target in a given span of time depend entirely upon one
thing, one thing that you never even consider: The odds that a
potential target within an unknown location will be within a given
distance of a known starting point.
Even with predicting who will be president, knowing the likely pool
from which the president will be drawn does improve the odds of a
successful pick, but the odds are still there. There are non-winner
options. You don't consider any odds of success vs. failure
whatsoever in your "theory". You don't use any odds analysis at all.
You simply argue that eventually it will be known, with a 1:2 odds of
success, who will be president.
Of course, if you actually know that the starting point is so close to
the target ahead of time, you can get very very accurate. Using this
analogy you actually claim that the odds of finding novel targets in
sequence space in a given span of time can be known to be as high as
50%? - regardless of the level of functional complexity under
consideration?
Do you not understand how strained this argument really is? Again,
you are in fact arguing that what is possible is what is likely
again. In reality, you have no idea as to the actual odds of success
without actually knowing the location of both the starting point AND
the target points in sequence space ahead of time. You don't know the
location of the target point(s) ahead of time like you know the target
point of the presidency ahead of time (or the actual final two
candidates ahead of time).
Determining the odds of success when it comes to finding targets in
sequence space involves at least some understanding of the likely
ratio and distribution of potential targets vs. non-targets in
sequence space at various sizes of sequence space. That's it. Yet,
you don't even consider such odds. You simply state that it is
possible. What about considering the likelihood of what is possible
Howard? That's the science part of the problem.
You're problem is that you assume that the ratios remain essentially
the same regardless of the size of sequence space. You simply assume
that because it is possible to have the minimum gap distance of one at
any size of sequence space that this is also likely. That's not
true. What is possible is not necessarily what is likely. You need
to actually consider the odds of what is likely. You don't do this.
> Real analysis of real historical events that have already happened do
> not, as you do, assume that all the precursors were equally likely to
> exist. It looks for *evidence* of precursors that would made the
> event that actually happened possible. In the world of the evolution
> of protein systems, that means looking for evidence of useful
> subfunctions that parts of the current modern function could do
> without major change in function or structure.
You have to consider the odds that you will actually find something
close enough Howard. You can search all you want, but the odds that
you will find something depend upon the nature of sequence space.
And, the search itself demonstrates my very point. Finding targets
within one or two mutations of each other gets exponentially more and
more difficult at higher and higher levels of functional complexity.
This is a fact. Like 3-letter words, lower-level targets are commonly
within one or two character changes of each other. This is not as
often the case for meaningfully beneficial 100-character sequences,
and exponentially less so for 1000-character sequences . . . etc.
You can't simply search without any idea as to what you're likely to
find. That sort of search is based on nothing but wishful thinking -
not science.
> > Your position can't be falsified, even in
> > theory, because everything is possible.
> > Science deals with estimates
> > of likelihood - not imagined possibilities.
>
> And for historical events, it looks for evidence of how that event
> actually happened by *possible* mechanisms,
We are talking about what is likely here, not about what is merely
possible. What is the likelihood that your proposed mechanism did the
job Howard? You don't even consider that question. You simply argue
that "it's possible" like a mantra. That's not science.
> not the probability of
> recurrence based on a process that is unlikely to be the one that was
> actually used, such as the idea that Obama became president by a
> random lottery pick from the total sequence space of total sequence
> space of legally possible candidates.
As I've told you before, the gap distance in real life is ALWAYS
smaller than the size of total sequence space - always. The pool of
likely starting positions is much smaller than the total space of
potential starting points. This doesn't remove the need for odds
analysis - of how many mutations it will likely take to find a novel
target when the location of potential targets is not already known
ahead of time. All that is known is that they are almost certainly
closer than the maximum possible distance.
> Hint: The *real* historical process of Obama becoming president
> involved a series of events, some of which were due to chance (such as
> the Jack Ryann Senate candidacy imploding in a sex scandal), some of
> which involved the character and qualifications of the candidate. The
> probability of the last step (or gap) in the process was essentially 1
> out of 2. There are ways of identifying evidence for the steps in the
> historical process. None of them involve assuming that Obama became
> president in a single step gap-crossing with a probability due to
> division by the total number of legally possible candidates for
> president.
We are talking about a situation where the actual gap distance is not
already known ahead of time Howard. We are talking about predicting
the gap distance. What gap distance is likely? That's the question
here. In order to determine this without actually knowing ahead of
time, you need to do some real science Howard. If you already know,
you don't need science. Since you do NOT already know what the actual
gap distances were, you DO need science. That means you need to start
using some real statistical analysis Howard - some real numbers. You
need to go beyond your mantra that "It's possible" to "It's likely"
based on some real mathematical analysis. I know that's tough for
someone who has spent his whole life telling just-so stories, but
until to go beyond this, what you're doing is not real science.
Sean Pitman
www.DetectingDesign.com
Ron O
> On Nov 27, 10:15 am, hersheyh <hershe...@yahoo.com> wrote:
>
> > > Again, you confuse what is possible with what is likely . . .
>
> > And you think it "likely" that there is only one possible "gap"
> > involved in going from your "hypothetical unnamed undescribed"
> > starting point to the final teleologic "system" you name?
>
> You simply can't stop using the word "possible". You just did it
> again here. Anything is possible. There are many "possible" gap
> distances. Which of these possibilities is most likely without
> knowing the answer ahead of time? That's the question here.
>
Just face this simple fact. According to your own standards your
alternatives don't even rate as "possible."
You can run and pretend, but that doesn't change such a simple fact,
does it?
Just how bogus can you get. Deflection and obfuscation are all you
have left. You know it and have known it for years. How long have
you been running and pretending from your claim that you had an
alternative to common descent that had evidence backing it up that was
just as good as the scientific evidence that you didn't like? It must
be going on 8 years now. 8 years of denial, and dishonest bogus
behaviour. Where is that intelligent design science that you would
have taught to school kids? Probably going into 6 years on running
from that claim. What does that mean for the title of your web site
when you know for a fact that the design science never existed? No
alternative worth mentioning, no science worth presenting, no argument
worth jack.
Running and pretending is just a bogus form of argument. You know it,
so why is it acceptable for you to do it?
Ron Okimoto
'Rev Dr' Lenny Flank
(snip)
> Name a unique functional difference between humans and chimps that
> isn't just quantitative but qualitative . . . Then, once you have
> done this, show the minimum number of genetic differences needed to
> produce this novel functional difference.
(snip)
I'm a little curious here . . .
Humans and chimps are closer to each other, genetically, than many
other species are which creationists consider to be the same "kind" --
horses and donkeys, for instance, or cheetahs and jaguars.
Why then do you consider it utterly absolutely completely impossible
for humans to have "micro-evolved" their genetic differencesd with
chimps, but NOT utterly absolutely completely impossible for members
of other "kinds" to have "micro-evolved" their LARGER genetic
differences with each other?
If the genetic differences between jaguars and cheetahs can have
evolved, then why do you insist that the SMALLER genetic differences
between chimps and humans, can not have?
Besides, of course, your religious opinion that humans are special and
simply cannot be related through descent to any other animal, no
matter what . . .
================================================
Lenny Flank
"There are no loose threads in the web of life"
Editor, Red and Black Publishers
http://www.RedandBlackPublishers.com
wf3h
>
> > > Again, you confuse what is possible with what is likely . . .
>
> > And you think it "likely" that there is only one possible "gap"
> > involved in going from your "hypothetical unnamed undescribed"
> > starting point to the final teleologic "system" you name?
>
> You simply can't stop using the word "possible". You just did it
> again here. Anything is possible. There are many "possible" gap
> distances. Which of these possibilities is most likely without
> knowing the answer ahead of time? That's the question here.
actually what sean ignores is the fact that the impossible is not
possible.
sean says that scientific data must be evaluated statistically. if the
data does not support the hypothesis, the hypothesis must be rejected.
sean says this is how science is done
however, creationism has been used to explain features of nature. sean
thinks it's true. but it has a 100% track record of failure. it's
ALWAYS failed. 100% of the time.
but sean doesn't reject it. why? why does he not use his OWN criteria
for rejecting a failed hypothesis.
anwer: because of his religion. his reliigon teaches that creationism
is correct. so sean is incapable of evaluating data objectively.
he is not a scientist...even by his own criteria.
>
> The problem here, of course is that no one knows anything about such
> functional differences between humans and chimps - at least not
> adequately at this point.
except that sean routinely asserts we know ALOT about DNA...we know
how it is formed and changed in nature. we know enough to exclude
natural processes.
how does he know this? well, hell he just admitted we know very little
about DNA. but he says we know ALOT about DNA...if it suits his
religious beliefs
That is why you use this example all the
> time. You're conveniently hiding behind a lack of information.
sean says that scientists should stop doing DNA research because it
gives the impression that creationism is false. he himself hides
behind his 'god of the gaps' ignorant view of science
Try
> dealing with examples that we know more about - like subcellular
> systems.
gee sean i thought you said we know all we need to know about DNA and
can exclude natural processes
>
> You're argument is not based on any form of statistical analysis
> whatsoever
well yours is. unfortunately it has failed. always. but you dont
reject it
why?
R. Baldwin
42ff8b...@g17g2000prg.googlegroups.com:
> On Nov 27, 10:15 am, hersheyh <hershe...@yahoo.com> wrote:
>
[big snip for brevity]
Sean, that whooshing sound over your head is the same point you have missed
over and over again, despite the numerous times it has been explained to
you by many posters.
YOU ARE APPLYING THE WRONG MODEL TO THE PROBLEM.
Rooting around in seuence space by random search on a Uniform distribution
is inapplicable to most problems in probability and statistics. BEFORE you
can use this model, you have to DEMONSTRATE WHY IT APPLIES to the problem
at hand. AFTER you use this model, you have to DEMONSTRATE THAT IT FITS the
data observed. You've never done either of these things. If you had, your
model would be in the dustbin where it belongs.
Frank J
> On Nov 28, 11:11 am, Seanpit <sean...@gmail.com> wrote:> On Nov 27, 10:15 am, hersheyh <hershe...@yahoo.com> wrote:
>
> > > > Again, you confuse what is possible with what is likely . . .
>
> > > And you think it "likely" that there is only one possible "gap"
> > > involved in going from your "hypothetical unnamed undescribed"
> > > starting point to the final teleologic "system" you name?
>
> > You simply can't stop using the word "possible". You just did it
> > again here. Anything is possible. There are many "possible" gap
> > distances. Which of these possibilities is most likely without
> > knowing the answer ahead of time? That's the question here.
>
> SNIP
>
> Just face this simple fact. According to your own standards your
> alternatives don't even rate as "possible."
>
> You can run and pretend, but that doesn't change such a simple fact,
> does it?
>
> Just how bogus can you get. Deflection and obfuscation are all you
> have left. You know it and have known it for years. How long have
> you been running and pretending from your claim that you had an
> alternative to common descent that had evidence backing it up that was
> just as good as the scientific evidence that you didn't like?
If I thought I had an even slightly promising alternative to common
descent, the *first* if not *only* person that I'd try to persuade
would be Michael Behe. Since Behe does not have a prior commitment to
"naturalism," I could stick to "what happened, when and how" and not
let my opponent confuse the issue with whether or not a creator/
designer was involved.
Curiously, neither the old-style "scientific" creationists, nor "don't
ask, don't tell" IDers, nor hybrids like Sean, ever do that. I wonder
why? ;-)
Frank J
> On Nov 28, 12:11 pm, Seanpit <sean...@gmail.com> wrote:
>
> (snip)> Name a unique functional difference between humans and chimps that
> > isn't just quantitative but qualitative . . . Then, once you have
> > done this, show the minimum number of genetic differences needed to
> > produce this novel functional difference.
>
> (snip)
>
> I'm a little curious here . . .
>
> Humans and chimps are closer to each other, genetically, than many
> other species are which creationists consider to be the same "kind" --
> horses and donkeys, for instance, or cheetahs and jaguars.
>
> Why then do you consider it utterly absolutely completely impossible
> for humans to have "micro-evolved" their genetic differencesd with
> chimps, but NOT utterly absolutely completely impossible for members
> of other "kinds" to have "micro-evolved" their LARGER genetic
> differences with each other?
>
> If the genetic differences between jaguars and cheetahs can have
> evolved, then why do you insist that the SMALLER genetic differences
> between chimps and humans, can not have?
>
> Besides, of course, your religious opinion that humans are special and
> simply cannot be related through descent to any other animal, no
> matter what . . .
As you know, even Michael Behe and a few other *anti-evolutionists*
admitted that this is a bait-and-switch. Although for political
reasons they probably now wish they hadn't.
For the benefit of other readers, what I mean is that, even if they
are right that "RM+NS", "naturalism" etc. can't cause the required
changes, the simplest alternate explanation still maintains a
"biological continuum", which means that humans are still related to
other animals, plants, etc.
Most science-literate theists have no problem with being related to
other species, because if God gave us free will, we are not
constrained to act like them. Anti-evolutionists claim to believe in
free will, but can't bear the thought of being related to broccoli,
yet have no problem being much more closely related to people who fly
planes into buildings.
As I said to Ron, the fact that anti-evolutionists increasingly
refrain from challenging *each other* on these fundamental differences
(& others like the age of life, earth) suggests that those who do seem
to take their own ideas seriously (e.g AIG, RTB) are slowly going
extinct .
TomS
<c586eb45-2b46-44e0...@y18g2000yqn.googlegroups.com>, Frank J
stated..."
>
>On Nov 28, 12:50=A0pm, "'Rev Dr' Lenny Flank" <lfl...@yahoo.com> wrote:
>> On Nov 28, 12:11=A0pm, Seanpit <sean...@gmail.com> wrote:
>>
>> (snip)> Name a unique functional difference between humans and chimps tha=
>t
>> > isn't just quantitative but qualitative . . . =A0Then, once you have
>> > done this, show the minimum number of genetic differences needed to
>> > produce this novel functional difference.
>>
>> (snip)
>>
>> I'm a little curious here . . .
>>
>> Humans and chimps are closer to each other, genetically, than many
>> other species are which creationists consider to be the same "kind" --
>> horses and donkeys, for instance, or cheetahs and jaguars.
>>
>> Why then do you consider it utterly absolutely completely impossible
>> for humans to have "micro-evolved" their genetic differencesd with
>> chimps, but NOT utterly absolutely completely impossible for members
>> of other "kinds" to have "micro-evolved" their LARGER genetic
>> differences with each other?
>>
>> If the genetic differences between jaguars and cheetahs can have
>> evolved, then why do you insist that the SMALLER genetic differences
>> between chimps and humans, can not have?
>>
>> Besides, of course, your religious opinion that humans are special and
>> simply cannot be related through descent to any other animal, no
>
>As you know, even Michael Behe and a few other *anti-evolutionists*
>admitted that this is a bait-and-switch. Although for political
>reasons they probably now wish they hadn't.
>
>For the benefit of other readers, what I mean is that, even if they
>are right that "RM+NS", "naturalism" etc. can't cause the required
>changes, the simplest alternate explanation still maintains a
>"biological continuum", which means that humans are still related to
>other animals, plants, etc.
>
>Most science-literate theists have no problem with being related to
>other species, because if God gave us free will, we are not
>constrained to act like them. Anti-evolutionists claim to believe in
>free will, but can't bear the thought of being related to broccoli,
>yet have no problem being much more closely related to people who fly
>planes into buildings.
If, on the other hand, the reason that we are so much like
chimps and other apes is that some intelligent designer(s)
purposefully, deliberately, designed us that way, shouldn't
we consider that we ought to follow the intentions of our
designers, and act like apes?
>
>As I said to Ron, the fact that anti-evolutionists increasingly
>refrain from challenging *each other* on these fundamental differences
>(& others like the age of life, earth) suggests that those who do seem
>to take their own ideas seriously (e.g AIG, RTB) are slowly going
>extinct .
>
>>
>> =3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=
>=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D
>> Lenny Flank
>> "There are no loose threads in the web of life"
>>
>> Editor, Red and Black Publishershttp://www.RedandBlackPublishers.com
>
--
---Tom S.
"As scarce as truth is, the supply has always been in excess of the demand."
attributed to Josh Billings
Ron O
It is worse than that for Sean because he seems to have this evidence
thing and backing up your own notions out of whack with reality. If
Sean wants to contend that he has something Sean has to come up with
examples that we can't explain. I haven't heard of any "qualitiative"
rather than "quantitative" difference that exist between humans and
chimps. Intellectually, chimps are about equivalent to 4 year old
humans. We share all our tissues and organs. Heck, we have about the
same number of hair folicles on our bodies as a chimp. The only
differences in our brains seems to be the size of the different
sections. We seem to share all brain parts. Sean has to demonstrate
that his type of gap exists.
What probably gets to Sean is how his bogus 1000 aa argument breaks
down with closely related species like chimps and humans. Sean comes
face to face with one obvious fact. Any change in any gene, protein,
whatever, has to work within the whole. Whether some new change is
part of a large existing complex or the start of some future large
complex it has to work within what already exists. If it doesn't it
has to limp along and exist against selection to remove it, and most
likely it is lost. What we see are the changes that fit well enough
to make it. Sean can't cope with that fact. His whole 1000 aa bull
pucky is based on some stupid reality that doesn't exist. He comes
face to face with that reality with chimps and humans, and has to
demand that his opposition provide what he cannot. Sean has to
demonstrate that his type of gaps ever existed. He can't do that with
the human and chimp example.
Ron Okimoto
heekster
wrote:
You are exactly right.
When he gets backed into a corner like this, he usually switches to
his imbecilic SETI analogy. He gets backed into a corner there, and
switches back to the 1000 aa idiocy.
What is truly entertaining, is that he sees himself as some sort of
authority. An imbecility on the level of adman's benighted
bloviations.
No observations.
No data, just some half-baked statistical manipulations, and a
cheesecake pinup of Ellen G. White.
Vend
<snip>
> > Hint: The *real* historical process of Obama becoming president
> > involved a series of events, some of which were due to chance (such as
> > the Jack Ryann Senate candidacy imploding in a sex scandal), some of
> > which involved the character and qualifications of the candidate. The
> > probability of the last step (or gap) in the process was essentially 1
> > out of 2. There are ways of identifying evidence for the steps in the
> > historical process. None of them involve assuming that Obama became
> > president in a single step gap-crossing with a probability due to
> > division by the total number of legally possible candidates for
> > president.
>
> We are talking about a situation where the actual gap distance is not
> already known ahead of time Howard. We are talking about predicting
> the gap distance. What gap distance is likely?
Sean, it appears that you keep repeating the same error.
Biological evolution isn't a search algorithm that moves form one
target to another.
There is no concept of 'target' and therefore no concept of 'gap
distance between targets' in biological evolution.
(M)-adman
If a gene can "limp along and exist against selection to remove it" as you say, then that kinda
shoots evolution down to ZERO.
How can random mutations take place if a gene can limp along and exist against selection to
remove it?
What other genes have existed against selection to remove it? Is this resistance to selection
random? Is it planed for in the gnome we do not fully understand yet?
Another nail in the coffin of evolution.
--
It is all about the nails with:
^^^^^^^^^^^^^^^^^^^^^
·.¸Adman¸.·
^^^^^^^^^^^
'Rev Dr' Lenny Flank
(snicker) (giggle)
Not terribly bright, are you, Adman . . . . .
(snicker) (giggle)
hersheyh
>
> > > Again, you confuse what is possible with what is likely . . .
>
> > And you think it "likely" that there is only one possible "gap"
> > involved in going from your "hypothetical unnamed undescribed"
> > starting point to the final teleologic "system" you name?
>
> You simply can't stop using the word "possible". You just did it
> again here. Anything is possible. There are many "possible" gap
> distances.
Learn to read. *You* are assuming a single gap. I am saying that
there are many gaps, each one smallish. What mechanism is involved if
there is only a single gap? Thus the question is "What evidence do
you have to support your hypothesis of evolution involving a *single*
gap that is a function of the end size of the system?" Other than
assertion.
> Which of these possibilities is most likely without
> knowing the answer ahead of time? That's the question here.
Predicting what *will* evolve is not the question. Determining how
structures that actually exist *did* evolve is.
>
> You simply assume that the minimum possible gap distance is likely
> without actually doing any statistical analysis to support this
> assumption - nor have you presented any actual demonstration or direct
> observational evidence. All you really have are bald assertions and
> just-so stories. That's not science.
You are the one making bald assertions. You don't, apparently,
understand the basic form of your argument.
Your basic argument is "If NOT X, then Y." Specifically, it is that
"If system X with the property of being larger than 1000aa in size
cannot reasonably evolve by the mechanism I describe in the time
available, then 'intelligent design', for which I have no independent
evidence, is the only other *possible* mechanism by which this system
can occur." The usefulness of such an argument depends crucially on X
and Y being a true dichotomy with no *possible* alternatives to X.
First, this is an argument about the mechanism by which things that
*actually* did occur could have occurred. It is not an argument about
the probability that such an event could happen in the future. The
probability that a failed assassination attempt on Ronald Reagan would
be due to the infatuation of the would-be assassin with an actress
would have been essentially nil even a few hours before it happened.
A few seconds later, the probability would have been one.
http://en.wikipedia.org/wiki/Reagan_assassination_attempt
The probability that president-elect Obama will be assassinated before
(or during) the inauguration is clearly not zero, but it is not
calculable either. *If* it happens, then the probability of it
happening will be one. *If* it happens, we will be able to use
analysis of the evidence to ascribe methods, motives, and other
features of the crime. But we would not be able to predict the
probability of it happening again.
Second, your assumption that the mechanism you describe, to the extent
you do, in which there is a single functionless gap that is a function
of the size of the end system, is NOT the only possible mechanism by
which the event that *did* happen could have happened. I have already
pointed out that your mechanism, which is nothing but the "747 in a
tornado" straw man is NOT the only possible mechanism by which
observed features could have occurred. Specifically, I point out that
it is stupid (not ignorant, stupid) to imply that only a single gap
between functions was involved. That you fail to specify functional
starting point and end point and the evidence to support the existence
of such in cells (the very evidence that analysis of the structure and
sequence provides) is telling.
> > > It
> > > isn't enough to present what is possible Howard.
Actually that *is* all I have to do to demonstrate that your argument
is a *false* dichotomy. All I have to do is show that there is a
different mechanism (one involving multiple intermediate gaps being
crossed) that could, in principle, produce the result. That such a
process is much more probable and much more evidenced than the
mechanism you describe, which no one thinks is how evolution works, is
gravy.
> > > You have to actually
> > > show that what you're presenting is even remotely likely in a given
> > > span of time . . .
>
> > Yes. Which is exactly what the evidence shows for humans and
> > chimpanzees.
>
> Name a unique functional difference between humans and chimps that
> isn't just quantitative but qualitative . . . Then, once you have
> done this, show the minimum number of genetic differences needed to
> produce this novel functional difference.
You have a failure to communicate. I am saying that 1) there either
is no such difference you would call a "novel functional difference"
or 2) such differences, if present, were not due to crossing large
functionless gaps impossible for the known rates of selective change.
I would be happy with either alternative. That is, there is
sufficient evidence to claim that there is no difference between
humans and chimps that meet the large functionless gap requirements
you posit.
> The problem here, of course is that no one knows anything about such
> functional differences between humans and chimps - at least not
> adequately at this point. That is why you use this example all the
> time. You're conveniently hiding behind a lack of information.
I am pointing out that the existing evidence of the genomes of these
two organisms is adequate to say that one or the other of your
premises about the existence of "large functionless gaps impossible to
be crossed in real time" is wrong for these two species. Either there
are no such "system" differences or, if any are found that you are
willing to call novel, it did not involve crossing large functionless
gaps impossible for NS for change.
> Try
> dealing with examples that we know more about - like subcellular
> systems.
So where are the 'subcellular' novel large system of function that
spontaneously appeared in organisms with a common ancestor 5 million
years in the past? Beyond a certain time of divergence (or apparent
divergence if you don't like common descent as the explanation for the
pattern), it is more difficult to trace sequence homology.
> You're argument is not based on any form of statistical analysis
> whatsoever when it comes to known differences in levels of functional
> complexity.
What is the statistical probability that Obama will be assassinated on
Inauguration Day by a deranged black American? Before Reagan was
shot, what was the probability that a President would be shot by a
deranged white man with an obsession for Jodi Foster? What was the
probability after he was shot?
Ron O
We know of examples of this. You can go into any extant population
and find deleterious mutations segregating. Just look up any paper on
mutation selection balance. We have examples where gene knockouts
have been fixed in populations and those species have had to deal with
loss of the gene. The gene responsible for vitamin C defficiency in
humans and other primates down to Monkeys is due to the knock out of a
single gene. The common ancestor of monkeys including the lineage
that evolved into humans is descended from a population where this
gene knock out got fixed due to genetic drift or founder effects or
some combination of such factors. Scurvy is the result of not having
enough vitamin C in our diets due to this gene loss. Evolution
doesn't necessarily allow only good things to happen. If it did
extinction would not be as common as it is.
>
> How can random mutations take place if a gene can limp along and exist against selection to
> remove it?
Really, just look up mutation selection balance and learn something.
Populations can exist with quite a load of deleterious mutations. It
isn't just theory, we have done genetic analysis of populations like
flies and even population studies of humans to demonstrate it. What
do you think it means when they estimate that every human carries a
genetic load of around 2.5. This means that the average human has the
equivalent of 2.5 recessive lethals in their genomes.
This isn't all bad. There are plenty of examples of where a second
mutation can "fix" the detrimental effects of another mutation. Look
up papers on second site reversions. This increases the evolutionary
potential of any population since Sean's gaps of 2 or 3 mutations can
obviously be crossed under such conditions. Just as Sean why he went
from demanding examples of 3 mutation gaps to his 1000 aa bull pucky.
He did the calculations himself and figured out that 3 mutation gaps
aren't that much of a problem. So he had to go into gap inflation.
It went from 3 to 20 and then 40 fairly quickly and then he settled on
the 1000 aa junk.
>
> What other genes have existed against selection to remove it? Is this resistance to selection
> random? Is it planed for in the gnome we do not fully understand yet?
Seems to be pretty random. You can look into the data and try to find
any pattern that everyone else has missed.
>
> Another nail in the coffin of evolution.
Just something else you are going to have to ignore or refuse to
understand.
I think all those nails are just getting pounded into your head
instead of the coffin you think that you are building. Maybe you
should try to point the nail gun in the right direction. Applying the
pressure safety to your forehead is not recommended in the manual.
Ron Okimoto
> --
>
> It is all about the nails with:
> ^^^^^^^^^^^^^^^^^^^^^
> ·.¸Adman¸.·
> ^^^^^^^^^^^- Hide quoted text -
>
> - Show quoted text -
(M)-adman
No. Either natural selection works or it does not work. Because what other genes have existed
against selection to remove it? This would mean that natural selection does not work in all
cases therefore cannot be responsible for such wide spread evolution over millions of years
because genes are know to remain regardless of selection against it.
The selection process has broken down.
Ron O
Selection doesn't work on miracles. It has to work under natural
conditions within the system that selection is working in. Lots of
scientists have worked this stuff out for nearly a century. Selection
isn't immediate except for certain mutations like ones that are
dominant lethals. Dominant lethals are where just one mutant allele
is enough to affect the embryo enough to kill it. Most detrimental
mutations are recessive lethals. This just means that before
selection can act to remove the mutation you have to have a high
enough frequency of the mutation in the population for homozygotes to
form and be selected against. You can look at standard Mendelian
genetics and see that even when you mate two carriers with the same
mutation together only 1/4 of their progeny will be selected against.
1/2 of their progeny will be heterozygous carriers like the parents
and will not be selected against. It is all just genetics. If you
would look it up instead of coming up with your brain dead
pronoucements you would be much better off. Didn't I tell you to look
up mutation selection balance? This is just the state where the rate
of new mutation occurring is balanced by the number of mutations taken
out of the population by selection. This balance can result in more
or less detrimental and lethal alleles in the population depending on
factors like mating behaviour and number of progeny produced. Humans
have suffered a recent bottle neck and likely inbreeding due to small
bands and villages that was the human population before the last few
thousand years and we have a genetic load of 2.5, but there are
species that do not inbreed (they do not mate with relatives) and
maintain a genetic load of over 15. This is just the genetic load of
detrimental variation allowed and doesn't say anything about the
variation in the population that is neutral.
Humans are short on genetic variation compared to other species. We
think that this is due to a population bottle neck where the effective
population size of the human race may have dropped to around 1000
individuals within the last 100,000 years. Some posit more than one
bottleneck event. If you take any two humans you will find them
different in about 1 in 1000 base-pairs of their DNA. If you looked
at a group of around 30 distantly related humans you would find
differences more frequently that 1 in 300 base-pairs. There are three
billion base-pairs in a haploid human genome. If you took the entire
human population of over 7 billion people, everyone has 200 or more
new mutations that they have inherited from both of their parents.
Nearly every site in the human genome has been hit multiple times by
new mutations just in the extant population. About the only mutations
that you will not observe in the extant population are the dominant
lethals that are already dead.
Most species have about 5 times the genetic variation found in humans,
but some like Cheetahs have even less genetic variation. If you took
around 30 relatively unrelated domestic chickens you would likely find
genetic variants around 1 in every 30 base-pairs. Chickens have a
genetic load of around 6, so there isn't a linear relationship between
detrimental variation carried in a population and the total genetic
variation.
So populations have a boat load of genetic variation in them. You
can't counter that fact with inane blather, or deny that selection is
taking place when even you could go out and measure it if you took the
time to learn how to do it.
Ron Okimoto
'Rev Dr' Lenny Flank
like Ray, is fit only to be laughed at. Since the creationist
movement is dead as a mackerel anyway, they simply no longer matter.
Let them shriek all they want to. (shrug)
Woland
I am continually amazed at how dense and faithless you are.
(M)-adman
Well *Ron*. If it is "all just genetics" as you claim, then genetically speaking, there is no
need for selection to have such a high priority regarding evolution because if it cannot breed
and produce a fertile offspring then it is not genetically the same. Selection is only
'observed' to produce a sub-species such as the dog within their kind.
"Each After His kind". Exactly as the bible says.
Example: Dogs are after his own "kind" called "wolf"
It really is THAT simple.
--
It is all about the genetic truth with:
'Rev Dr' Lenny Flank
> Selection is only
> 'observed' to produce a sub-species such as the dog within their kind.
>
Why can't emmer grass breed with wheat, Adman.
(sound of crickets chirping)
(snicker) (giggle)
Ron O
> Ron O wrote:
> > On Nov 29, 12:45 pm, "\(M\)-adman" <g...@hotmail.ed> wrote:
> >> Ron O wrote:
> >>> On Nov 29, 9:45 am, "\(M\)-adman" <g...@hotmail.ed> wrote:
> >>>> Ron O wrote:
> >>>>> On Nov 28, 11:50 am, "'Rev Dr' Lenny Flank" <lfl...@yahoo.com>
> >>>>> wrote:
> >>>>>> On Nov 28, 12:11 pm, Seanpit <sean...@gmail.com> wrote:
>
SNIP:
Do you actually think before you write? What do you think the
genetics are? Do you think that the genetics is going to
independently produce an organism? Doesn't it have to work within the
environment? Doesn't it have to interact with the environment? What
do you think natural selection is? It is basically the interaction of
the environment with the organism, and this includes the organisms
genetics.
What is a kind? Look up ring species. How are you going to stop the
evolution from continuing?
>
> "Each After His kind". Exactly as the bible says.
>
> Example: Dogs are after his own "kind" called "wolf"
>
> It really is THAT simple.
The guys that wrote the Bible didn't understand genetics, selection,
genetic drift, mutation, recombination etc. Can you deny that? You
live in a world that does, so what is your excuse?
So what about all the genetic variation? Why get off on this kind
kick when you were such a basket case on the previous point? Two
wrongs don't make a right.
Ron Okimoto
Seanpit
> On Nov 29, 9:45 am, "\(M\)-adman" <g...@hotmail.ed> wrote:
>
>
>
> > Ron O wrote:
> > > On Nov 28, 11:50 am, "'Rev Dr' Lenny Flank" <lfl...@yahoo.com> wrote:
> > >> On Nov 28, 12:11 pm, Seanpit <sean...@gmail.com> wrote:
>
> > >> (snip)> Name a unique functional difference between humans and
> > >> chimps that
> > >>> isn't just quantitative but qualitative . . . Then, once you have
> > >>> done this, show the minimum number of genetic differences needed to
> > >>> produce this novel functional difference.
>
> > >> (snip)
>
> > >> I'm a little curious here . . .
>
> > >> Humans and chimps are closer to each other, genetically, than many
> > >> other species are which creationists consider to be the same "kind"
> > >> -- horses and donkeys, for instance, or cheetahs and jaguars.
We don't know enough about the genetics of humans and apes to be
definitive in this matter. That's the point. However, there are
clues that humans and apes do not have the same kind of gene pool of
options as, say, horses and donkeys or cheetahs and jaguars. The most
obvious difference is that humans and apes cannot produce viable
offspring. And yes, this has been tested.
Another difference is the cellular and structural differences of major
organ systems like the brain. It seems like these differences are not
so much based on significant differences in coding genes or protein
building-block products, but in differences in non-coding DNA that
manipulates the coding portions of the genomes. A significant number
of non-coding DNA sequences have been discovered and this number and
percentage is growing.
"For example, miRNAs recently have been implicated in synaptic
development and in memory formation. As the species specific miRNAs
described here are expressed in the brain, which is the most complex
tissue in the human body, with an estimated 10,000 different cell
types, these miRNAs could have a role in establishing or maintaining
cellular diversity and could thereby contribute to the differences in
human and chimpanzee brain ... function."
Eugene Berezikov, Fritz Thuemmler, Linda W van Laake, Ivanela Kondova,
Ronald Bontrop4, Edwin Cuppen & Ronald H A Plasterk, "Diversity of
microRNAs in human and chimpanzee brain", Nature Genetics, Vol 38 |
Number 12 | December 2006 pp. 1375-1377.
http://www.detectingdesign.com/earlyman.html#Key
> > >> Why then do you consider it utterly absolutely completely impossible
> > >> for humans to have "micro-evolved" their genetic differencesd with
> > >> chimps, but NOT utterly absolutely completely impossible for members
> > >> of other "kinds" to have "micro-evolved" their LARGER genetic
> > >> differences with each other?
I've repeatedly explained in this forum that I do not think there is
enough evidence to adequately exclude human-ape common ancestry on a
genetic basis at this point. If you would have read the rest of my
comments on this topic instead of snipping them, you would have
understood this in this particular thread as well.
> > >> If the genetic differences between jaguars and cheetahs can have
> > >> evolved, then why do you insist that the SMALLER genetic differences
> > >> between chimps and humans, can not have?
>
> > >> Besides, of course, your religious opinion that humans are special
> > >> and simply cannot be related through descent to any other animal, no
> > >> matter what . . .
I've never said that . . .
> > >> ================================================
> > >> Lenny Flank
> > >> "There are no loose threads in the web of life"
>
> > >> Editor, Red and Black Publishershttp://www.RedandBlackPublishers.com
>
> > > It is worse than that for Sean because he seems to have this evidence
> > > thing and backing up your own notions out of whack with reality. If
> > > Sean wants to contend that he has something Sean has to come up with
> > > examples that we can't explain. I haven't heard of any "qualitiative"
> > > rather than "quantitative" difference that exist between humans and
> > > chimps.
That's because no one knows enough about the genetics of either humans
or apes. We know that there probably are qualitative differences due
to the fact that humans and apes cannot produce viable offspring while
other species pairs, like donkeys and horses, can. Again, there are
hints of key qualitative genetic differences, especially now that we
are learning more about non-coding DNA. However, at this point, we
simply do not know enough about these differences to adequately
propose an overwhelming block to RM/NS.
> > > Intellectually, chimps are about equivalent to 4 year old
> > > humans. We share all our tissues and organs. Heck, we have about the
> > > same number of hair follicles on our bodies as a chimp. The only
> > > differences in our brains seems to be the size of the different
> > > sections. We seem to share all brain parts. Sean has to demonstrate
> > > that his type of gap exists.
We do not share certain features of cellular structure and
organization within the brain - for example. Again, such differences
are understood well enough at this point to say anything definitive.
We know far more about less complex systems, like subcellular systems,
that do show very clear limitations to the mechanism of RM/NS.
> > > What probably gets to Sean is how his bogus 1000 aa argument breaks
> > > down with closely related species like chimps and humans. Sean comes
> > > face to face with one obvious fact. Any change in any gene, protein,
> > > whatever, has to work within the whole. Whether some new change is
> > > part of a large existing complex or the start of some future large
> > > complex it has to work within what already exists.
That's right . . .
> > > If it doesn't it
> > > has to limp along and exist against selection to remove it, and most
> > > likely it is lost.
Right again . . .
> > > What we see are the changes that fit well enough
> > > to make it. Sean can't cope with that fact.
Where have I said anything else but this? This is a big part of my
own position on this topic.
> > > His whole 1000 aa bull
> > > pucky is based on some stupid reality that doesn't exist.
There are lots of known systems that require far more than 1000 fsaar
at minimum to work. Tell me, how can you make a flagellar system with
less than 1000 fsaar? Think you can do it? How?
> > > He comes
> > > face to face with that reality with chimps and humans, and has to
> > > demand that his opposition provide what he cannot. Sean has to
> > > demonstrate that his type of gaps ever existed. He can't do that with
> > > the human and chimp example.
You guys hide behind creatures and systems which are largely unknown
instead of even trying to deal with those systems that are much better
known and understood. What a crock . . .
> > > Ron Okimoto
>
> > If a gene can "limp along and exist against
> > selection to remove it" as you say, then that kinda
> > shoots evolution down to ZERO.
>
> We know of examples of this. You can go into any extant population
> and find deleterious mutations segregating. Just look up any paper on
> mutation selection balance. We have examples where gene knockouts
> have been fixed in populations and those species have had to deal with
> loss of the gene. The gene responsible for vitamin C defficiency in
> humans and other primates down to Monkeys is due to the knock out of a
> single gene. The common ancestor of monkeys including the lineage
> that evolved into humans is descended from a population where this
> gene knock out got fixed due to genetic drift or founder effects or
> some combination of such factors. Scurvy is the result of not having
> enough vitamin C in our diets due to this gene loss. Evolution
> doesn't necessarily allow only good things to happen. If it did
> extinction would not be as common as it is.
That's right . . . In fact, "devolution" or significant ongoing
genetic losses are a real problem to the overall ToE.
http://www.detectingdesign.com/dnamutationrates.html#Detrimental
> > How can random mutations take
> > place if a gene can limp along and exist against selection to
> > remove it?
>
> Really, just look up mutation selection balance and learn something.
> Populations can exist with quite a load of deleterious mutations. It
> isn't just theory, we have done genetic analysis of populations like
> flies and even population studies of humans to demonstrate it. What
> do you think it means when they estimate that every human carries a
> genetic load of around 2.5. This means that the average human has the
> equivalent of 2.5 recessive lethals in their genomes.
It is actually worse than that when one considers all the non-lethal
deleterious mutations that are present in the genomes of humans and
all other slowing reproducing creatures.
> This isn't all bad. There are plenty of examples of where a second
> mutation can "fix" the detrimental effects of another mutation. Look
> up papers on second site reversions.
That's right. It is fairly easy to step back onto a beneficial island
which a population has taken a very short step off of in the past.
> This increases the evolutionary
> potential of any population since Sean's gaps of 2 or 3 mutations can
> obviously be crossed under such conditions.
It is one thing to step off of an island that one was already on in
the past. It is quite another think to find a novel beneficial island
to begin with.
> Just ask Sean why he went
> from demanding examples of 3 mutation gaps to his 1000 aa bull pucky.
> He did the calculations himself and figured out that 3 mutation gaps
> aren't that much of a problem. So he had to go into gap inflation.
> It went from 3 to 20 and then 40 fairly quickly and then he settled on
> the 1000 aa junk.
It is just amazing to me that you still do not understand, despite my
explaining it to you dozens and dozens of times, that the structural
threshold of 1000 fsaar is NOT a measure of the gap distance. It is
the measure of a level of functional complexity. Functional
complexity is not the same thing as the likely gap distance. The
likely minimum gap distance is always smaller than the level of
functional complexity - always. The smallest gap distance between an
existing starting point and a potential target at the 1000 fsaar level
is likely to be only a few dozen mutational changes wide.
I've been explaining this for over ten years now. There's been no
"inflation" here. That's just your strawman misrepresentation.
< snip >
Sean Pitman
www.DetectingDesign.com
Seanpit
> On Nov 28, 11:11 am, Seanpit <sean...@gmail.com> wrote:> On Nov 27, 10:15 am, hersheyh <hershe...@yahoo.com> wrote:
>
>
> > > And you think it "likely" that there is only onepossible"gap"
> > > involved in going from your "hypothetical unnamed undescribed"
> > > starting point to the final teleologic "system" you name?
>
> > You simply can't stop using the word "possible". You just did it
> > distances. Which of these possibilities is mostlikelywithout
> > knowing the answer ahead of time? That's the question here.
>
> SNIP
>
> Just face this simple fact. According to your own standards your
> alternatives don't even rate as "possible."
>
> You can run and pretend, but that doesn't change such a simple fact,
> does it?
>
> Just how bogus can you get. Deflection and obfuscation are all you
> have left. You know it and have known it for years. How long have
> you been running and pretending from your claim that you had an
> alternative to common descent that had evidence backing it up that was
> just as good as the scientific evidence that you didn't like? It must
> be going on 8 years now. 8 years of denial, and dishonest bogus
> behaviour. Where is that intelligent design science that you would
> have taught to school kids? Probably going into 6 years on running
> from that claim. What does that mean for the title of your web site
> when you know for a fact that the design science never existed? No
> alternative worth mentioning, no science worth presenting, no argument
> worth jack.
>
> Running and pretending is just a bogus form of argument. You know it,
> so why is it acceptable for you to do it?
Just answer the simple question Ron - what are the odds that the
proposed evolutionary steppingstones is a system known as well as the
flagellar system are likely to have existed in real life? Do you have
any idea? - any idea at all? - based on real statistical analysis?
It is your position that the mechanism of the ToE is based on real
scientific understanding of its creative powers. Yet, where is the
statistical basis of this understanding? Where is the actual
"science"?
> Ron Okimoto
Sean Pitman
www.DetectingDesign.com
Seanpit
>
> > "Each After His kind". Exactly as the bible says.
>
> > Example: Dogs are after his own "kind" called "wolf"
>
> > It really is THAT simple.
>
> The guys that wrote the Bible didn't understand genetics, selection,
> genetic drift, mutation, recombination etc. Can you deny that? You
> live in a world that does, so what is your excuse?
>
> So what about all the genetic variation? Why get off on this kind
> kick when you were such a basket case on the previous point? Two
> wrongs don't make a right.
The basis point is that the term "species" is very subjective. It
doesn't really consider the functional similarities and differences
between different kinds of creatures. It is largely based on very
subjective interpretations of morphologic differences of creatures
that can in fact interbreed and produce viable and sometimes fertile
offspring. In fact, on occasion, different "species" have been
defined only to find out later that they were part of the same
breeding pool or even part of the same organism (i.e., like different
parts of the same plant).
Seanpit
wrote:
> Seanpit <sean...@gmail.com> wrote in news:67075dc7-0ffd-4739-9efd-
> 42ff8b15e...@g17g2000prg.googlegroups.com:
>
> > On Nov 27, 10:15 am, hersheyh <hershe...@yahoo.com> wrote:
>
> [big snip for brevity]
>
> Sean, that whooshing sound over your head is the same point you have missed
> over and over again, despite the numerous times it has been explained to
> you by many posters.
>
> YOU ARE APPLYING THE WRONG MODEL TO THE PROBLEM.
>
> is inapplicable to most problems in probability and statistics. BEFORE you
> can use this model, you have to DEMONSTRATE WHY IT APPLIES to the problem
> at hand. AFTER you use this model, you have to DEMONSTRATE THAT IT FITS the
> data observed. You've never done either of these things. If you had, your
> model would be in the dustbin where it belongs.
Rather, you have to explain your own model of sequence space and why
it is likely to be true. No one in the scientific community has done
this. It is simply assumed that RM/NS did the job without actually
subjecting this idea to any real statistically supported model of
sequence space. No mathematical odds analysis is performed. There's
simply nothing but assumptions when it comes to the proposed mechanism
of RM/NS.
Beyond this, my model of sequence space does fit the data. My model
suggests that non-beneficial sequences increase at an exponential rate
compared with potentially beneficial sequences as overall sequence
space increases in size. My model also suggests that those areas
within sequence space that have a clustering of potentially beneficial
targets will not be so clustered at higher and higher levels of
functional complexity. This in turn will result in an exponential
stalling out effect of RM/NS when it comes to finding novel island
targets within sequence space.
This model is exactly what is observed in real life. That's a simple
fact for anyone who cares to look. This is exactly why evolution
happens, quite commonly, below the 1000 fsaar threshold, but not at
all above it in a given span of observable time. There simply is no
comparable evolutionary model of sequence space - none whatsoever.
Sean Pitman
www.DetectingDesign.com
Seanpit
> On 28 Nov, 18:11, Seanpit <sean...@gmail.com> wrote:
> <snip>
>
> > > Hint: The *real* historical process of Obama becoming president
> > > involved a series of events, some of which were due to chance (such as
> > > the Jack Ryann Senate candidacy imploding in a sex scandal), some of
> > > which involved the character and qualifications of the candidate. The
> > > probability of the last step (or gap) in the process was essentially 1
> > > out of 2. There are ways of identifying evidence for the steps in the
> > > historical process. None of them involve assuming that Obama became
> > > president in a single step gap-crossing with a probability due to
> > > president.
>
> > We are talking about a situation where the actual gap distance is not
> > already known ahead of time Howard. We are talking about predicting
> > the gap distance. What gap distance islikely?
>
> Sean, it appears that you keep repeating the same error.
> Biological evolution isn't a search algorithm that moves form one
> target to another. There is no concept of 'target'
> and therefore no concept of 'gap
> distance between targets' in biological evolution.
LOL - What do you think the concept of RM/NS is based on? What does
"natural selection" select? Obviously, NS selects those random
mutations that produce new genetic sequences that are more
functionally beneficial compared to what came before. There are many
such sequences that exist in the potential of undiscovered sequence
space. These sequences are potential "targets" for the evolutionary
mechanism. the only problem is that non-target sequences vastly
outnumber the potential targets within sequence space and this ratio
only gets exponentially worse and worse with each increase in the
level of functional complexity.
Sean Pitman
www.DetectingDesign.com
Seanpit
> On Nov 28, 12:11 pm, Seanpit <sean...@gmail.com> wrote:
>
> > On Nov 27, 10:15 am, hersheyh <hershe...@yahoo.com> wrote:
>
> > > > Again, you confuse what is possible with what is likely . . .
>
> > > And you think it "likely" that there is only one possible "gap"
> > > involved in going from your "hypothetical unnamed undescribed"
> > > starting point to the final teleologic "system" you name?
>
> > You simply can't stop using the word "possible". You just did it
> > again here. Anything is possible. There are many "possible" gap
> > distances.
>
> Learn to read. *You* are assuming a single gap. I am saying that
> there are many gaps, each one smallish. What mechanism is involved if
> there is only a single gap? Thus the question is "What evidence do
> you have to support your hypothesis of evolution involving a *single*
> gap that is a function of the end size of the system?" Other than
> assertion.
There isn't a single gap. There are many many gaps. However, the
odds of success are based on the smallest gap distance that exists
between the starting points and the closest beneficial target in
sequence space. There are many potentially beneficial targets of
course - and therefore many gap distances. However, it is the
smallest gap distance that is statistically important here.
You keep asserting, without any odds analysis whatsoever, that this
smallest gap distance is likely to be the minimum possible gap
distance of one. Your argument is that because this is possible, it
is likely. That's ludicrous Howard! That's not a scientific argument
at all!
> > Which of these possibilities is most likely without
> > knowing the answer ahead of time? That's the question here.
>
> Predicting what *will* evolve is not the question. Determining how
> structures that actually exist *did* evolve is.
You can't directly know how structures that actually exist did
evolve. You can only predict how they *likely* evolved. Scientific
predictions require odds analysis - something you do you provide.
Therefore, your predictions of how something likely evolved are not
scientific. They're just-so stories at best.
> > You simply assume that the minimum possible gap distance is likely
> > without actually doing any statistical analysis to support this
> > assumption - nor have you presented any actual demonstration or direct
> > observational evidence. All you really have are bald assertions and
> > just-so stories. That's not science.
>
> You are the one making bald assertions. You don't, apparently,
> understand the basic form of your argument.
>
> Your basic argument is "If NOT X, then Y." Specifically, it is that
> "If system X with the property of being larger than 1000aa in size
> cannot reasonably evolve by the mechanism I describe in the time
> available, then 'intelligent design', for which I have no independent
> evidence, is the only other *possible* mechanism by which this system
> can occur." The usefulness of such an argument depends crucially on X
> and Y being a true dichotomy with no *possible* alternatives to X.
Like SETI, it depends upon a lack of "known" alternatives to X - not
the complex exclusion of all possibilities with 100% assurance.
That's not a requirement of science Howard. In fact, if this degree
of certainty were ever possible, science would no longer be needed.
It is because there is a lack of complete knowledge that science is
useful here.
> First, this is an argument about the mechanism by which things that
> *actually* did occur could have occurred.
Again with your argument that what is possible is therefore
likely . . . Please stop using this nonsense argument.
> It is not an argument about
> the probability that such an event could happen in the future.
That's right. It is an argument about the probability of something
happening in the past. It is the same difference. If the odds
against it happening in the future are X, these same odds likely hold
for analyzes of the past as well. The only way you can overcome these
odds analyzes is to show that there is some sort of direct observation
where odds are no longer needed. That would, of course, remove the
need for science as well.
> The
> probability that a failed assassination attempt on Ronald Reagan would
> be due to the infatuation of the would-be assassin with an actress
> would have been essentially nil even a few hours before it happened.
> A few seconds later, the probability would have been one.
This isn't probability or science Howard. This is direct knowledge -
something you don't have for the mechanism of the ToE. What you are
left with is real science Howard - and that is based on real odds
analysis.
> http://en.wikipedia.org/wiki/Reagan_assassination_attempt
>
> The probability that president-elect Obama will be assassinated before
> (or during) the inauguration is clearly not zero, but it is not
> calculable either. *If* it happens, then the probability of it
> happening will be one. *If* it happens, we will be able to use
> analysis of the evidence to ascribe methods, motives, and other
> features of the crime. But we would not be able to predict the
> probability of it happening again.
The probability of finding novel targets within sequence space can be
roughly determined. You don't have to directly observe it to predict
when it is likely to happen with at least some useful level of
predictive value. You are trying to compare apples and oranges
here.
> Second, your assumption that the mechanism you describe, to the extent
> you do, in which there is a single functionless gap that is a function
> of the size of the end system, is NOT the only possible mechanism by
> which the event that *did* happen could have happened.
Of course it isn't the only possible scenario. Again, you are stuck
on this idea that just because there are other possibilities that the
one most favorable to your position is therefore "likely". That's
nonsense.
> I have already
> pointed out that your mechanism, which is nothing but the "747 in a
> tornado" straw man is NOT the only possible mechanism by which
> observed features could have occurred.
We are talking about what is likely here, not just what is
possible . . .
And yes, purely random mutations do have to cross the gap before the
guiding force of NS can come into play. In a sense, this is likely a
mini random tornado-type action finding something useful within a junk-
yard gap where potential targets have an unknown location.
> Specifically, I point out that
> it is stupid (not ignorant, stupid) to imply that only a single gap
> between functions was involved. That you fail to specify functional
> starting point and end point and the evidence to support the existence
> of such in cells (the very evidence that analysis of the structure and
> sequence provides) is telling.
If it was possible to specify both starting and ending points at the
same time, you wouldn't need any odds analysis here - and therefore
you wouldn't need science. What don't you understand about this
concept Howard? This isn't that hard. You don't know one or the
other with certainty here. You have to predict the likelihood of one
based on the other and knowledge of the ratio and distribution of
sequence space.
> > > > It
> > > > isn't enough to present what is possible Howard.
>
> Actually that *is* all I have to do to demonstrate that your argument
> is a *false* dichotomy.
LOL - That's not science. It's like arguing that it is possible to
win the CA Lottery 10 times in a row . . . therefore it's likely?
>All I have to do is show that there is a
> different mechanism (one involving multiple intermediate gaps being
> crossed) that could, in principle, produce the result.
This is a just-so story that could always be proposed without any need
for odds analysis at all. It is possible - absolutely! But, is such
a story likely? That's the real question here. You have no idea. It
is very easy to simply dream up such stories. It is quite another
thing to back them up with real science.
> That such a
> process is much more probable and much more evidenced than the
> mechanism you describe, which no one thinks is how evolution works, is
> gravy.
LOL - Again, you use words like "probable" without using any odds
analysis whatsoever - amazing! What is the actual probability
Howard? Have any real numbers to back up your baldly asserted just-so
stories? Any real science?
< snip rest >
Sean Pitman
www.DetectingDesign.com
hersheyh
What evidence do you have that functional and non-functional sequences
are randomly distributed in total sequence space? And how can you
define "function" in the absence of an organism and environment in
which to function? From my knowledge of genetics (and yours too) it
is clear that a single point mutational event can eliminate the
current function of gene and reversion of point mutations can usually
also occur (deletions do not revert). Thus, if you cluster sequences
on the basis of similarity, sequences that have a specified function
and those that don't will be intermeshed and in intimate contact.
Moreover, that a particular sequence lacks the *named function*
doesn't mean it lacks all useful functionality. I don't see *real*
sequence space dividing neatly into functionless sequences and
sequences that have a specific named function. Can you elaborate on
how your "total sequence space" is arranged wrt sequence and
function? Do all three sequences that can perform the function of
cellulase map together? Do both of the rotary flagella map together
by function? Or do they map together by sequence? Or structure? Or
what? And what is the starting point for your generating "the" gap
size? Curious minds want to know.
You apparently have a clear vision of "total sequence space" and how
it is arranged wrt sequence and/or function and/or structure. Perhaps
you would like to tell us your vision rather than have us continue to
claim that you are proposing the "747 in a tornado" straw man version
of evolution?
Ron O
When are you going to stop running and pretending? Why try some
dishonest deflection ploy to side track the issues that you know that
you have to address, but can't?
Where is that alternative to common descent that you claimed to have
and the evidence for it that was just as good as the evidence you
claim that real science doesn't have? What good is your above
dishonest deflection and misdirection ploy above when you don't have
jack?
>
> It is your position that the mechanism of the ToE is based on real
> scientific understanding of its creative powers. Yet, where is the
> statistical basis of this understanding? Where is the actual
> "science"?
Where is that science of intelligent design that you were going to
teach to school kids. Why haven't you changed the name of your web
page when you know for a fact that intelligent design was just a bogus
creationist scam with no science to back it up? Why are the same
dishonest perps that ran the teach ID scam running a dishonest bait
and switch scam on all their supporters if they really had any
intelligent design junk worth teaching. You even know that the switch
scam doesn't even mention that intelligent design ever existed. How
bogus can you get?
Why is dishonesty all you have? Why employ misdirection when you
could be making good on the claims that you know that you absolutely
require in order to have any type of valid argument. No science, no
alternative, no scientific argument.
Ron Okimoto
>
> > Ron Okimoto
>
> Sean Pitmanwww.DetectingDesign.com- Hide quoted text -
Ron O
You know why the term is subjective. It is because life is evolving.
There are all intermediate shades of gray when it comes to species
because there are all kinds of populations in various degrees of
speciation and differentiation. How does your alternative explain the
current facts that have to go into defining known species? It doesn't
does it? If everything was specially created why is there a continuum
of variation in the differences between species?
Where is that alternative to common descent and the evidence to back
it up that was just as good as the real scientific evidence that you
don't think is good enough? Where is that science of intelligent
design that you claimed to have to teach to school kids. No
alternative, no science just obfuscation and dishonest and bogus smoke
like this species bull pucky above. Why blow smoke if you really have
an argument? Why blow smoke about a subject when you don't have a
good explanation for it and the explanation that we have works? How
do you explain the variation that has to be incorporated in any
species definition? There isn't another explanation as good as what
we already have, is there?
Seanpit
> > flagellar system are likely to have existed in real life? Do you have
> > any idea? - any idea at all? - based on real statistical analysis?
>
> When are you going to stop running and pretending? Why try some
> dishonest deflection ploy to side track the issues that you know that
> you have to address, but can't?
>
> Where is that alternative to common descent that you claimed to have
> and the evidence for it that was just as good as the evidence you
> claim that real science doesn't have? What good is your above
> dishonest deflection and misdirection ploy above when you don't have
> jack?
I'll take that as a no - you have no idea as to the likelihood of your
proposed mechanism to do the job you claim it did. Where's the
science Ron? Who's running from a request to demonstrate a real
scientific basis for what is supposed to be a well-established
scientific theory?
> > It is your position that the mechanism of the ToE is based on real
> > scientific understanding of its creative powers. Yet, where is the
> > statistical basis of this understanding? Where is the actual
> > "science"?
>
> Where is that science of intelligent design that you were going to
> teach to school kids. Why haven't you changed the name of your web
> page when you know for a fact that intelligent design was just a bogus
> creationist scam with no science to back it up? Why are the same
> dishonest perps that ran the teach ID scam running a dishonest bait
> and switch scam on all their supporters if they really had any
> intelligent design junk worth teaching. You even know that the switch
> scam doesn't even mention that intelligent design ever existed. How
> bogus can you get?
>
> Why is dishonesty all you have? Why employ misdirection when you
> could be making good on the claims that you know that you absolutely
> require in order to have any type of valid argument. No science, no
> alternative, no scientific argument.
All I've done is asked you a simple question. I've asked for at least
a rough basis in real statistical analysis for your theory. Is the
very best you have in response a list of non-sense pejoratives? Why
not simply answer a very simple question? I'm sure others in this
forum, besides me, would love to hear the answer . . .
TomS
<59817049-4996-430f...@d23g2000yqc.googlegroups.com>, hersheyh
stated..."
>
>On Nov 30, 11:17=A0am, Seanpit <sean...@gmail.com> wrote:
>> On Nov 29, 7:19=A0am, Vend <ven...@virgilio.it> wrote:
>>
>>
>>
>> > On 28 Nov, 18:11, Seanpit <sean...@gmail.com> wrote:
>> > <snip>
>>
>> > > > Hint: The *real* historical process of Obama becoming president
> as
>> > > > the Jack Ryann Senate candidacy imploding in a sex scandal), some o=
>f
>> > > > which involved the character and qualifications of the candidate. =
>=A0The
>> > > > probability of the last step (or gap) in the process was essentiall=
>y 1
>> > > > out of 2. =A0There are ways of identifying evidence for the steps i=
>n the
>> > > > historical process. =A0None of them involve assuming that Obama bec=
>ame
>> > > > president in a single step gap-crossing with a probability due to
>> > > > division by the total number of legallypossiblecandidates for
>> > > > president.
>>
>> > > We are talking about a situation where the actual gap distance is not
>g
>> > > the gap distance. =A0What gap distance islikely?
>>
>> > Sean, it appears that you keep repeating the same error.
>> > Biological evolution isn't a search algorithm that moves form one
>> > target to another. There is no concept of 'target'
>> > and therefore no concept of 'gap
>> > distance between targets' in biological evolution.
>>
>> "natural selection" select? =A0Obviously, NS selects those random
>> mutations that produce new genetic sequences that are more
>> such sequences that exist in the potential of undiscovered sequence
>> mechanism. =A0the only problem is that non-target sequences vastly
>> outnumber the potential targets within sequence space and this ratio
>> only gets exponentially worse and worse with each increase in the
>> level of functional complexity.
>>
>> Sean Pitmanwww.DetectingDesign.com
>
>What evidence do you have that functional and non-functional sequences
>are randomly distributed in total sequence space?
Excuse me. Do you mean something like "uniformly distributed"?
That is to say, are you questioning what are the the proper
statistics to calculate the probabilities? It appears that the
probability as calculated by the anti-evolutionists assumes a
certain distribution, something like this: A certain convention
for describing the structure of molecules corresponds one-for-
one with equally likely events. It is not obvious that that
assignment is correct - some molecular structures may be more
or less likely than others. And I gather that you are asking
for a reason to accept this "uniform distribution". Am I
correct?
Seanpit
>
> > > Sean, it appears that you keep repeating the same error.
> > > Biological evolution isn't a search algorithm that moves form one
> > > target to another. There is no concept of 'target'
> > > and therefore no concept of 'gap
> > > distance between targets' in biological evolution.
>
> > LOL - What do you think the concept of RM/NS is based on? What does
> > "natural selection" select? Obviously, NS selects those random
> > mutations that produce new genetic sequences that are more
> > functionally beneficial compared to what came before. There are many
> > such sequences that exist in the potential of undiscovered sequence
> > space. These sequences are potential "targets" for the evolutionary
> > mechanism. the only problem is that non-target sequences vastly
> > outnumber the potential targets within sequence space and this ratio
> > only gets exponentially worse and worse with each increase in the
> > level of functional complexity.
>
> > Sean Pitmanwww.DetectingDesign.com
>
> What evidence do you have that functional and non-functional sequences
> are randomly distributed in total sequence space?
There is a loose clustering effect, certainly, but this clustering
effect gets less and less clustered with each increase in the size and
specificity requirements of sequence space.
Where is your evidence that there is no change in the clustering of
targets within sequence spaces of different sizes?
> And how can you
> define "function" in the absence of an organism and environment in
> which to function?
I don't defined a beneficial function in the absence of an organism or
the environment. That's what makes a functional system "beneficial".
> From my knowledge of genetics (and yours too) it
> is clear that a single point mutational event can eliminate the
> current function of gene and reversion of point mutations can usually
> also occur (deletions do not revert).
Absolutely. Deletions do not usually, but can, at least
theoretically, revert. The reason why they almost never do revert is,
again, based on the gap problem. Multicharacter losses are much
harder to replace via random mutations than single character losses -
statistically.
> Thus, if you cluster sequences
> on the basis of similarity, sequences that have a specified function
> and those that don't will be intermeshed and in intimate contact.
Sequences that require greater specificity are much more widely spaced
in sequence space than those of similar size that require much less
specificity. Therefore, finding a target with lower specificity will
be far easier than finding one with higher specificity. Getting from
a starting point with lower specificity to a target with higher
specificity is not enhanced just because the edges of the lower-
specificity island overlap the edges of the higher specificity
target. Why not? Because, finding the target is still based on
searching randomly within a very large sequence space of the lower-
specificity target. There is no improvement of the odds here.
> Moreover, that a particular sequence lacks the *named function*
> doesn't mean it lacks all useful functionality.
Nothing is absolute here. There could be some unknown useful function
to an intermediate sequence. All things are possible. However, not
all that is possible is likely. That's what you have to consider
here.
> I don't see *real*
> sequence space dividing neatly into functionless sequences and
> sequences that have a specific named function. Can you elaborate on
> how your "total sequence space" is arranged wrt sequence and
> function? Do all three sequences that can perform the function of
> cellulase map together?
No. There are many completely different non-clustered islands within
sequence space that could produce a particular type of function - like
cellulase or citrase or lactase or flagellar motility. It is just
that all islands, beyond the 1000 fsaar threshold are widely separated
from each other.
> Do both of the rotary flagella map together
> by function? Or do they map together by sequence? Or structure? Or
> what? And what is the starting point for your generating "the" gap
> size? Curious minds want to know.
We are only talking about sequence/structure space here and those
sequences/structures that could produce a selectively beneficial
function if found. Many completely different sequences could produce
the same type of function. That has nothing to do with the fact that
the ratio of these potential targets vs. non-target sequences does in
fact decline, exponentially, with increasing size and specificity
requirements of overall sequence space.
> You apparently have a clear vision of "total sequence space" and how
> it is arranged wrt sequence and/or function and/or structure. Perhaps
> you would like to tell us your vision rather than have us continue to
> claim that you are proposing the "747 in a tornado" straw man version
> of evolution?
I've already told you. You're the one building non-sense strawman
misrepresentations that you know do not actually represent my
position. You are also the one who will not, to save your life,
present any statistical view of sequence space yourself. All you
present are your just-so stories of what could possibly happen,
without actually considering the odds of these various possibilities
of yours being remotely likely . . .
Sean Pitman
www.DetectingDesign.com
Ron O
> On Nov 29, 10:16 am, Ron O <rokim...@cox.net> wrote:
>
> > On Nov 29, 9:45 am, "\(M\)-adman" <g...@hotmail.ed> wrote:
>
> > > Ron O wrote:
> > > > On Nov 28, 11:50 am, "'Rev Dr' Lenny Flank" <lfl...@yahoo.com> wrote:
> > > >> On Nov 28, 12:11 pm, Seanpit <sean...@gmail.com> wrote:
>
> > > >> (snip)> Name a unique functional difference between humans and
> > > >> chimps that
> > > >>> isn't just quantitative but qualitative . . . Then, once you have
> > > >>> done this, show the minimum number of genetic differences needed to
> > > >>> produce this novel functional difference.
>
> > > >> (snip)
>
> > > >> I'm a little curious here . . .
>
> > > >> Humans and chimps are closer to each other, genetically, than many
> > > >> other species are which creationists consider to be the same "kind"
> > > >> -- horses and donkeys, for instance, or cheetahs and jaguars.
>
> We don't know enough about the genetics of humans and apes to be
> definitive in this matter. That's the point. However, there are
> clues that humans and apes do not have the same kind of gene pool of
> options as, say, horses and donkeys or cheetahs and jaguars. The most
> obvious difference is that humans and apes cannot produce viable
> offspring. And yes, this has been tested.
I don't think that I wrote what you are responding to.
So what? There are probably more closely related species than chimps
and humans that can't produce viable offspring. Horses and Donkeys
are probably less related genetically than humans and chimps. So your
point is that you have no point. There seems to be a wide range of
species in various degrees of being different. I wonder how that
could happen....
>
> Another difference is the cellular and structural differences of major
> organ systems like the brain. It seems like these differences are not
> so much based on significant differences in coding genes or protein
> building-block products, but in differences in non-coding DNA that
> manipulates the coding portions of the genomes. A significant number
> of non-coding DNA sequences have been discovered and this number and
> percentage is growing.
Too bad for you that there don't seem to be any major differences
between chimps and humans in this regard that relate to the brain or
just about anything else. There has to be a punch line somewhere.
Where do you start explaining why science has to solve your made up
problems for you? Just because you can't come up with what you wanted
someone else to justify doesn't mean that rambling around and blowing
smoke makes everything better.
>
> "For example, miRNAs recently have been implicated in synaptic
> development and in memory formation. As the species specific miRNAs
> described here are expressed in the brain, which is the most complex
> tissue in the human body, with an estimated 10,000 different cell
> types, these miRNAs could have a role in establishing or maintaining
> cellular diversity and could thereby contribute to the differences in
> human and chimpanzee brain ... function."
So how does this solve your problem? It is your problem. You make
the contention, you have to demonstrate that there is something that
we have to explain.
>
> Eugene Berezikov, Fritz Thuemmler, Linda W van Laake, Ivanela Kondova,
> Ronald Bontrop4, Edwin Cuppen & Ronald H A Plasterk, "Diversity of
> microRNAs in human and chimpanzee brain", Nature Genetics, Vol 38 |
> Number 12 | December 2006 pp. 1375-1377.
>
> http://www.detectingdesign.com/earlyman.html#Key
>
> > > >> Why then do you consider it utterly absolutely completely impossible
> > > >> for humans to have "micro-evolved" their genetic differencesd with
> > > >> chimps, but NOT utterly absolutely completely impossible for members
> > > >> of other "kinds" to have "micro-evolved" their LARGER genetic
> > > >> differences with each other?
>
> I've repeatedly explained in this forum that I do not think there is
> enough evidence to adequately exclude human-ape common ancestry on a
> genetic basis at this point. If you would have read the rest of my
> comments on this topic instead of snipping them, you would have
> understood this in this particular thread as well.
I think that you should go up the thread and answer the specific
posters because I did not write this what you are responding to.
More smoke. Smoking is bad for your health. Your type of smoking is
bad for your mental health.
Can't do what you need to do so you are willing to just blow smoke.
>
> > > > Intellectually, chimps are about equivalent to 4 year old
> > > > humans. We share all our tissues and organs. Heck, we have about the
> > > > same number of hair follicles on our bodies as a chimp. The only
> > > > differences in our brains seems to be the size of the different
> > > > sections. We seem to share all brain parts. Sean has to demonstrate
> > > > that his type of gap exists.
>
> We do not share certain features of cellular structure and
> organization within the brain - for example. Again, such differences
> are understood well enough at this point to say anything definitive.
> We know far more about less complex systems, like subcellular systems,
> that do show very clear limitations to the mechanism of RM/NS.
Work it out and come back with your explanation. First you will have
to define these differences enough so that they have to be explained.
>
> > > > What probably gets to Sean is how his bogus 1000 aa argument breaks
> > > > down with closely related species like chimps and humans. Sean comes
> > > > face to face with one obvious fact. Any change in any gene, protein,
> > > > whatever, has to work within the whole. Whether some new change is
> > > > part of a large existing complex or the start of some future large
> > > > complex it has to work within what already exists.
>
> That's right . . .
So when does a complex become your 1000aa complex. With the first
mutation in an existing large complex or when the function changes
enough to be said to be doing something else, or something new? How
long does it take for these things to change enough to suit you? Your
flagellum example probably evolved billions of years ago, and you
don't have the faintest idea of when the flagellum started to evolve
because no one knows what parts and what order things started. We
have a bunch of genes that obviously evolved from duplciated genes,
and we can get some estimates of when the duplications occurred. The
parts don't seem to all have evolved at the same time. It would be
nice if you could work it all out for everyone and tell us why it is
impossible to evolve a flagellum the way it probably evolved. Can you
do that? Maybe you can start with what the ATPases in the rotary
motor were doing before they became part of the complex that
eventually would become the motor, and work up from there. You even
admit that your 1000aa gap thingy doesn't mean that all 1000aa had to
evolve all at once, so shouldn't you be able to figure out a
reasonable order of events before you claim that it is impossible.
You admit that all new mutations have to work within the whole
already, so put up or shut up.
>
> > > > If it doesn't it
> > > > has to limp along and exist against selection to remove it, and most
> > > > likely it is lost.
>
> Right again . . .
>
> > > > What we see are the changes that fit well enough
> > > > to make it. Sean can't cope with that fact.
>
> Where have I said anything else but this? This is a big part of my
> own position on this topic.
Well see just about every mutation is part of some elaborate system
that it has to function within. So you don't seem to have much of an
argument.
>
> > > > His whole 1000 aa bull
> > > > pucky is based on some stupid reality that doesn't exist.
>
> There are lots of known systems that require far more than 1000 fsaar
> at minimum to work. Tell me, how can you make a flagellar system with
> less than 1000 fsaar? Think you can do it? How?
Isn't that your problem? You are the one that claims to know enough
to claim it could not happen, so you are the one that has to
demonstrate it. We just have to point to obvious signatures of
evolution like gene duplication and the fact that we can determine
that a lot of the parts did something else in the cells before they
were coopted to work in the flagellum. Why can we claim that there
are ATPases in the motor? What are these ATPases related to? What do
you have to compare to these facts?
>
> > > > He comes
> > > > face to face with that reality with chimps and humans, and has to
> > > > demand that his opposition provide what he cannot. Sean has to
> > > > demonstrate that his type of gaps ever existed. He can't do that with
> > > > the human and chimp example.
>
> You guys hide behind creatures and systems which are largely unknown
> instead of even trying to deal with those systems that are much better
> known and understood. What a crock . . .
What are these better understood systems? Aren't you the one that is
using some stupid 1000aa bull pucky from some unknown system where you
don't have the faintest idea of how to demonstrate that any
substantial gaps ever existed?
Why keep going with dishonest obfuscation ploys. Why should
misdirection be your primary tool? Why not make good on your claim
about having an alternative to common descent and the evidence to back
it up that is just as good as the evidence that you claim isn't good
enough? Why keep blowing smoke if you have some real substantial
argument?
>
> > > > Ron Okimoto
>
> > > If a gene can "limp along and exist against
> > > selection to remove it" as you say, then that kinda
> > > shoots evolution down to ZERO.
>
> > We know of examples of this. You can go into any extant population
> > and find deleterious mutations segregating. Just look up any paper on
> > mutation selection balance. We have examples where gene knockouts
> > have been fixed in populations and those species have had to deal with
> > loss of the gene. The gene responsible for vitamin C defficiency in
> > humans and other primates down to Monkeys is due to the knock out of a
> > single gene. The common ancestor of monkeys including the lineage
> > that evolved into humans is descended from a population where this
> > gene knock out got fixed due to genetic drift or founder effects or
> > some combination of such factors. Scurvy is the result of not having
> > enough vitamin C in our diets due to this gene loss. Evolution
> > doesn't necessarily allow only good things to happen. If it did
> > extinction would not be as common as it is.
>
> That's right . . . In fact, "devolution" or significant ongoing
> genetic losses are a real problem to the overall ToE.
>
> http://www.detectingdesign.com/dnamutationrates.html#Detrimental
What an idiot. The example given probably happened over 30 or 40
million years ago. It is just a fact of evolution. What is your
explanation for it? All the species of monkeys and apes (including
humans) have evolved around this change. Genes are lost all the time
in evolution. New genes evolve to do other things.
>
> > > How can random mutations take
> > > place if a gene can limp along and exist against selection to
> > > remove it?
>
> > Really, just look up mutation selection balance and learn something.
> > Populations can exist with quite a load of deleterious mutations. It
> > isn't just theory, we have done genetic analysis of populations like
> > flies and even population studies of humans to demonstrate it. What
> > do you think it means when they estimate that every human carries a
> > genetic load of around 2.5. This means that the average human has the
> > equivalent of 2.5 recessive lethals in their genomes.
>
> It is actually worse than that when one considers all the non-lethal
> deleterious mutations that are present in the genomes of humans and
> all other slowing reproducing creatures.
The genetic load incorporates all detrimental mutations that affect
viability. If humans are like Drosophila in their genetic load, than
over half the load is due to recessive detrimentals with only around
10% lethality. This just means that 10% of the homozygotes die. This
just means that everyone has a lot of detrimentals in their genomes
not just 5 recessive fully lethals.
>
> > This isn't all bad. There are plenty of examples of where a second
> > mutation can "fix" the detrimental effects of another mutation. Look
> > up papers on second site reversions.
>
> That's right. It is fairly easy to step back onto a beneficial island
> which a population has taken a very short step off of in the past.
>
> > This increases the evolutionary
> > potential of any population since Sean's gaps of 2 or 3 mutations can
> > obviously be crossed under such conditions.
>
> It is one thing to step off of an island that one was already on in
> the past. It is quite another think to find a novel beneficial island
> to begin with.
Sean doesn't know this. All we know is that finding new function is
nearly trivial in protein evolution. He knows the sequence space for
things like antibodies and yet we know that in less than 10^12 trials
new functions can be evolved from a given protein sequence. This is
such a small sampling of the existing sequence space that claiming
anything about "novel beneficial island" is pretty darn stupid. A new
function isn't a new island? Sean can define his terms any way that
he wants to, but that doesn't mean that they conform to reality in any
respect.
>
> > Just ask Sean why he went
> > from demanding examples of 3 mutation gaps to his 1000 aa bull pucky.
> > He did the calculations himself and figured out that 3 mutation gaps
> > aren't that much of a problem. So he had to go into gap inflation.
> > It went from 3 to 20 and then 40 fairly quickly and then he settled on
> > the 1000 aa junk.
>
> It is just amazing to me that you still do not understand, despite my
> explaining it to you dozens and dozens of times, that the structural
> threshold of 1000 fsaar is NOT a measure of the gap distance. It is
> the measure of a level of functional complexity. Functional
> complexity is not the same thing as the likely gap distance. The
> likely minimum gap distance is always smaller than the level of
> functional complexity - always. The smallest gap distance between an
> existing starting point and a potential target at the 1000 fsaar level
> is likely to be only a few dozen mutational changes wide.
Yeah, we've all heard it before. It is only a gap when I need it to
be a gap in my probability calculations, but it really isn't a gap....
no really it isn't a gap until...well... I need it to be a gap. Geez
it must be a few dozen somethings in the gap that isn't a gap. Sean
can't tell us what those 12 somethings are, but he knows that they are
there and part of his 1000 aa bull pucky. Sean, just take your
flagellar example and show us the 12 somethings that aren't really a
gap.
>
> I've been explaining this for over ten years now. There's been no
> "inflation" here. That's just your strawman misrepresentation.
You have been running and pretending for most of that time. It has to
be going on 8 years that you have been running from the claim you made
about having an alternative to common descent and the evidence to back
it up that was just as good as the evidence science had that wasn't
good enough for you. So why blow smoke if you really have an
alternative? Where is that science of intelligent design that you
would have taught to school kids? Why run and pretend and perpetrate
stupid obfuscation ploys if you really have something worth
supporting? Lying about it isn't going to solve any of your problems.
Ron Okimoto
>
> < snip >
>
> Sean Pitmanwww.DetectingDesign.com
heekster
wrote:
A meaningless question, since Pitman willfully misunderstands ToE at a
fundamental level. This has been explained to him by others, in great
detail, yet he refuses to acknowledge or understand. He also refuses
to answer questions, preferring instead to attempt a goal post move,
by asking irrelevant questions to redirect attention away from the
gaping chasm of his adventist ignorance. As seen above
>It is your position that the mechanism of the ToE is based on real
>scientific understanding of its creative powers. Yet, where is the
>statistical basis of this understanding? Where is the actual
>"science"?
>
Another IDiotic question, which has already been answered. Pitman
chooses to conveniently ignore the uncomfortable fact (to him) that
ToE is based on a century and a half of observation and analysis.
Pitman has his own definition of scientific theory, which in part,
helps to explain his galactic obtuseness. He thinks that it is
actually statistical analysis.
When I attempted to disabuse him of this imbecility:
>> ToE isn't a statistically derived theory.
Pitman responded with
>LOL -
> Oh really? Don't you realize that all scientific theories must
>have some sort of statistical analysis to establish predictive value?
my response:
Don't you realize that statistical analysis is a tool, not a
requirement? Besides, Popper said a hypothesis has to be able to
make "falsifiable predictions", not "statistical falsifiable
predictions".
A scientific theory is a unifying and self-consistent explanation of
fundamental natural processes or phenomena that is totally constructed
of corroborated hypotheses. A theory, therefore, is built of reliable
knowledge--built of scientific facts--and its purpose is to explain
major natural processes or phenomena. Scientific theories explain
nature by unifying many once-unrelated facts or corroborated
hypotheses; they are the strongest and most truthful explanations of
how the universe, nature, and life came to be, how they work, what
they are made of, and what will become of them.
Pitman:
>Without at least some basis so suggest that future observations are at
>least likely to occur with a particular frequency, you don't have a
>real scientific theory.
My response:
Most of science was deterministic,until quantum mechanics, in the late
19th century.
Pitman:
> There is no real science without mathematics
My response:
No one claimed that. Why the strawman?
[Still waiting for a response on that one.]
>and statistically supported predictions.
>
Yep, one doesn't need the century and a half of observations, actual
examples, fossil evidence or any of those silly things, just
statistics.
Pitman would probably have to do a statistical analysis of 2 + 2,
before he could set it equal to 4.
Darwin developed the ToE through NS in order to explain what had been
observed. Pitman hasn't shown anything yet, that indicates that his
"calculations" reflect what has been observed. In fact, he
conspicuously avoids reference to observations, or else places absurd
limitations on them, like they have to occur within 50 years, and
involve at least 1000 amino acids. He does not seem to have a working
functional understanding of what ToE is. If one peruses his website,
one will find fairy tales, cartoon characters, Seventh Day Adventist
links, and lots of condescension, just not a whole lot of actual
science.
http://www.detectingdesign.com/images/Methinks/Weasel.jpg
http://www.detectingdesign.com/images/Goldberg/Rooster.jpg
http://www.detectingdesign.com/PDF%20Files/History%20of%20the%20Sabbath.doc
hersheyh
> "On Sun, 30 Nov 2008 08:45:48 -0800 (PST), in article
Sean's model seems to assume that sequences with a named (teleologic)
function are clustered together on an "island" of functionality having
similar sequences that all have the named function. I am asking how,
given that all he uses is sequence similarity, he manages to exclude
the single point mutants that have 'lost' the named function from this
functional island and where he places them in this imaginary
geography. And how he knows that all sequences with similar functions
and related structure are present in separate islands that are
randomly placed in the ocean of intervening sequences. I am asking,
if I have a specific sequence, how I can know where to place it in
this imaginary landscape or locate it on the surface. What is the
more relevant feature, sequence or function?
Using metaphor is nice for generating mental images, but it isn't
science.
Ron O
You know how you should take it. You should understand that it is
your that are running the bogus misdirection ploy. You are the one
that is running and pretending. I never made any such claims to
defend. This is just your dishonest and pathetic attempt to deflect
the issue from your bogus dishonesty so that you can just blow smoke.
Why should I let you do that?
Why run and pretend? Where is that alternative to common descent and
the evidence that you claimed to have that was just as good as the
evidence that science had that you think isn't good enough? Why try
and dishonestly transfer your own bogousity onto someone else. What
kind of person would do something like that? Obviously, not the type
of person that you want others to think that you are, but what are you
doing? You are the one that is running, and you have to lie about it
and try to blame someone else for your own shortcomings.
>
> > > It is your position that the mechanism of the ToE is based on real
> > > scientific understanding of its creative powers. Yet, where is the
> > > statistical basis of this understanding? Where is the actual
> > > "science"?
>
> > Where is that science of intelligent design that you were going to
> > teach to school kids. Why haven't you changed the name of your web
> > page when you know for a fact that intelligent design was just a bogus
> > creationist scam with no science to back it up? Why are the same
> > dishonest perps that ran the teach ID scam running a dishonest bait
> > and switch scam on all their supporters if they really had any
> > intelligent design junk worth teaching. You even know that the switch
> > scam doesn't even mention that intelligent design ever existed. How
> > bogus can you get?
>
> > Why is dishonesty all you have? Why employ misdirection when you
> > could be making good on the claims that you know that you absolutely
> > require in order to have any type of valid argument. No science, no
> > alternative, no scientific argument.
>
> All I've done is asked you a simple question. I've asked for at least
> a rough basis in real statistical analysis for your theory. Is the
> very best you have in response a list of non-sense pejoratives? Why
> not simply answer a very simple question? I'm sure others in this
> forum, besides me, would love to hear the answer . . .
You've just tried a dishonest ploy to deflect the issue. You got
caught. You obviously do not know when to give up. This type of
degenerate behavior is what we can expect from the anti-science
creationists from a whole lot of past experience. Why don't you want
to be different? Why resort to dishonest behaviour? Why spend years
lying to yourself and everyone else about it? Who is the one that is
running? Who is the bogus liar? Who is the guy that has to depend on
trying to blame others for their own dishonest behaviour? Just look
in the mirror Sean. They aren't non-sense pejoratives when they are
true, and you know that they are true or you wouldn't be trying these
dishonest ploys. If they were not true you would be addressing them
and demonstrating that they are not true. That should be obvious to
anyone that reads this junk.
'Rev Dr' Lenny Flank
That's nice.
Why is it that creationists think the genetic difference between
jaguars and lions could have evolved, but the much smaller genetic
difference between humans and chimps could have evolved under any
circumstances whatever?
'Rev Dr' Lenny Flank
The most
> obvious difference is that humans and apes cannot produce viable
> offspring. And yes, this has been tested.
(snip)
That's nice.
Domestic wheat and emmer grass can't produce viable offspring either.
And yet we know for an absolute historical fact that one descended
from the other.
The two North American species of grey tree frog, H versicolor and H
chrysoscelis, also can't produce viable offspring. Yet we know that
one is a polyploid of the other.
So I will ask again ---- why is it that you think the genetic
difference between jaguars and cheetahs can have evolved, but the much
smaller genetic difference between humans and chimps could not have?
Other than your religious opinion that humans are special and must be
separate from the whole animal kingdom . . . .
(snip)
> > > >> Why then do you consider it utterly absolutely completely impossible
> > > >> for humans to have "micro-evolved" their genetic differencesd with
> > > >> chimps, but NOT utterly absolutely completely impossible for members
> > > >> of other "kinds" to have "micro-evolved" their LARGER genetic
> > > >> differences with each other?
>
> I've repeatedly explained in this forum that I do not think there is
> enough evidence to adequately exclude human-ape common ancestry on a
> genetic basis at this point.
Then, uh, what are you bitching about?
<snip)
>
> > > >> Besides, of course, your religious opinion that humans are special
> > > >> and simply cannot be related through descent to any other animal, no
> > > >> matter what . . .
>
> I've never said that . . .
Don't bullshit us, Sean.
heekster
wrote:
Pitman conflates religion with science.
"* Distinguishing “Truth” from “Error”, concerning ideas about the
world around the mind requires the same “not true” filter
Can be used by both science and religion, making both the same thing"
He followed the above with this,
"Ellen White comments that in Heaven the study of the plan of
salvation will be our science and our song"
which hardly seems relevant.
See slide 56 of this powerpoint.
http://www.detectingdesign.com/Presentations/Intelligent%20Design%20as%20a%20True%20Science%202.ppt
'Rev Dr' Lenny Flank
I'm still confused. Why is this, uh "odds problem" you keep yammering
about, any better for any OTHER species to species evolution? If, as
you seem to believe, moving from one spot in sequence space (one
species) to another spot in sequence space (another species) is "too
improbable", then, uh, how can ANY species evolve into ANY other
species? They ALL have to cross a "sequence space" to reach another
point in it.
Or do you agree with Ray that NO species-to-species evolution is
possible?
If not, then why is the problem of "moving in sequence space" between
"jaguar" and "cheetah" any more or less "probable" than moving between
"human" and "chimp" -- particularly since humans and chimps are much
closer together in your "sequence space" than jaguars and cheetahs
are.
So why is it "statistically possible" for ONE of these crosses in
"sequence space", but not "statistically possible" for the
OTHER . . . ?
Other than your religious belief that humans are "special" and simply
cannot have evolved . . . .
R. Baldwin
news:43ae29de-a316-462e...@35g2000pry.googlegroups.com:
No, I don't. I have not suggested any model of sequence space, so I have
nothing to defend. You have suggested a model, therefore the burden is
on you to defend it.
Your language, by the way, is hopelessly imprecise. Sequence space is a
term that belongs primarily to mathematics, and you are attempting to
apply it to genome sequences as a specific problem. Rather than asking
someone to defend a model of sequence space, you should be asking
someone to defend a model of biology.
> No one in the scientific community has done
> this.
Probably because no one in the scientific community is idiotic enough.
> It is simply assumed that RM/NS did the job without actually
> subjecting this idea to any real statistically supported model of
> sequence space.
Actually, the real statistical work is done within valid frameworks,
which are different from your sequence space model.
> No mathematical odds analysis is performed. There's
> simply nothing but assumptions when it comes to the proposed mechanism
> of RM/NS.
The mechanisms causing random mutation and natural selection are readily
observed and understood (mutagens, predation, environmental stress,
etc.), so that is a very silly statement. But perhaps you meant the
proposed *processes* of random mutation and natural selection? In which
case, I would have to ask, how do you *know* there are only assumptions?
That is an exceptionally strong statement, and would require many
lifetimes of research to demonstrate that no facts have ever been
produced regarding random mutation and natural selection.
>
> Beyond this, my model of sequence space does fit the data.
What data? Who has the data? Who has validated the model against the
data besides you?
> My model
> suggests that non-beneficial sequences increase at an exponential rate
> compared with potentially beneficial sequences as overall sequence
> space increases in size. My model also suggests that those areas
> within sequence space that have a clustering of potentially beneficial
> targets will not be so clustered at higher and higher levels of
> functional complexity. This in turn will result in an exponential
> stalling out effect of RM/NS when it comes to finding novel island
> targets within sequence space.
We are all familiar with what you claim.
>
> This model is exactly what is observed in real life.
Again, based on what data? Who has the data> Who has validated the model
against the data besides you? Where are the results published?
> That's a simple
> fact for anyone who cares to look.
Your assertion of this does not make it so. Why don't you try to publish
your results, and obtain peer review? If the facts are so simple and
easy to find, this should not be hard for you.
> This is exactly why evolution
> happens, quite commonly, below the 1000 fsaar threshold, but not at
> all above it in a given span of observable time.
Your frequent assertions are not convincing.
> There simply is no
> comparable evolutionary model of sequence space - none whatsoever.
Again, because it is the WRONG MODEL!
Ron O
> On Sun, 30 Nov 2008 08:54:06 -0800 (PST), Ron O <rokim...@cox.net>
The sad thing is that around three years before this power point is
dated Sean came to the realization using his "truth filter" that there
was no science of intelligent design worth teaching. Even after the
bogus ID perps that had lied to Sean about the non existant science of
intelligent design had given up on teaching the bogus junk and had
started running the bait and switch on any creationist rube like Sean
that had believed them, Sean made the claim inspite of the fact that
he knew that the switch was in, that he had the science of intelligent
design to teach to school kids even if the dishonest blowhards at the
Discovery Institute had given up and decided to run in the switch scam
instead of putting up anything to teach about intelligent design.
That was sometime in 2003. Sean was running and pretending that he
had the science of intelligent design for around 3 years by the time
this power point got dated.
Hey, Sean, where is that science of intelligent design that you would
have taught to school kids. None of it is obviously in this bogus
power point presentation or you wouldn't be running from that claim,
but trying to support it. We are going into 6 years of running and
pretending while you can lie to the guys that you showed this
presentation to. What a dishonest crock. The only people that
support the anti-evolution creationists are ignorant, incompetent and
or dishonest. We know where Sean fits in. At least the ignorant and
incompetent have some kind of excuse. They haven't run this junk
through their "truth filter."
Ron Okimoto
R. Baldwin
news:319ed711-37ba-4fe7...@w3g2000yqc.googlegroups.com:
> On Nov 30, 12:31 pm, TomS <TomS_mem...@newsguy.com> wrote:
>> "On Sun, 30 Nov 2008 08:45:48 -0800 (PST), in article
>> <59817049-4996-430f-8c43-377a1db54...@d23g2000yqc.googlegroups.com>,
>> hers
> heyh
>> stated..."
>>
>>
>>
>> >On Nov 30, 11:17=A0am, Seanpit <sean...@gmail.com> wrote:
>> >> On Nov 29, 7:19=A0am, Vend <ven...@virgilio.it> wrote:
>>
>> >> > On 28 Nov, 18:11, Seanpit <sean...@gmail.com> wrote:
>> >> > <snip>
>>
>> >> > > > Hint: The *real* historical process of Obama becoming
>> >> > > > president involved a series of events, some of which were
>> >> > > > due to chance (s
> uch> > as
>> >> > > > the Jack Ryann Senate candidacy imploding in a sex scandal),
>> >> > > > som
> e o> >f
>> >> > > > which involved the character and qualifications of the
>> >> > > > candidate
> . > >=A0The
>> >> > > > probability of the last step (or gap) in the process was
>> >> > > > essenti
> all> >y 1
>> >> > > > out of 2. =A0There are ways of identifying evidence for the
>> >> > > > st
> eps i> >n the
>> >> > > > historical process. =A0None of them involve assuming that
>> >> > > > Obam
> a bec> >ame
>> >> > > > president in a single step gap-crossing with a probability
>> >> > > > due t
> o
>> >> > > > division by the total number of legallypossiblecandidates
>> >> > > > for president.
>>
>> >> > > We are talking about a situation where the actual gap distance
>> >> > > is
> not
>> >> > > already known ahead of time Howard. =A0We are talking about
>> >> > > pred
> ictin> >g
Tagging on:
Sean's model is hopelessly unrelated to reality. He assumes a random walk
through a "sequence space" defined by a given length of amino acid
residues. Since there are 20 possible values for each digit, there are 20^N
possible sequences, which he assumes will be arrived at through a random
walk, one point mutation at a time, with all point mutations being
equiprobable at the codon level (Uniform distribution). He then assumes
that beneficial sequences are sparsely populated through the space, and
argues that getting from one to the next becomes hopelessly improbable.
Sean's model makes no account for facts.
First, the distribution of point mutations in the amino acid residue
sequence space is non-Uniform. Point mutations occur at base pairs, with
transitions (purine to purine: A to G, G to A, our pyramidine to
pyramidine: C to T, or T to C) being most common and transversions (purine
to pyramidine or pyramidine to purine) being less common. This is further
complicated by codon degeneracy. There are six different codon spellings
for arginine (CGT, CGC, CGA, CGG, AGA, and AGG).For four of then (CGN), any
point mutation in the third nucleotide will leave the amino acid uncanged.
It is still arginine. For the other two (AGR), the amino acid is unchanged
under transition mutation. Methionine, on the other hand, has only one
spelling (ATG), and any point mutation will change it into a different
codon.
By point mutation, codons can only change to a different codon that differs
by only one base pair. Glycine to valine occurs with transversion G->T in
the center nucleic acid, but glycine to proline requires two point
mutations: transversions in the first two nucleic acid (GG ->
CC).Asparagine to histine requires only a transition in the first base
pair. Thus, asparagine to histine is far more probable than glycine to
proline.
Second, even under point mutation the sequence size is subject to change.
Glutamine to Stop or the reverse involves a transition in the first base
pair.
Third, point mutations are not then only kind of mutation, Under an
insertion, deletion, or inverson, a huge leap is taken across the sequence
space, not a step in a random walk.
Fourth, Sean is only modeling a single open reading frame with no
relationship to the rest of the genome, yet mutations may occur in other
regions such as promoters.
I believe Howard Hershey has already explained many times why the
beneficial seuences are not sparsely populated with a Uniform distribution
over the sequence space.
wf3h
> On Nov 30, 8:44 am, Ron O <rokim...@cox.net> wrote:
> >
> > When are you going to stop running and pretending? Why try some
> > dishonest deflection ploy to side track the issues that you know that
> > you have to address, but can't?
>
> > Where is that alternative to common descent that you claimed to have
> > and the evidence for it that was just as good as the evidence you
> > claim that real science doesn't have? What good is your above
> > dishonest deflection and misdirection ploy above when you don't have
> > jack?
>
> I'll take that as a no - you have no idea as to the likelihood of your
> proposed mechanism to do the job you claim it did. Where's the
> science Ron? Who's running from a request to demonstrate a real
> scientific basis for what is supposed to be a well-established
> scientific theory?
says the man who thinks creationism...the most used failed idea in
history...is science.
god, talk about a hypocrite. he INSISTS others reject a hypothesis if
it fails, yet he refuses to do so on the basis of what his church
tells him to do.
>
> > Why is dishonesty all you have? Why employ misdirection when you
> > could be making good on the claims that you know that you absolutely
> > require in order to have any type of valid argument. No science, no
> > alternative, no scientific argument.
>
> All I've done is asked you a simple question. I've asked for at least
> a rough basis in real statistical analysis for your theory.
and i have asked you the EXACT SAME QUESTION a number of times.
your response? none.
Is the
> very best you have in response a list of non-sense pejoratives? Why
> not simply answer a very simple question? I'm sure others in this
> forum, besides me, would love to hear the answer . . .
>
and ditto for your view that 'god did it' is science
RAM
Ron this is a very good sequence of responses to Sean. I appreciate
the your efforts here.
RAM
Kent Paul Dolan
> Well *Ron*. If it is "all just genetics" as you
> claim, then genetically speaking, there is no need
> for selection to have such a high priority
> regarding evolution because if it cannot breed and
> produce a fertile offspring then it is not
> genetically the same.
You might want to fill in some of the referent-free
pronouns there to turn that word-hash into a
sensible statement in the English language. As it
stands, it just highlights you as a sufferer of some
brain damage event in your past.
> Selection is only 'observed' to produce a
> sub-species such as the dog within their kind.
That is a simple falsehood, and you are not going to
convince a single sane person here otherwise.
Speciation is an _observed_ phenomenon in nature,
full stop.
> "Each After His kind". Exactly as the bible says.
The bible is not only not an authority about
evolution, a concept of which it contains not the
first clue, it is not an authority on anything,
being rife with easily seen errors which only those
who tap-dance themselves into a stupor trying to
"explain" have any trouble understanding.
> Example: Dogs are after his own "kind" called
> "wolf"
Dogs and wolves are inter-fertile [a bit more than
horses and donkeys are], but are separate species
due to geographical and sympatric separation that
usually prevents them from interbreeding.
There is no such biological concept as your "kind";
that is pure religious flummery.
> It really is THAT simple.
No, but as often mentioned here, _you_ are that
simple-minded, and so you try to crush all
observational evidence science has provided to you
under your only tool, an immense stack of bibles.
That doesn't work.
Unfortunately for that method of obfuscation of
observed fact, piling up bibles doesn't make the
stack of them any more true than the first one,
which first one is untrue on its face and easily
shown to be so.
Do that proof this way.
Just start mentioning, one after another, in a list,
the lies the bible contains and watch the
creationists' biblical-error-dismissing tap-dancing
grow ever more frenetic.
When tap-dancing creationists have vibrated
themselves into a hot plasma of incoherence, you've
got your proof that the bible is untrue.
Were the bible true, such _incoherent_ defenses, as
yours here, of its contents would not be necessary.
xanthian.
Vend
Ok.
> There are many
> such sequences that exist in the potential of undiscovered sequence space.
Ok.
> These sequences are potential "targets" for the evolutionary
> mechanism.
There is no reason to call them "targets", since evolution isn't aimed
at finding any of them.
> the only problem is that non-target sequences vastly
> outnumber the potential targets within sequence space and this ratio
> only gets exponentially worse and worse with each increase in the
> level of functional complexity.
What do you mean by "non-target" sequence?
Vend
> On Nov 30, 8:45 am, hersheyh <hershe...@yahoo.com> wrote:
>
>
>
>
>
> > > > Sean, it appears that you keep repeating the same error.
> > > > Biological evolution isn't a search algorithm that moves form one
> > > > target to another. There is no concept of 'target'
> > > > and therefore no concept of 'gap
> > > > distance between targets' in biological evolution.
>
> > > LOL - What do you think the concept of RM/NS is based on? What does
> > > "natural selection" select? Obviously, NS selects those random
> > > mutations that produce new genetic sequences that are more
> > > functionally beneficial compared to what came before. There are many
> > > such sequences that exist in the potential of undiscovered sequence
> > > space. These sequences are potential "targets" for the evolutionary
> > > mechanism. the only problem is that non-target sequences vastly
> > > outnumber the potential targets within sequence space and this ratio
> > > only gets exponentially worse and worse with each increase in the
> > > level of functional complexity.
>
> > > Sean Pitmanwww.DetectingDesign.com
>
> > What evidence do you have that functional and non-functional sequences
> > are randomly distributed in total sequence space?
>
> There is a loose clustering effect, certainly, but this clustering
> effect gets less and less clustered with each increase in the size and
> specificity requirements of sequence space.
Even if that is correct, why would it be a problem for the theory of
evolution and common descent?
> Where is your evidence that there is no change in the clustering of
> targets within sequence spaces of different sizes?
You are claiming that the theory of evolution isn't a sufficient
explanation for the variety of life on earth, thus the burden is on
you to support your claim.
> > And how can you
> > define "function" in the absence of an organism and environment in
> > which to function?
>
> I don't defined a beneficial function in the absence of an organism or
> the environment. That's what makes a functional system "beneficial".
"beneficial" can be a property of a mutation, not a system.
Systems can be viable or not viable.
> > From my knowledge of genetics (and yours too) it
> > is clear that a single point mutational event can eliminate the
> > current function of gene and reversion of point mutations can usually
> > also occur (deletions do not revert).
>
> Absolutely. Deletions do not usually, but can, at least
> theoretically, revert. The reason why they almost never do revert is,
> again, based on the gap problem. Multicharacter losses are much
> harder to replace via random mutations than single character losses -
> statistically.
>
> > Thus, if you cluster sequences
> > on the basis of similarity, sequences that have a specified function
> > and those that don't will be intermeshed and in intimate contact.
>
> Sequences that require greater specificity are much more widely spaced
> in sequence space than those of similar size that require much less
> specificity. Therefore, finding a target with lower specificity will
> be far easier than finding one with higher specificity. Getting from
> a starting point with lower specificity to a target with higher
> specificity is not enhanced just because the edges of the lower-
> specificity island overlap the edges of the higher specificity
> target. Why not? Because, finding the target is still based on
> searching randomly within a very large sequence space of the lower-
> specificity target. There is no improvement of the odds here.
If fitness increases with specificity then an high specific sequence
can be quickly evolved form a low specific sequence.
Consider a simple genetic algorithm that manipulates strings of
letters, for instance. The string length is fixed and equal to the
length of the English version of "War and Peace". To keep it simple,
there are only point mutations.
Fitness is proportional to string length minus the Hamming distance to
"War and Peace".
How long does it take, on average, to evolve the maximal specific
string from a population of randomly generated initial strings?
<snip>
Seanpit
> true, and you know that they are true or you wouldn't be trying these
> dishonest ploys. If they were not true you would be addressing them
> and demonstrating that they are not true. That should be obvious to
> anyone that reads this junk.
This is really all anyone can expect from Ron O - lame attempt at
personal attacks while only very very rarely dealing with the actual
issue or questions at hand. Worthless babel - I've come to expect it.
Seanpit
> > There simply is no
> > comparable evolutionary model of sequence space - none whatsoever.
>
> Again, because it is the WRONG MODEL!
Sequence space does exist. Potentially beneficial targets do exist
within that space. There is a ratio of potential targets vs. non-
targets within sequence space. Different levels of functional
complexity have different ratios of targets vs. non-targets. All of
these are non-arguable facts. What model of sequence space do you
have if you think my model is wrong? Please, do explain your own
model - or the model of anyone else that you think has a better idea
for that matter. I'm asking for a model of the appearance or
character of something we know does actually exist. What is your
model?
Sean Pitman
www.DetectingDesign.com
Seanpit
> function are clustered together on an "island" of functionality having
> similar sequences that all have the named function. I am asking how,
> given that all he uses is sequence similarity, he manages to exclude
> the single point mutants that have 'lost' the named function from this
> functional island and where he places them in this imaginary
> geography. And how he knows that all sequences with similar functions
> and related structure are present in separate islands that are
> randomly placed in the ocean of intervening sequences. I am asking,
> if I have a specific sequence, how I can know where to place it in
> this imaginary landscape or locate it on the surface. What is the
> more relevant feature, sequence or function?
>
> Using metaphor is nice for generating mental images, but it isn't
> science.
If you have a particular sequence that is only one point mutation away
from some functional island cluster with a particular type of
beneficial function, you would place it right next to that island -
one step away from it. What about this is mysterious to you?
The question here is not if it is possible to be just one step away
from a high-level beneficial island, but is it likely to be just one
step away from the perspective of a given genome. Again, you have to
go beyond your idea that what is possible = what is likely. That's
just not true.
Sean Pitman
www.DetectingDesign.com
wf3h
>
> This is really all anyone can expect from Ron O - lame attempt at
> personal attacks while only very very rarely dealing with the actual
> issue or questions at hand. Worthless babel - I've come to expect it.
>
says the man who insisted i provide him with proof of my 'scientific'
credentials...and then ignored every request i put to him for
information supporting his view of creationism
wf3h
> < snip>
> Sequence space does exist. Potentially beneficial targets do exist
> within that space. There is a ratio of potential targets vs. non-
> targets within sequence space. Different levels of functional
> complexity have different ratios of targets vs. non-targets. All of
> these are non-arguable facts. What model of sequence space do you
> have if you think my model is wrong? Please, do explain your own
> model - or the model of anyone else that you think has a better idea
> for that matter. I'm asking for a model of the appearance or
> character of something we know does actually exist. What is your
> model?
of course, the same can be asked of sean. he's committed a type I
(alpha) error in supporting creationism...seeing a pattern where none
exists. while routinely says that evolution is false based on stats,
he uses a type I error to claim (without statistics) that ID is
presents...based on no stats at all
hersheyh
The question of whether you are ordering the sequences into clusters
based on function or based on sequence. The two are not the same
thing and either will be problematic wrt producing actual clusters.
If you arrange proteins so that, in a 1000 aa system, each *sequence*
is surrounded by the 999 different one-aa different *sequences*, most
of the surrounding *sequences* will have at least some of the same
named teleologic function as the sequence you specified as the
teleologic goal. But there will be significant variation in
functionality for the named function. If you then vary each of the
999 proteins by one aa, most of the ones that will have lost the named
function will remain lacking in the named teleologic function. But
not all of them will. There are many examples of compensatory
intragenic reversion where a second mutation restores function that
was lost by the first mutation. In fact, for some mutations,
heterozygosity between two different mutations, neither of which
produces function by itself, can restore function. What do we
consider such features. Worse, we know that, for some ancient
functions, there can be so much sequence change that the proteins are
not identifiable as similar on the basis of sequence (but they do have
the same structure). Worse yet, there can be (and often are)
sequences that are similar in sequence to the starting (named)
sequence, but that have different, but related, *functions* at various
levels of *function*. In fact *some* of the sequences have dual or
multiple functions. Say by binding both aldosterone and cortisol. Or
by both acting as an organismal motility organ and a toxin export
machine. When that happens, then further changes might emphasize one
of these secondary functions, providing a chain of linkage with the
function you claim is on an isolated functional island.
Thus, if you arrange your surface geography on the basis of *sequence*
you do not get a tight clustering on the basis of *function*. You get
a fuzzy network filled with holes of non-function and chains of
functional linkage to distant sequences that don't resemble the
starting point. I fail to see how arranging on the basis of sequence
produces your model of compact single functions.
*And* that is not even thinking about the possible ways that the same
function can arise by an entirely independent mechanism (as in lactase
from antibodies or flagella like that seen in archaebacteria).
In contrast, if you organize your surface geography in your model on
the basis of level of a particular *function*, you will wind up with
quite different sequences being close together and quite similar
sequences being far apart (with the non-functional ones being
"offshore", so to speak. And you would still have the problem of
overlapping functionality (as in flagella that also act as adhesion
systems or toxin transport systems or receptors that can bind both
cortisol and aldosterone).
This problem is a problem at *any* level of function.
Not to mention that no *actual* organism has ever had the capacity to
search total sequence space.
But I am sure that you already have answers to these minor problems.
hersheyh
>
> > > There simply is no
> > > comparable evolutionary model of sequence space - none whatsoever.
>
> > Again, because it is the WRONG MODEL!
>
> Sequence space does exist.
The only part of sequence space that is relevant is that which
actually exists in the relevant organisms. Total sequence space has
about as much relevance as the size of the universe does to the space
taken up by starbucks coffee shops. My understanding is that
starbucks does not place its shops randomly in the universe, but tend
to place them in places close that get a certain amount of human
traffic.
> Potentially beneficial targets do exist
> within that space.
Which space? Total or relevant?
> There is a ratio of potential targets vs. non-
> targets within sequence space.
Which space? Total or relevant? And if relevant space, I would point
out that organisms are different.
> Different levels of functional
> complexity have different ratios of targets vs. non-targets.
In total sequence space. Not necessarily in relevant sequence space.
> All of
> these are non-arguable facts. What model of sequence space do you
> have if you think my model is wrong? Please, do explain your own
> model - or the model of anyone else that you think has a better idea
> for that matter.
One where the chain of functional intermediate steps matter. And
where things do not evolve in a single giant leap. You know, the one
that involves *actual* evolution rather than straw man evolution.
> I'm asking for a model of the appearance or
> character of something we know does actually exist. What is your
> model?
I have given you some. You reject them because it doesn't consider
the size of total sequence space.
>
> Sean Pitmanwww.DetectingDesign.com
Seanpit
wrote:
>
> Sean'smodel is hopelessly unrelated to reality. He assumes a random walk
> through a "sequence space" defined by a given length of amino acid
> residues. Since there are 20 possible values for each digit, there are 20^N
> possible sequences, which he assumes will be arrived at through a random
> walk, one point mutation at a time, with all point mutations being
> equiprobable at the codon level (Uniform distribution).
Sequence space, by definition, is 20^N in size. Searching this
sequence space for potentially beneficial sequences (i.e., "target"
sequences) can be done with a very wide variety of random mutation
types - - to include point mutations and various kinds of
multicharacter or indel-type mutations. While point mutations and
other small indel-type mutations are more common than larger
multicharacter mutations, point mutations are by not means the only
type of mutation available. However, regardless of type, all have
essentially the same odds of successfully landing upon a target
sequence. There simply is no statistical advantage of one type of a
random mutation over any other type when it comes to finding targets
with unknown locations in sequence space.
> He then assumes
> that beneficial sequences are sparsely populated through the space,
They are. Even at low levels of functional complexity, potentially
beneficial sequences are significantly outnumbered by non-beneficial
sequences. And, this ratio only gets worse, exponentially worse, with
increasing size and/or specificity requirements.
> and
> argues that getting from one to the
> next becomes hopelessly improbable.
That's exactly right . . .
> Sean's model makes no account for facts.
>
> First, the distribution of point mutations in the amino acid residue
> sequence space is non-Uniform. Point mutations occur at base pairs, with
> transitions (purine to purine: A to G, G to A, our pyramidine to
> pyramidine: C to T, or T to C) being most common and transversions (purine
> to pyramidine or pyramidine to purine) being less common. This is further
> complicated by codon degeneracy. There are six different codon spellings
> for arginine (CGT, CGC, CGA, CGG,
> AGA, and AGG). For four of them (CGN), any
> point mutation in the third nucleotide will leave the amino acid uncanged.
> It is still arginine. For the other two (AGR), the amino acid is unchanged
> under transition mutation. Methionine, on the other hand, has only one
> spelling (ATG), and any point mutation will change it into a different
> codon.
Non-uniform distribution of various types of point mutation do not
significantly affect the odds of finding a target with an unknown
location in sequence space.
For example, say I have a blind man who has a limp that favors his
right side. This means that without some sort of outside direction,
he tends to walk in elliptical circles toward the right. Say that I
have a field that is 100 x 100 meters. In this field there are 5 red
1m square panels with an unknown location. On average, starting from
any one of these panels, how many steps would it take for our blind
man with the limp to find another panel?
The answer is the same regardless of if the blind man did or did not
have a limp or took 1 meter steps or 10 meter leaps. The odds of
success are essentially the same regardless.
> By point mutation, codons can only change to a different codon that differs
> by only one base pair. Glycine to valine occurs with transversion G->T in
> the center nucleic acid, but glycine to proline requires two point
> mutations: transversions in the first two nucleic acid (GG ->
> CC).Asparagine to histine requires only a transition in the first base
> pair. Thus, asparagine to histine is far more probable than glycine to
> proline.
Very good. But it doesn't make a significant difference when it comes
to finding targets in sequence space.
Oh, but you'll no doubt argue that functionally beneficial sequences
are more likely to have more higher-odds residues. That's a
reasonable argument. And, it would help a little bit, but not to any
significant degree. The basic problem remains the same - an
exponential decline in potential targets with increasing functional
complexity vs. non-target sequences.
Your argument is kinda like a situation where the dice are loaded to
favor a sixes over the other numbers by, say, 10%. Such loading would
certainly favor the production of a sequence with 10% more sixes.
However, this isn't enough to find a target sequence since the actual
location of the sixes within the sequence is also important due to the
"specificity" criterion. The same thing is true of the other
characters in the sequence. Producing the right ratio of characters
is nice, but it isn't enough. The specific location of the characters
in the sequence is also important to finding target sequences in
sequence space.
> Second, even under point mutation the sequence size is subject to change.
> Glutamine to Stop or the reverse involves a transition in the first base
> pair.
>
> Third, point mutations are not then only kind of mutation, Under an
> insertion, deletion, or inverson, a huge leap is taken across the sequence
> space, not a step in a random walk.
While true, as noted above, this doesn't improve the odds of success.
The odds of landing on a target with a leap or a small step are
essentially the same. You really do need to actually try and do some
real calculations for yourself here instead of spewing out a bunch of
facts that don't really have any bearing on the question at hand -
i.e., how to finding targets with unknown locations in sequence space
by a random search algorithm more effectively.
> Fourth, Sean is only modeling a single open reading frame with no
> relationship to the rest of the genome, yet mutations may occur in other
> regions such as promoters.
I'm taking the entire genomes of billions of individuals into account
as a starting point - coding and non-coding regions.
> I believe Howard Hershey has already explained many times why the
> beneficial sequences are not sparsely populated with a Uniform distribution
> over the sequence space.
There is a clustering effect to be sure. What you and Howard ignore
is the fact that this clustering effect gets less and less clustered
with each step up the ladder of functional complexity.
Howard's entire argument is based on what could exist without any
actual consideration of the odds that what is possible is also
likely. He argues that because the clustering seen at lower levels
could be maintained at higher levels as well, that it obviously
happened this way. That's a nice story, but what are the odds of it
actually representing reality? Howard doesn't produce such
statistical odds analysis - and neither do you. It seems good enough
for you to simply assert it without demonstration or predictive value
of any kind - not even an attempt at producing any odds analysis
whatsoever. Go figure . . .
Sean Pitman
www.DetectingDesign.com
Bruce Stephens
[...]
> While point mutations and other small indel-type mutations are more
> common than larger multicharacter mutations, point mutations are by
> not means the only type of mutation available. However, regardless
> of type, all have essentially the same odds of successfully landing
> upon a target sequence. There simply is no statistical advantage of
> one type of a random mutation over any other type when it comes to
> finding targets with unknown locations in sequence space.
As far as I understand it (and I don't know a great deal about the
field) that's not the experience of people who use genetic algorithms.
In that field the balance of the various kinds of mutation can make a
significant difference in finding maxima (where by "maxima" I think
typically one's looking for local maxima that are "good" rather than
actual global maxima).
[...]
heekster
Your knowledge of high school geometry even seems to be stunted. He
either walked in an ellipse or a circle. "Elliptical circles", like
so much of the other bullshit that you sling in here, is a nonsensical
term.
You still don't get it, do you?
You're using the wrong model, with the wrong assumptions, and no
facts. Facts are not what your statistical model says.
You failed.
Seanpit
>
> > If you have a particular sequence that is only one point mutation away
> > from some functional island cluster with a particular type of
> > beneficial function, you would place it right next to that island -
> > one step away from it. What about this is mysterious to you?
>
> The question of whether you are ordering the sequences into clusters
> based on function or based on sequence. The two are not the same
> thing and either will be problematic wrt producing actual clusters.
The clusters are based on sequences which happen to have a beneficial
function of a particular type.
> If you arrange proteins so that, in a 1000 aa system, each *sequence*
> is surrounded by the 999 different one-aa different *sequences*, most
> of the surrounding *sequences* will have at least some of the same
> named teleologic function as the sequence you specified as the
> teleologic goal.
Pretty much all of the 999aa surrounding sequences are likely to have
at least some useful level of the function in question. That's what
makes up the "island" of beneficial sequences of a certain type. The
island itself can be quite large in absolute numbers - into the
trillions of sequences. However, it can also be quite tiny relative
to the total size of sequence space. All that a search algorithm
needs to do is find at least the "edge" of any target island of
sequences within sequence space to be successful. Landing upon any
sequence that is part of a target island of sequences counts as a
success.
> But there will be significant variation in
> functionality for the named function.
As I've explained many times to you, quantitative differences don't
matter in this game. The very edge of the island where only the
tiniest degree of selective advantage of a certain type of function
still counts as a successful search.
> If you then vary each of the
> 999 proteins by one aa, most of the ones that will have lost the named
> function will remain lacking in the named teleologic function. But
> not all of them will. There are many examples of compensatory
> intragenic reversion where a second mutation restores function that
> was lost by the first mutation. In fact, for some mutations,
> heterozygosity between two different mutations, neither of which
> produces function by itself, can restore function. What do we
> consider such features. Worse, we know that, for some ancient
> functions, there can be so much sequence change that the proteins are
> not identifiable as similar on the basis of sequence (but they do have
> the same structure).
That's fine. Different widely separated islands in sequence space can
and often do carry essentially the same type of functionality. This
doesn't change the fact that the ratio of potentially beneficial vs.
non-beneficial is a tiny fraction and gets exponentially smaller and
smaller with each increase in the size and/or specificity
requirements.
> Worse yet, there can be (and often are)
> sequences that are similar in sequence to the starting (named)
> sequence, but that have different, but related, *functions* at various
> levels of *function*. In fact *some* of the sequences have dual or
> multiple functions. Say by binding both aldosterone and cortisol. Or
> by both acting as an organismal motility organ and a toxin export
> machine. When that happens, then further changes might emphasize one
> of these secondary functions, providing a chain of linkage with the
> function you claim is on an isolated functional island.
At lower levels, islands can and do overlap each other. Given the
relatively high-ratio of beneficial vs. non-beneficial at low-levels
of functional complexity, this is only to be expected on a fairly
common basis.
Tell me, what other higher-level system of equivalent functional
complexity overlaps a flagellar motility system?
> Thus, if you arrange your surface geography on the basis of *sequence*
> you do not get a tight clustering on the basis of *function*. You get
> a fuzzy network filled with holes of non-function and chains of
> functional linkage to distant sequences that don't resemble the
> starting point. I fail to see how arranging on the basis of sequence
> produces your model of compact single functions.
Again, at lower levels the islands have a bubble-gum type appearance
with holes and stretched bridges and the like. However, as the levels
of functional complexity increase, these hole grow exponentially
bigger and bigger and the bridges start to thin and then to snap until
the entire island is very quite isolated indeed.
For example, you could probably take a flagellar system and change
every single one of the underlying bp of DNA, on an individual basis,
without completely loosing the flagellar motility function. You could
probably change any two or three sequences at the same time as well -
or at least the vast majority of such options. There certainly is a
fair degree of flexibility. However, there is also a fair degree of
specificity to such a system that, though the island seems large in
absolute numbers, is very very tiny compared to the size of overall
sequence space. There is no known overlap with other systems of the
same, higher, or lower levels when it comes to minimum size and
specificity requirements.
> *And* that is not even thinking about the possible ways that the same
> function can arise by an entirely independent mechanism (as in lactase
> from antibodies or flagella like that seen in archaebacteria).
Again, many different islands can have the same basic function.
> In contrast, if you organize your surface geography in your model on
> the basis of level of a particular *function*, you will wind up with
> quite different sequences being close together and quite similar
> sequences being far apart (with the non-functional ones being
> "offshore", so to speak. And you would still have the problem of
> overlapping functionality (as in flagella that also act as adhesion
> systems or toxin transport systems or receptors that can bind both
> cortisol and aldosterone).
>
> This problem is a problem at *any* level of function.
There is no problem. The islands are arranged according to sequence
similarities that carry a particular type of function. Islands with
the same type of function can be multiple. They can also overlap.
None of these are actual problems for my view of sequence space. And,
none of these solve your problem for determining the odds of
successfully finding any part of a novel target island.
> Not to mention that no *actual* organism has ever had the capacity to
> search total sequence space.
That's a limitation for your view of evolution - not mine. Limited
search algorithms do not help find targets with unknown locations any
faster. All random search algorithms have essentially the same odds
of success.
> But I am sure that you already have answers to these minor problems.
And I'm sure you don't have any statistical odds analyzes as to how
your own search algorithm is likely to find a target over a given span
of time. Yeah yeah, I know that if the starting and ending points are
known ahead of time the problem is easy. The problem for you is that
this isn't the problem at hand. You only know one or the other, not
both, ahead of time.
Sean Pitman
www.DetectingDesign.com
Seanpit
wrote:
Have an actual reference?
Statistically, you understand, there is no advantage over one form of
random search vs. any other when it comes to finding targets with an
unknown location in a given space.
Sean Pitman
www.DetectingDesign.com
Seanpit
>
> >> First, the distribution of point mutations in the amino acid residue
> >> sequence space is non-Uniform. Point mutations occur at base pairs, with
> >> transitions (purine to purine: A to G, G to A, our pyramidine to
> >> pyramidine: C to T, or T to C) being most common and transversions (purine
> >> to pyramidine or pyramidine to purine) being less common. This is further
> >> complicated by codon degeneracy. There are six different codon spellings
> >> for arginine (CGT, CGC, CGA, CGG,
> >> AGA, and AGG). For four of them (CGN), any
> >> point mutation in the third nucleotide will leave the amino acid uncanged.
> >> It is still arginine. For the other two (AGR), the amino acid is unchanged
> >> under transition mutation. Methionine, on the other hand, has only one
> >> spelling (ATG), and any point mutation will change it into a different
> >> codon.
>
> >Non-uniform distribution of various types of point mutation do not
> >significantly affect the odds of finding a target with an unknown
> >location in sequence space.
>
> >For example, say I have a blind man who has a limp that favors his
> >right side. This means that without some sort of outside direction,
> >he tends to walk in elliptical circles toward the right.
>
> Your knowledge of high school geometry even seems to be stunted. He
> either walked in an ellipse or a circle. "Elliptical circles", like
> so much of the other bullshit that you sling in here, is a nonsensical
> term.
I'm just describing a circular path that isn't a perfect circle -
obviously.
> >> Fourth,Seanis only modeling a single open reading frame with no
> >> relationship to the rest of the genome, yet mutations may occur in other
> >> regions such as promoters.
>
> >I'm taking the entire genomes of billions of individuals into account
> >as a starting point - coding and non-coding regions.
>
> >> I believe Howard Hershey has already explained many times why the
> >> beneficial sequences are not sparsely populated with a Uniform distribution
> >> over the sequence space.
>
> >There is a clustering effect to be sure. What you and Howard ignore
> >is the fact that this clustering effect gets less and less clustered
> >with each step up the ladder of functional complexity.
>
> >Howard's entire argument is based on what could exist without any
> >actual consideration of the odds that what is possible is also
> >likely. He argues that because the clustering seen at lower levels
> >could be maintained at higher levels as well, that it obviously
> >happened this way. That's a nice story, but what are the odds of it
> >actually representing reality? Howard doesn't produce such
> >statistical odds analysis - and neither do you. It seems good enough
> >for you to simply assert it without demonstration or predictive value
> >of any kind - not even an attempt at producing any odds analysis
> >whatsoever. Go figure . . .
>
> You still don't get it, do you?
I guess not ; )
> You're using the wrong model, with the wrong assumptions, and no
> facts. Facts are not what your statistical model says. You failed.
What are the "facts"? Where, exactly, is my model or assumptions
mistaken? Where is your statistical model? Do you have any
statistical basis at all? Any odds analyzes whatsoever?
Sean Pitman
www.DetectingDesign.com
Seanpit
Humans and chimps do not produce viable much less fertile offspring -
lions and jaguars do.
Obviously then, there is a much greater genetic difference between
humans and chimps vs. lions and jaguars. Although not very much is
know about this genetic difference yet, recent research suggests that
the most significant functional genetic differences are to be found in
non-coding DNA.
> ================================================
> Lenny Flank
> "There are no loose threads in the web of life"
>
> Editor, Red and Black Publishershttp://www.RedandBlackPublishers.com
Sean Pitman
www.DetectingDesign.com
'Rev Dr' Lenny Flank
Again, you have to
> go beyond your idea that what is possible = what is likely. That's
> just not true.
Offhand, I'd say that something that actually happened, is, uh,
possible. Furthermore, it is, um, really really likely to have
happened.
Just a guess.
'Rev Dr' Lenny Flank
wrote:
(snip lots of arm-waving)
Sean, why is the move in "sequence space" from ape to human utterly
impossible, but the move in sequence space from ANY OTHER species to
another is NOT utterly impossible (particularly since humans and apes
are closer, genetically, than many other species that we KNJOW evolved
from each other)?
Would you answer that simple question for me, please?
Why is the move from the point in sequence space labelled "ape" to the
one labelled "human", more "statistically impossible" than the move
from the point in sequence space labelled "jaguar" to the one labelled
"cheetah"?
Other than your religious opinion that humans are special and simply
can not have evolved.
================================================
R. Baldwin
2b6759...@a29g2000pra.googlegroups.com:
As I told you, I have not proposed a model, so I don't need to defend
one. We are discussing YOUR model and whether it has merit.
Sequence space does not exist in the way you suppose, because sequence
length is variable, and it is modified by both genetic and environmental
factors that effect gene expression.
Potentially beneficial sequences do exist within sequence space to the
extent it can be defined. They change over time. They are not targets.
There is no goal involved in evolution. Sequences mutate over time, just
as the fitness landscape for the phenotype changes over time, and move
in whatever interesting direction they happen to move in by point
mutation, indels, or inversions.
"Different levels of functional complexity" is meaningless gibberish
that you have made up.
R. Baldwin
99f0-4cfe-8c6...@o40g2000prn.googlegroups.com:
WRONG! There is no advantage over random search when it comes to finding
targets with an unlocation in the set of ALL spaces. This is because the
set of all spaces includes mostly very random, very chaotic spaces.
There is a tremendous advantage when a search is tailored to a given space.
R. Baldwin
news:e66b0d5d-2338-4d5e...@i18g2000prf.googlegroups.com:
> On Nov 30, 1:31 pm, "R. Baldwin" <res0k...@nozirevBACKWARDS.net>
> wrote:
>>
>> Sean'smodel is hopelessly unrelated to reality. He assumes a random
>> walk through a "sequence space" defined by a given length of amino
>> acid residues. Since there are 20 possible values for each digit,
>> there are 20^N possible sequences, which he assumes will be arrived
>> at through a random walk, one point mutation at a time, with all
>> point mutations being equiprobable at the codon level (Uniform
>> distribution).
>
> Sequence space, by definition, is 20^N in size. Searching this
> sequence space for potentially beneficial sequences (i.e., "target"
> sequences) can be done with a very wide variety of random mutation
> types - - to include point mutations and various kinds of
> multicharacter or indel-type mutations. While point mutations and
> other small indel-type mutations are more common than larger
> multicharacter mutations, point mutations are by not means the only
> type of mutation available. However, regardless of type, all have
> essentially the same odds of successfully landing upon a target
> sequence. There simply is no statistical advantage of one type of a
> random mutation over any other type when it comes to finding targets
> with unknown locations in sequence space.
For DNA open reading frames, sequence space is by definition VARIABLE
in size, not 20^N in size, because the Stop delimeter is one of the
codons.
Mutations most expressly do NOT have the same odds of successfully
landing upon a "target sequence," for a variety of reasons that you
apparently don't get. (Hint one: the NFL Theorem does tell you anything
about one given search space). (Hint two: evolution does not have
targets).
>
>> He then assumes
>> that beneficial sequences are sparsely populated through the space,
>
> They are. Even at low levels of functional complexity, potentially
> beneficial sequences are significantly outnumbered by non-beneficial
> sequences. And, this ratio only gets worse, exponentially worse, with
> increasing size and/or specificity requirements.
Kindly forgive us for not taking your word for it.
>
>> and
>> argues that getting from one to the
>> next becomes hopelessly improbable.
>
> That's exactly right . . .
>
>> Sean's model makes no account for facts.
>>
>> First, the distribution of point mutations in the amino acid residue
>> sequence space is non-Uniform. Point mutations occur at base pairs,
>> with transitions (purine to purine: A to G, G to A, our pyramidine to
>> pyramidine: C to T, or T to C) being most common and transversions
>> (purine to pyramidine or pyramidine to purine) being less common.
>> This is further complicated by codon degeneracy. There are six
>> different codon spellings for arginine (CGT, CGC, CGA, CGG,
>> AGA, and AGG). For four of them (CGN), any
>> point mutation in the third nucleotide will leave the amino acid
>> uncanged. It is still arginine. For the other two (AGR), the amino
>> acid is unchanged under transition mutation. Methionine, on the other
>> hand, has only one spelling (ATG), and any point mutation will change
>> it into a different codon.
>
> Non-uniform distribution of various types of point mutation do not
> significantly affect the odds of finding a target with an unknown
> location in sequence space.
Yes, they do, if they also happen to have some correlation to the
"targets", as you insist on calling them.
>
> For example, say I have a blind man who has a limp that favors his
> right side. This means that without some sort of outside direction,
> he tends to walk in elliptical circles toward the right. Say that I
> have a field that is 100 x 100 meters. In this field there are 5 red
> 1m square panels with an unknown location. On average, starting from
> any one of these panels, how many steps would it take for our blind
> man with the limp to find another panel?
That would depend entirely on the distribution.
>
> The answer is the same regardless of if the blind man did or did not
> have a limp or took 1 meter steps or 10 meter leaps. The odds of
> success are essentially the same regardless.
Wrong. If the tendancies of the path taken happen to correspond with the
distribution, then the odds are affected.
>
>> By point mutation, codons can only change to a different codon that
>> differs by only one base pair. Glycine to valine occurs with
>> transversion G->T in the center nucleic acid, but glycine to proline
>> requires two point mutations: transversions in the first two nucleic
>> acid (GG -> CC).Asparagine to histine requires only a transition in
>> the first base pair. Thus, asparagine to histine is far more probable
>> than glycine to proline.
>
> Very good. But it doesn't make a significant difference when it comes
> to finding targets in sequence space.
Kindly demonstrate this assertion with math.
>
> Oh, but you'll no doubt argue that functionally beneficial sequences
> are more likely to have more higher-odds residues. That's a
> reasonable argument. And, it would help a little bit, but not to any
> significant degree. The basic problem remains the same - an
> exponential decline in potential targets with increasing functional
> complexity vs. non-target sequences.
Why don't you SHOW THE MATH, Sean? How do you know what a "significant
degree" is? How can you demonstrate this supposed exponential decline
when you abandon your Uniform distribution in favor of one that might
actually exist?
>
> Your argument is kinda like a situation where the dice are loaded to
> favor a sixes over the other numbers by, say, 10%. Such loading would
> certainly favor the production of a sequence with 10% more sixes.
> However, this isn't enough to find a target sequence since the actual
> location of the sixes within the sequence is also important due to the
> "specificity" criterion. The same thing is true of the other
> characters in the sequence. Producing the right ratio of characters
> is nice, but it isn't enough. The specific location of the characters
> in the sequence is also important to finding target sequences in
> sequence space.
>
Proove this. It is your model on the line. Remember, I am not the one
proposing a model of any sort.
>> Second, even under point mutation the sequence size is subject to
>> change. Glutamine to Stop or the reverse involves a transition in the
>> first base pair.
>>
>> Third, point mutations are not then only kind of mutation, Under an
>> insertion, deletion, or inverson, a huge leap is taken across the
>> sequence space, not a step in a random walk.
>
> While true, as noted above, this doesn't improve the odds of success.
> The odds of landing on a target with a leap or a small step are
> essentially the same. You really do need to actually try and do some
> real calculations for yourself here instead of spewing out a bunch of
> facts that don't really have any bearing on the question at hand -
> i.e., how to finding targets with unknown locations in sequence space
> by a random search algorithm more effectively.
Why don't YOU provide the real calculations, if you are all that
interested in anyone buying into your model?
>
>> Fourth, Sean is only modeling a single open reading frame with no
>> relationship to the rest of the genome, yet mutations may occur in
>> other regions such as promoters.
>
> I'm taking the entire genomes of billions of individuals into account
> as a starting point - coding and non-coding regions.
>
>> I believe Howard Hershey has already explained many times why the
>> beneficial sequences are not sparsely populated with a Uniform
>> distribution over the sequence space.
>
> There is a clustering effect to be sure. What you and Howard ignore
> is the fact that this clustering effect gets less and less clustered
> with each step up the ladder of functional complexity.
And you know this how? By misinterpreting one article in Pub Med?
>
> Howard's entire argument is based on what could exist without any
> actual consideration of the odds that what is possible is also
> likely. He argues that because the clustering seen at lower levels
> could be maintained at higher levels as well, that it obviously
> happened this way. That's a nice story, but what are the odds of it
> actually representing reality? Howard doesn't produce such
> statistical odds analysis - and neither do you. It seems good enough
> for you to simply assert it without demonstration or predictive value
> of any kind - not even an attempt at producing any odds analysis
> whatsoever. Go figure . . .
Again, I don't have to produce statistical analysis. I am not proposing
a model. You are proposing a model. I'm pointing out why it is a bad
one. You've at least admitted that I've offered reasonable points, which
is huge for you. But you are arm-waving them away without thinking. Show
us the math, Sean.
R. Baldwin
news:d95aa89a-dba2-4450...@r40g2000yqj.googlegroups.com:
> On 30 Nov, 17:17, Seanpit <sean...@gmail.com> wrote:
>> On Nov 29, 7:19 am, Vend <ven...@virgilio.it> wrote:
>>
>>
[snip]
>
>> the only problem is that non-target sequences vastly
>> outnumber the potential targets within sequence space and this ratio
>> only gets exponentially worse and worse with each increase in the
>> level of functional complexity.
>
> What do you mean by "non-target" sequence?
>
All the ones that weren't found?
:D
R. Baldwin
8052-65c...@v42g2000yqv.googlegroups.com:
> On Dec 1, 3:01 pm, Seanpit <sean...@gmail.com> wrote:
>
> Again, you have to
>> go beyond your idea that what is possible = what is likely. That's
>> just not true.
>
>
> Offhand, I'd say that something that actually happened, is, uh,
> possible. Furthermore, it is, um, really really likely to have
> happened.
>
> Just a guess.
Perhaps you need to consider sufficiently small values of 1.
wf3h
wrote:
>
> What are the "facts"? Where, exactly, is my model or assumptions
> mistaken? Where is your statistical model? Do you have any
> statistical basis at all? Any odds analyzes whatsoever?
>
we await the same for sean...he's presented precisely
no
evidence in favor of his use of the most failed idea in human history
Kent Paul Dolan
> Non-uniform distribution of various types of point
> mutation do not significantly affect the odds of
> finding a target with an unknown location in
> sequence space.
You keep pimping this "odds of finding' bogosity,
because you just can't get your mind around the idea
that evolution isn't _trying_ to find anything, is
not doing a deterministic search for what it
eventually finds, but is behaving as if it were
doing a fuzzily directed search for _anything that
improves fitness_.
You are trying to look backward from the end product
and claim that "evolution was obviously seeking this
result".
Well, no it wasn't, that's teleology.
Try to distinguish the intent-free observed behavior
of evolution from the claimed intent-laden behavior
of your purported deity.
Your faux deity "wanted" to create a strong,
look-alike intelligent organism to be the residence
of "souls", and an interesting collection of
species by which that boss organism could be
entertained, assisted, and/or fed...
Evolution has no intent, it is just math in action.
Evolution isn't even anthropomorphic, so it doesn't
seek _at all_. When improved fitness enters the
breeding cohort, the math of evolution raises the
fraction of alleles in the population that encode
the improvement, pretty much full stop.
Something called crossovers then randomly match up
improved alleles once upon a time on different
strands of DNA to be on the same strand, and the
math of evolution again aimlessly but persistently,
enhances the fraction of DNA strands containing a
superior fraction of fitness from its combined
alleles.
This simple, easily understood characterization of
how evolution works, makes all your talk about the
difficulty of crossing gaps just so much word salad.
Evolution has no goals, no intents, no required
directions, does no working backwards in time to
lure itself to a highly fit newly evolved species.
Evolution just has purely mathematical behaviors, so
if a gap is somehow "too big", evolution doesn't get
hurt feelings about that fact. Natural selection,
the directional part of evolution, doesn't cross
gaps _at all_, it just takes advantage of random
variation's having done so entirely by accident.
Evolution's behavior is just unlikely to include
crossing that big gap in a single jump, or maybe
ever, and so what?
Natural selection grades on a fitness curve.
NS will instead amplify the breeding cohort allele
fraction of recently arrived or long advancing
variations that _do_ provide improved fitness, but
it doesn't go have a few beers with the boys
afterwards to celebrate.
Math is a total abstainer.
Lots of those little improvements, by the nature of
vector addition, result in a big improvement,
usually but not always, eventually one associated
with a big change in the phenotype, again, pretty
much, full stop.
When you learn to "do the math" at a gut level, this
stuff won't be so utterly incomprehensible to you.
But of course to do that, you'd have to junk
everything you learned in bible school.
xanthian.
TomS
<d77727e0-4c2c-4b6b...@w3g2000yqc.googlegroups.com>, hersheyh
stated..."
>
>On Dec 1, 2:57=A0pm, Seanpit <sean...@gmail.com> wrote:
>> < snip >
>>
>> > > There simply is no
>> > > comparable evolutionary model of sequence space - none whatsoever.
>>
>> > Again, because it is the WRONG MODEL!
>>
>
>The only part of sequence space that is relevant is that which
>actually exists in the relevant organisms. Total sequence space has
>about as much relevance as the size of the universe does to the space
>taken up by starbucks coffee shops. My understanding is that
>starbucks does not place its shops randomly in the universe, but tend
>to place them in places close that get a certain amount of human
>traffic.
However, what part of the sequence space is relevant to an
"intelligent designer"?
As long as we have no restrictions on what an ID might do,
it seems that it is the whole sequence space. (One could
argue that what is relevant to an ID is much more than the
sequence space, but let's be conservative about this.)
This particular argument for ID, if it were really a sound
argument, would be an argument *against* ID. It would show
that ID is *less* probable than evolution.
Ron O
Lying again. Just what you can expect from Sean. Running and
pretending is just a way of life for someone like you. You can't even
deny it because then you would be openly telling a lie, and for some
reason your weird mentality won't allow you to do that. All you can
do is blame someone else for your own problem and run and pretend that
you aren't lying and just trying to deflect the issue. Your running
and pretending is the issue at hand. Just deny that you have been
running.
Ron Okimoto
Seanpit
> Seanpit <seanpitnos...@naturalselection.0catch.com> wrote in news:de975572-
> 99f0-4cfe-8c63-991fdfa4f...@o40g2000prn.googlegroups.com:
Not if you don't already know that that space contains target
sequences . . .
Sean Pitman
www.DetectingDesign.com
Seanpit
The targets are protein-based. It is the structural thresholds of the
target systems that are in question here. These targets are in
sequence spaces of 20^N and the N in this formula is defined by the
minimum size requirement of the target systems.
> Mutations most expressly do NOT have the same odds of successfully
> landing upon a "target sequence," for a variety of reasons that you
> apparently don't get. (Hint one: the NFL Theorem does tell you anything
> about one given search space).
I'm not sure what you are talking about. If the search space has very
rare targets, and this ratio of potentail targets vs. non-targets gets
more and more rare at higher and higher levels of functional
complexity, I'm not sure I see that you have any argument here . . .
> (Hint two: evolution does not have targets).
That's where you're wrong. The "targets" for the evolutionary
mechanism of RM/NS are functionally beneficial sequences in sequence
space. Those are in fact the "targets" for evolution. If RM/NS does
not find such targets, evolution simply doesn't happen.
> >> He then assumes
> >> that beneficial sequences are sparsely populated through the space,
>
> > They are. Even at low levels of functional complexity, potentially
> > beneficial sequences are significantly outnumbered by non-beneficial
> > sequences. And, this ratio only gets worse, exponentially worse, with
> > increasing size and/or specificity requirements.
>
> Kindly forgive us for not taking your word for it.
Who asked you to take my word for it? Produce your own counter
analysis to prove me wrong . . .
http://www.detectingdesign.com/flagellum.html#Calculation
> > Non-uniform distribution of various types of point mutation do not
> > significantly affect the odds of finding a target with an unknown
> > location in sequence space.
>
> Yes, they do, if they also happen to have some correlation to the
> "targets", as you insist on calling them.
Not if the non-uniformitarity of targets is itself fairly uniformly
distributed - as in non-uniform clusters of beneficial targets into
islands that are themselves widely scattered throughout sequence
space. And, at higher and higher levels of functional complexity,
this scattering effect becomes more and more pronounced. This is in
fact reflected in actual sequence comparisons of known beneficial
protein-based systems. Look it up.
In short, potentially beneficial targets simply are not all clustered
together into one tiny corner of sequence space like they would have
to be for your proposed mechanism to actually work effectively beyond
extremely low levels of functional complexity.
> > For example, say I have a blind man who has a limp that favors his
> > right side. This means that without some sort of outside direction,
> > he tends to walk in elliptical circles toward the right. Say that I
> > have a field that is 100 x 100 meters. In this field there are 5 red
> > 1m square panels with an unknown location. On average, starting from
> > any one of these panels, how many steps would it take for our blind
> > man with the limp to find another panel?
>
> That would depend entirely on the distribution.
Not if you don't know the actual location or distribution relative to
your starting point ahead of time.
> > The answer is the same regardless of if the blind man did or did not
> > have a limp or took 1 meter steps or 10 meter leaps. The odds of
> > success are essentially the same regardless.
>
> Wrong. If the tendancies of the path taken happen to correspond with the
> distribution, then the odds are affected.
You don't know the distribution ahead of time. So, the odds of
success are not affected a priori. If you think the odds are good
that the targets are going to be significantly clustered around your
starting point, by all means, please do provide the statistical
evidence to support this otherwise bald assertion.
> >> By point mutation, codons can only change to a different codon that
> >> differs by only one base pair. Glycine to valine occurs with
> >> transversion G->T in the center nucleic acid, but glycine to proline
> >> requires two point mutations: transversions in the first two nucleic
> >> acid (GG -> CC).Asparagine to histine requires only a transition in
> >> the first base pair. Thus, asparagine to histine is far more probable
> >> than glycine to proline.
>
> > Very good. But it doesn't make a significant difference when it comes
> > to finding targets in sequence space.
>
> Kindly demonstrate this assertion with math.
http://www.detectingdesign.com/flagellum.html#Calculation
Now it is your turn to kindly demonstrate your assertion of
significant clustering, regardless of the level of functional
complexity, with math - some real odds analysis please . . .
> > While true, as noted above, this doesn't improve the odds of success.
> > The odds of landing on a target with a leap or a small step are
> > essentially the same. You really do need to actually try and do some
> > real calculations for yourself here instead of spewing out a bunch of
> > facts that don't really have any bearing on the question at hand -
> > i.e., how to finding targets with unknown locations in sequence space
> > by a random search algorithm more effectively.
>
> Why don't YOU provide the real calculations, if you are all that
> interested in anyone buying into your model?
I have provided real calculations. You have yet to do so. Please,
where are your own counter calculations? I've yet to see even an
attempt by you or anyone else in this forum to use real math or odds
analysis. It is like you guys have some sort of aversion to sticking
real numbers into real formulas to back up your bald assertions. Why
is that? Scared of the implications of potential falsification?
< snip >
Sean Pitman
www.DetectingDesign.com
wf3h
> > interested in anyone buying into your model?
>
> I have provided real calculations. You have yet to do so. Please,
> where are your own counter calculations? I've yet to see even an
> attempt by you or anyone else in this forum to use real math or odds
> analysis. It is like you guys have some sort of aversion to sticking
> real numbers into real formulas to back up your bald assertions. Why
> is that? Scared of the implications of potential falsification?
>
double standard.
what we see is sean 'offering proof' that evolution is false. be that
as it may, it in no way supports sean's position that creationism is
true because evolution is false. sean thinks that, because he's
'demonstrated evolution is false', he need offer no proof at all
supporting creationism...it's simply true by default
given the fact that creationism is the most commonly used failed idea
in history...it's failed 100% of the time it's been used, sean should
at least make a faint hearted effort at meeting his own standards. he
insists scientists do statistical analysis on prospective mechanisms.
he, however, seems to be immune from his own standards of proof
which is what one expects from a creationist.
hersheyh
Which, in fact, is the case. The searchable space for *real*
biological systems starts with a genome highly enriched in functional
sequences and modifies them *to the extent* that can reasonably
reached by RM given NS. Not surprisingly, this tends to keep the
modifications within the realm of sequences that have some functional
utility. And the end points also wind up in the subset of sequences
that have function. Thus we observe gene families and sequence
homology as a consequence of the search mechanism.
>
> Sean Pitmanwww.DetectingDesign.com
gregwrld
I can't wait for Sean to
demonstrate how he knows
how many possible solutions
("targets" in his personal
nomenclature) there are for any
problem evolution must
overcome for a species to
adapt (i.e., continue to
reproduce) or why that lack
of a number doesn't affect his
odds.
gregwrld
_Arthur
HH, is it a valid hypothesis that using a sequence encoding a
demonstrably useful protein, is _more_ likely to lead to a protein
with a "new" biological usefulness, as opposed to starting from a
"junk" DNA sequence, with a start and a stop codon, but random, or
repetitive, or frame-shifted, content ?
hersheyh
And the search space you mention has no connection to *real* search
spaces. It *assumes* that real search space is either "total sequence
space", which no real genome has or "random samples of total sequence
space". *Real* starting points match neither assumption. *Real*
genomes are a highly biased subset of "total sequence space". It is
*even* a highly biased subset of "viable protein sequence space".
That renders any probability based on this false assumption GIGO. One
of the most ignorant and simple violations of using probability is to
*assume* randomness where it does not exist. You cannot do a
probability that *requires* the assumption of randomness when the
evidence directly tells you that that assumption is bull shit.
>
> > Mutations most expressly do NOT have the same odds of successfully
> > landing upon a "target sequence," for a variety of reasons that you
> > apparently don't get. (Hint one: the NFL Theorem does tell you anything
> > about one given search space).
>
> I'm not sure what you are talking about. If the search space has very
> rare targets, and this ratio of potentail targets vs. non-targets gets
> more and more rare at higher and higher levels of functional
> complexity, I'm not sure I see that you have any argument here . . .
>
> > (Hint two: evolution does not have targets).
>
> That's where you're wrong. The "targets" for the evolutionary
> mechanism of RM/NS are functionally beneficial sequences in sequence
> space. Those are in fact the "targets" for evolution. If RM/NS does
> not find such targets, evolution simply doesn't happen.
Yep. And to the extent that some "targets" did not exist within a
short mutational distance of some pre-existing sequence or set of
motifs in some genome, that particular evolutionary solution did not
happen. What you have to do is show that some *specific* step that
*did* happen could not, even in principle, have *actually* happened.
Using a probability based on a false assumption of randomness of the
starting point simply will not do that.
> > >> He then assumes
> > >> that beneficial sequences are sparsely populated through the space,
>
> > > They are. Even at low levels of functional complexity, potentially
> > > beneficial sequences are significantly outnumbered by non-beneficial
> > > sequences. And, this ratio only gets worse, exponentially worse, with
> > > increasing size and/or specificity requirements.
>
> > Kindly forgive us for not taking your word for it.
>
> Who asked you to take my word for it? Produce your own counter
> analysis to prove me wrong . . .
>
> http://www.detectingdesign.com/flagellum.html#Calculation
There is no relevant analysis of that specific point in this garbage
you call a "calculation". First you have to tell us how you organize
total sequence space: by sequence similarity or by function. Then you
have to demonstrate the relationship between these two features with
*specific* examples of the relationship between function and
sequence. That means you have to tell us about overlapping function,
about subfunction, and how you deal with chimeric duplications and
other mutational steps that are not point mutations. All I see is
hand-waving bull shit.
>
> > > Non-uniform distribution of various types of point mutation do not
> > > significantly affect the odds of finding a target with an unknown
> > > location in sequence space.
>
> > Yes, they do, if they also happen to have some correlation to the
> > "targets", as you insist on calling them.
>
> Not if the non-uniformitarity of targets is itself fairly uniformly
> distributed - as in non-uniform clusters of beneficial targets into
> islands that are themselves widely scattered throughout sequence
> space. And, at higher and higher levels of functional complexity,
> this scattering effect becomes more and more pronounced. This is in
> fact reflected in actual sequence comparisons of known beneficial
> protein-based systems. Look it up.
The above is completely incomprehensible. You have not demonstrated
that beneficial targets form islands if they are organized by sequence
*and* if you remember that the current distribution of functional
sequences does not necessarily (and, in fact, is unlikely to) the
totality of sequences that can perform a function.
As one of your citations points out, even random protein sequences
generate specific functions like ATP binding at much higher rates than
what you propose. And ATP-binding is certainly a "potentially
beneficial target". Of course, since *real* starting points involve
genomes that already have ATP-binding moieties, borrowing what already
exists is a more likely mechanism than random assembly.
>
> In short, potentially beneficial targets simply are not all clustered
> together into one tiny corner of sequence space like they would have
> to be for your proposed mechanism to actually work effectively beyond
> extremely low levels of functional complexity.
>
> > > For example, say I have a blind man who has a limp that favors his
> > > right side. This means that without some sort of outside direction,
> > > he tends to walk in elliptical circles toward the right. Say that I
> > > have a field that is 100 x 100 meters. In this field there are 5 red
> > > 1m square panels with an unknown location. On average, starting from
> > > any one of these panels, how many steps would it take for our blind
> > > man with the limp to find another panel?
>
> > That would depend entirely on the distribution.
>
> Not if you don't know the actual location or distribution relative to
> your starting point ahead of time.
>
> > > The answer is the same regardless of if the blind man did or did not
> > > have a limp or took 1 meter steps or 10 meter leaps. The odds of
> > > success are essentially the same regardless.
>
> > Wrong. If the tendancies of the path taken happen to correspond with the
> > distribution, then the odds are affected.
>
> You don't know the distribution ahead of time. So, the odds of
> success are not affected a priori. If you think the odds are good
> that the targets are going to be significantly clustered around your
> starting point, by all means, please do provide the statistical
> evidence to support this otherwise bald assertion.
New functions tend to have structures (and sequence to a lesser
extent) clustered near existing functions. Since existing functions
are the *real* starting points, calculations based on the assumption
that they are not the real starting points are pointless.
> > >> By point mutation, codons can only change to a different codon that
> > >> differs by only one base pair. Glycine to valine occurs with
> > >> transversion G->T in the center nucleic acid, but glycine to proline
> > >> requires two point mutations: transversions in the first two nucleic
> > >> acid (GG -> CC).Asparagine to histine requires only a transition in
> > >> the first base pair. Thus, asparagine to histine is far more probable
> > >> than glycine to proline.
>
> > > Very good. But it doesn't make a significant difference when it comes
> > > to finding targets in sequence space.
>
> > Kindly demonstrate this assertion with math.
>
> http://www.detectingdesign.com/flagellum.html#Calculation
>
> Now it is your turn to kindly demonstrate your assertion of
> significant clustering, regardless of the level of functional
> complexity, with math - some real odds analysis please . . .
>
> > > While true, as noted above, this doesn't improve the odds of success.
> > > The odds of landing on a target with a leap or a small step are
> > > essentially the same. You really do need to actually try and do some
> > > real calculations for yourself here instead of spewing out a bunch of
> > > facts that don't really have any bearing on the question at hand -
> > > i.e., how to finding targets with unknown locations in sequence space
> > > by a random search algorithm more effectively.
>
> > Why don't YOU provide the real calculations, if you are all that
> > interested in anyone buying into your model?
>
> I have provided real calculations.
Only if you consider calculations that are GIGO numerology (because
they are based on false assumptions that you *know* are false) to be
"real".
> You have yet to do so. Please,
> where are your own counter calculations?
Statistical calculations based on false assumptions of randomness are
bogus numerology.
> I've yet to see even an
> attempt by you or anyone else in this forum to use real math or odds
> analysis.
Nobody but you is ignorant enough to make calculations based on false
premises. You do it because such bogus numerology is all you have.
> It is like you guys have some sort of aversion to sticking
> real numbers into real formulas to back up your bald assertions. Why
> is that? Scared of the implications of potential falsification?
No. Not so arrogant and ignorant as to think that using false premises
to do bogus math is science.
> < snip >
>
> Sean Pitmanwww.DetectingDesign.com
wf3h
> On Dec 11, 11:17 am, Seanpit <sean...@gmail.com> wrote:
>
>
> > The targets are protein-based. It is the structural thresholds of the
> > target systems that are in question here. These targets are in
> > sequence spaces of 20^N and the N in this formula is defined by the
> > minimum size requirement of the target systems.
>
> And the search space you mention has no connection to *real* search
> spaces. It *assumes* that real search space is either "total sequence
> space", which no real genome has or "random samples of total sequence
> space". *Real* starting points match neither assumption. *Real*
> genomes are a highly biased subset of "total sequence space". It is
> *even* a highly biased subset of "viable protein sequence space".
> That renders any probability based on this false assumption GIGO. One
> of the most ignorant and simple violations of using probability is to
> *assume* randomness where it does not exist. You cannot do a
> probability that *requires* the assumption of randomness when the
> evidence directly tells you that that assumption is bull shit.
>
>
the path to creationism has, as its starting point, bullshit
in any case, i'm a physical chemist, not a biochemist, or biologist.
but it seems logical to exclude, as a part of the 'sequence space'
those permutations which are excluded by kinetics and thermodynamics.
DNA, as a molecule, has primary, secondary and tertiary structures.
mutations must happen governed by the laws of kinetics and thermo as
they apply to these.
is this what sean is ignoring?...at least part of what he's ignoring,
in addition to his ignorance of the whole protocol of scientific
methodology, which is another story...
John Stockwell
wrote:
The point is that it isn't random and we aren't talking about a
search. You are attempting to use (abuse) the NFL theorems in
the way that Dembski did in his book.
We are doing the equivalent
of firing a shotgun at a group of birds. While the odds of a
particular lead shot hitting a particular bird is low, the odds of
some
lead shot hitting some bird is 1. There is no predetermined
particular target.
-John
>
> Sean Pitmanwww.DetectingDesign.com
geo...@hotmail.com
> Seanpit <seanpitnos...@naturalselection.0catch.com> wrote in news:de975572-
> 99f0-4cfe-8c63-991fdfa4f...@o40g2000prn.googlegroups.com:
This is what annoyed me most about Dembski's papers and finally made
me realise he was a fraud.
The averaging-over-all-possible-spaces that he does is pure crap.
There is no reason to do it.
The amount of possible fitness spaces is quite a lot. Most are junk,
and Dembski reckons evolution is working on all those junky spaces.
Why? Because he's a fraud (I'm being polite here; I bet he's an
excellent mathematician, which means this mistake can only be intended
to deceive).
But it's quite obvious that nature's fitness space is not random.
Indeed, this is the whole point Darwin was making - it's why we have
natural selection! For example, leg sizes make nice curvy slopes in
fitness space, because long legs can mean more grub. Or better
escapes. Why is Dembski considering scenarios where leg size has
nothing to do with fitness? Because he's a fraud.
Nature's fitness space is full of hills and slopes. Dembski is lying
in his math when he adds the random ones. Perhaps he'll admit that in
ten years, eh?
hersheyh
sounds a lot like him) has done a video.
Paul J Gans
I, speaking as another physical chemist, theoritical type,
can't answer that. I think that his entire model is bad. It
reminds me of the old physicist joke about "consider a spherical
horse".
In its simplest form I assume that he is talking about a space
consisting of all possible amino acid sequences. I'd model a
sequence as a sequence of digits in base 20, each number
corresponding to a given amino acid. Then all possible sequences
of length N would be 20^N. For N of any real size, the number
of possible sequences would be quite large.
The problem is then to take a naturally occuring sequence, X, of
length LX and transform it to another sequence Y, of length LY.
Sean seems to want to calculate the ab initio probability of
such a process. That is already a problem since there are a
large number of proteins that could be transformed into Y. But
never mind that.
Sean seems to *assume* that the initial and final lengths are
the same, I.e. LX = LY. However that's not only not necessarily
true, but intermediate states could have totally different lengths.
Further, Sean seems to assume that the only change that is
possible is that one may change residue k (or digit k, if one
thinks of the sequence as a number) to another digit m, all
such changes being equally likely. That's wrong on the face
of it.
But putting that aside, there are many other possible mechanisms
to get from X to Y. Some involve inclusions of entire subsequences
and elisons of other subsequences. Some involve even more complex
changes.
As a result, Sean's model is fatally flawed. As a result, any
calculations based on it are fatally flawed. Do we have a better
model? That's outside my area of competence, but my *guess* is
that we don't know nearly enough about protein evolution, though
what we've seen certainly does not indicate that it is impossible.
--
--- Paul J. Gans
wf3h
>
> But putting that aside, there are many other possible mechanisms
> to get from X to Y. Some involve inclusions of entire subsequences
> and elisons of other subsequences. Some involve even more complex
> changes.
what i love is that sean says he knows enough about these mechanisms
to exclude them. who knew such encyclopedic knowledge existed!
>
> As a result, Sean's model is fatally flawed. As a result, any
> calculations based on it are fatally flawed. Do we have a better
> model? That's outside my area of competence, but my *guess* is
> that we don't know nearly enough about protein evolution, though
> what we've seen certainly does not indicate that it is impossible.
>
i know...it's risible that sean says, given the 'decades' of research,
no mechanisms are possible so only the god mechanism is left. he's
quite the comedian
Paul J Gans
Well, he's a true believer. I don't see much point in long
arguments with true believers. Reason won't get through. His
position is an item of faith.
Every so often I get involved with him, most recently was an
attempt to show that there are ways to get around the "exponential
difficulty" he talks about. But he'd have none of it.
Seanpit
> "'Rev Dr' Lenny Flank" <lfl...@yahoo.com> wrote in news:243ac663-0fa7-4fb8-
>
> > On Dec 1, 3:01 pm, Seanpit <sean...@gmail.com> wrote:
>
> > Again, you have to
> >> go beyond your idea that what is possible = what is likely. That's
> >> just not true.
>
> > Offhand, I'd say that something that actually happened, is, uh,
> > possible. Furthermore, it is, um, really really likely to have
> > happened.
>
> > Just a guess.
LOL - we all know it happened. After all, its here. The question
isn't if it happened or not. The question is if it happened via the
particular mechanism of RM/NS.
So, how do you "know" it happened by the particular mechanism of RM/
NS? Did you see it happen by that particular mechanism? If not, how
do you knpw that this mechanism actually did the job or is even
remotely likely to have done the job? Hmmm? What is the basis of
your belief in this mechanism? - besides blind faith, just-so stories,
and bald assertions that is?
> Perhaps you need to consider sufficiently small values of 1.
If only it were that easy . . .
Sean Pitman
www.DetectingDesign.com
'Rev Dr' Lenny Flank
> On Dec 1, 8:59 pm, "R. Baldwin" <res0k...@nozirevBACKWARDS.net> wrote:
>
> > "'Rev Dr' Lenny Flank" <lfl...@yahoo.com> wrote in news:243ac663-0fa7-4fb8-
> > 8052-65c58bb23...@v42g2000yqv.googlegroups.com:
>
> > > On Dec 1, 3:01 pm, Seanpit <sean...@gmail.com> wrote:
>
> > > Again, you have to
> > >> go beyond your idea that what is possible = what is likely. That's
> > >> just not true.
>
> > > Offhand, I'd say that something that actually happened, is, uh,
> > > possible. Furthermore, it is, um, really really likely to have
> > > happened.
>
> > > Just a guess.
>
> LOL - we all know it happened. After all, its here. The question
> isn't if it happened or not. The question is if it happened via the
> particular mechanism of RM/NS.
>
> So, how do you "know" it happened by the particular mechanism of RM/
> NS?
Because that's the ONLY mechanism we know that CAN produce it.
If you disagree, by all means go ahead and show us another mechanism.
Show us a gene that you think was designed, show us what mechanism the
designer used to produce it, then show us an example of the designer
using a similar mechanism today do . . . well . . ., anything.
Anything at all whatsoever anywhere.
Time for you to run away again,
Sean . . . . . . . . . . . . . . . . . . . . . . .. . . . . . .. . . . . . . . .. .
'Rev Dr' Lenny Flank
(snip)
> So, how do you "know" it happened by the particular mechanism of RM/
> NS? Did you see it happen by that particular mechanism? If not, how
> do you knpw that this mechanism actually did the job or is even
> remotely likely to have done the job? Hmmm? What is the basis of
> your belief in this mechanism? - besides blind faith, just-so stories,
> and bald assertions that is?
How do you "know" that Lee Harvey Oswald shot Kennedy? How do you
"know" that OJ Simpson killed his ex-wife? Did you see it happen?
Did ANYBODY see it happen? What then is the basis of your belief that
it happened? Hmmmm? Besides blind faith, just-so stories, and bald
assertions, that is?
Speaking of which . . .
Can you point me towards an example of any non-human intelligent
designer doing . . . well . . . anything? Anything at all? Anything
at all whatsoever? Anywhere? At any time?
Come on, Sean -- show me one gene that you think was intelligently
designed, and show me how the designer designed it.
Just one.
One?
ONE ????????????
Put up or shut up, Sean.
wf3h
>
> LOL - we all know it happened. After all, its here. The question
> isn't if it happened or not. The question is if it happened via the
> particular mechanism of RM/NS.
>
> So, how do you "know" it happened by the particular mechanism of RM/
> NS? Did you see it happen by that particular mechanism? If not, how
> do you knpw that this mechanism actually did the job or is even
> remotely likely to have done the job? Hmmm? What is the basis of
> your belief in this mechanism? - besides blind faith, just-so stories,
> and bald assertions that is?
gee. let me try a mechanism that will make sense to sean since it's
kind of what he believes....
in the beginning...
make you feel better?
seanpi...@naturalselection.0catch.com
> Seanpit <sean...@gmail.com> wrote in news:6a95e3f8-9b8f-4357-9047-
> 2b6759697...@a29g2000pra.googlegroups.com:
>
>
>
> > < snip >
>
> >> > There simply is no
> >> > comparable evolutionary model of sequence space - none whatsoever.
>
> >> Again, because it is the WRONG MODEL!
>
> > within that space. There is a ratio of potential targets vs. non-
> > targets within sequence space. Different levels of functional
> > complexity have different ratios of targets vs. non-targets. All of
> > these are non-arguable facts. What model of sequence space do you
> > have if you think my model is wrong? Please, do explain your own
> > model - or the model of anyone else that you think has a better idea
> > for that matter. I'm asking for a model of the appearance or
> > character of something we know does actually exist. What is your
> > model?
>
> As I told you, I have not proposed a model, so I don't need to defend
> one. We are discussing YOUR model and whether it has merit.
Ah, but you have proposed odds. You said that you believed that the
mechanism of RM/NS had a 100% chance of producing 1000+ fsaar systems
given a few billion years of time. That's what you said. So, you
must have some sort of basis for this claim - do you not?
Now, if your basis, as is common, is that sequence homologies indicate
a common origin of some kind, I most certainly agree! Of course
homologies strongly support the hypothesis of a common origin. That's
not in question here.
What is in question here is the mechanism that produced the functional
differences. Homologies aren't the problem. The functional
differences are the problem. How were these produced? By what
mechanism? You say that it is 100% certain that RM/NS did the job -
well beyond the 1000 fsaar threshold. Based on what? How do you
know?
> Sequence space does not exist in the way you suppose, because sequence
> length is variable,
So is sequence space. As length varies, so does sequence space - by
20^N. Is this mistaken? ; )
> and it is modified by both genetic and environmental
> factors that effect gene expression.
That's right . . . How is that a problem for my position?
> Potentially beneficial sequences do exist within sequence space to the
> extent it can be defined.
Again, right in line with my position . . .
> They change over time.
They certainly can change, but not just because of the elapse of
time. Target locations remain static if the only change is time.
Now, there can be a change in target expression over time with various
sequences on a given island expressed by a given population over time
- a kind of local random walk on the same functional island. However,
this doesn't explain how to find novel islands via RM/NS over a given
span of time - - even if that span seems like a long time (i.e., a
few billion years).
> They are not targets.
Yes, they are. If RM/NS didn't find these sequences, evolution
wouldn't happen.
> There is no goal involved in evolution.
There is no specific goal - that's true. But, this doesn't mean there
is no goal at all for evolution. That's most certainly not true. If
RM/NS never did find qualitatively new targets, Darwinian-style
evolution simply wouldn't happen. In order for this type of evolution
to take place, qualitatively novel targets do in fact need to be
found.
> Sequences mutate over time,
Yes they do . . .
> just
> as the fitness landscape for the phenotype changes over time,
It most certainly can.
> and move
> in whatever interesting direction they happen to move in by point
> mutation, indels, or inversions.
Right again . . .
It is just that the odds of moving a target so that it matches up with
a random searcher are the same as the odds of moving a searcher in
space to match up with a target. And, since targets move less often
than a large population of searchers, the odds of success are
essentially dependent upon the movements of the searchers over a given
span of time.
For example, say we have a target of a specific size in a large field
of a specific size. Let's say that our random walker takes random
steps of a certain size and that the target itself moves within the
field at a rate that is less than the rate of movement of the
searcher. Are the odds of the searcher finding the target improved
over having a static unmoving target?
> "Different levels of functional complexity" is meaningless gibberish
> that you have made up.
Ok, tell me how to make a flagellar motility system with less than
1000aa? - in any arrangement? Compare this to a lactase enzyme - no
more than 300aa needed. And you think these different functional
systems are on the same level of functional complexity? How is that
again?
Sean Pitman
www.DetectingDesign.com
seanpi...@naturalselection.0catch.com
Funny . . . I was just thinking this sounds a lot like Howard! ; )
Nice spoof - - of a strawman.
Sean Pitman
www.DetectingDesign.com
seanpi...@naturalselection.0catch.com
> wf3h <w...@vsswireless.net> wrote:
> >On Dec 11, 7:16 pm, Paul J Gans <g...@panix.com> wrote:
>
> >> But putting that aside, there are many other possible mechanisms
> >> to get from X to Y. Some involve inclusions of entire subsequences
> >> and elisons of other subsequences. Some involve even more complex
> >> changes.
> >what i love is that sean says he knows enough about these mechanisms
> >to exclude them. who knew such encyclopedic knowledge existed!
>
> >> As a result, Sean's model is fatally flawed. As a result, any
> >> calculations based on it are fatally flawed. Do we have a better
> >> model? That's outside my area of competence, but my *guess* is
> >> that we don't know nearly enough about protein evolution, though
> >> what we've seen certainly does not indicate that it is impossible.
>
> >i know...it's risible that sean says, given the 'decades' of research,
> >no mechanisms are possible so only the god mechanism is left. he's
> >quite the comedian
>
> Well, he's a true believer. I don't see much point in long
> arguments with true believers. Reason won't get through. His
> position is an item of faith.
Just like your blind faith in the ToE? ; )
> Every so often I get involved with him, most recently was an
> attempt to show that there are ways to get around the "exponential
> difficulty" he talks about. But he'd have none of it.
You went off on some method to produce non-repeating random walk
steps. I actually agree with your model for non-repeating random
walks. It just doesn't solve the problem when it actually comes to
finding rare targets in sequence space is all. That problem is still
an exponential problem. How so? Because, as the Hamming distance
increases in a linear manner, the average non-repeating random walk
distance increases exponentially. That's the problem. Your "method"
simply does not solve this problem.
> --- Paul J. Gans
Sean Pitman
www.DetectingDesign.com
seanpi...@naturalselection.0catch.com
>
> I, speaking as another physical chemist, theoritical type,
> can't answer that. I think that his entire model is bad. It
> reminds me of the old physicist joke about "consider a spherical
> horse".
>
> In its simplest form I assume that he is talking about a space
> consisting of all possible amino acid sequences. I'd model a
> sequence as a sequence of digits in base 20, each number
> corresponding to a given amino acid. Then all possible sequences
> of length N would be 20^N. For N of any real size, the number
> of possible sequences would be quite large.
Yes indeed . . .
> The problem is then to take a naturally occuring sequence, X, of
> length LX and transform it to another sequence Y, of length LY.
Right . . . with LY having a novel qualitatively different function
that is also selectably beneficial.
> Sean seems to want to calculate the ab initio probability of
> such a process. That is already a problem since there are a
> large number of proteins that could be transformed into Y. But
> never mind that.
Yes, but it is the mutation rate for each one of the starting points
that is important here. This number is limited. Therefore, so is the
searchable space per unit time.
> Sean seems to *assume* that the initial and final lengths are
> the same, I.e. LX = LY.
I do not make this assumption at all. The initial and final lengths
do not have to be the same. They can be very different. The only
thing that matters is the likely minimum Hamming distance between LX
and LY.
> However that's not only not necessarily
> true, but intermediate states could have totally different lengths.
Absolutely. Doesn't improve the odds of success.
> Further, Sean seems to assume that the only change that is
> possible is that one may change residue k (or digit k, if one
> thinks of the sequence as a number) to another digit m, all
> such changes being equally likely. That's wrong on the face
> of it.
How is that "wrong" on the face of it? Isn't this how random
mutations work? If the starting sequence is not changed, how does RM/
NS work to find novel target sequences?
> But putting that aside, there are many other possible mechanisms
> to get from X to Y. Some involve inclusions of entire subsequences
> and elisons of other subsequences. Some involve even more complex
> changes.
These are simply multi-character mutations or changes. Again, the
odds of success are not affected given a certain minimum Hamming
distance. You just don't seem to understand the concept of a random
walk or random leaps very well. All have essentially the same odds of
success.
Again, consider the average number of steps needed to find a target
location in a large field. It doesn't matter what size of random
steps you take. Odds are, it will take the same number of steps
regardless of the size of the steps taken.
> As a result, Sean's model is fatally flawed. As a result, any
> calculations based on it are fatally flawed.
You just don't understand the statistics of random walks . . .
> Do we have a better
> model? That's outside my area of competence, but my *guess* is
> that we don't know nearly enough about protein evolution, though
> what we've seen certainly does not indicate that it is impossible.
Again, anything is possible - - but not necessarily likely.
But, at least your honest enough to admit that you don't know of a
decent model for the mechanism of RM/NS. That's a start . . .
seanpi...@naturalselection.0catch.com
> Vend <ven...@virgilio.it> wrote innews:d95aa89a-dba2-4450...@r40g2000yqj.googlegroups.com:
>
>
>
> > On 30 Nov, 17:17, Seanpit <sean...@gmail.com> wrote:
> >> On Nov 29, 7:19 am, Vend <ven...@virgilio.it> wrote:
>
> [snip]
>
> >> the only problem is that non-target sequences vastly
> >> outnumber the potential targets within sequence space and this ratio
> >> only gets exponentially worse and worse with each increase in the
> >> level of functional complexity.
>
> > What do you mean by "non-target" sequence?
>
> All the ones that weren't found?
> :D
Rather, all the ones that would not be able to produce a selectably
beneficial function if they were found - i.e., non-beneficial
sequences.
Sean Pitman
www.DetectingDesign.com
seanpi...@naturalselection.0catch.com
> On Dec 12, 6:40 pm, Seanpit <sean...@gmail.com> wrote:
>
>
>
> > On Dec 1, 8:59 pm, "R. Baldwin" <res0k...@nozirevBACKWARDS.net> wrote:
>
> > > "'Rev Dr' Lenny Flank" <lfl...@yahoo.com> wrote in news:243ac663-0fa7-4fb8-
> > > 8052-65c58bb23...@v42g2000yqv.googlegroups.com:
>
> > > > On Dec 1, 3:01 pm, Seanpit <sean...@gmail.com> wrote:
>
> > > > Again, you have to
> > > >> go beyond your idea that what is possible = what is likely. That's
> > > >> just not true.
>
> > > > Offhand, I'd say that something that actually happened, is, uh,
> > > > possible. Furthermore, it is, um, really really likely to have
> > > > happened.
>
> > > > Just a guess.
>
> > LOL - we all know it happened. After all, its here. The question
> > isn't if it happened or not. The question is if it happened via the
> > particular mechanism of RM/NS.
>
> > So, how do you "know" it happened by the particular mechanism of RM/
> > NS?
>
> Because that's the ONLY mechanism we know that CAN produce it.
How do you "know" that? What is the likelihood that this mechanism
will produce a 1000 fsaar system in 4 billion years. Can you produce
such a calculated estimate? - for the mechanism of RM/NS? If so, I'd
love to see it. It will be a first.
> If you disagree, by all means go ahead and show us another mechanism.
Humans can and do produce such systems all the time . . .
> Show us a gene that you think was designed, show us what mechanism the
> designer used to produce it, then show us an example of the designer
> using a similar mechanism today do . . . well . . ., anything.
> Anything at all whatsoever anywhere.
It's happening right now . . . via human design.
> Time for you to run away again,
> Sean . . . . . . . . . . . . . . . . . . . . . . .. . . . . . .. . . . . . . . .. .
>
> ================================================
> Lenny Flank
> "There are no loose threads in the web of life"
>
> Editor, Red and Black Publishershttp://www.RedandBlackPublishers.com
Sean Pitman
www.DetectingDesign.com
wf3h
>
> But, at least your honest enough to admit that you don't know of a
> decent model for the mechanism of RM/NS. That's a start . . .
>
would that you could be so honest regarding the failure of YOUR idea...