Non-beneficial Gaps
Seanpit
concepts or ideas or forms of information require a greater number of
characters or a greater specificity of character arrangement, the
ratio of potentially meaningful or useful or functional systems
relative to the number of potential character arrangements drops off
*exponentially*.
This is true of the English language as well as all other spoken or
written human languages, computer codes and programs, and even of
genetic information and protein-based biosystems.
Let's start with the English language/information system. What is the
ratio of potentially meaningful vs. meaningless 2-character sequences
are there? Well, its around 1 in 7. What about 3-character
sequences? About 1 in 18. What about 7-character sequences? About 1
in 250,000.
Exactly the same pattern is present in computer codes and programs.
It is also present in the information systems of DNA and proteins.
There is a demonstrable decline in the ratio of useful genetic
sequences and protein-based systems, from the perspective of a given
life form, with each increase in either the minimum size requirement
or the minimum degree of sequence specificity needed for certain kinds
of higher-level systems to work. This decline is related to the
increase in minimum structural threshold requirements in an
exponential nature - just as it is for the decline in the ratio of
potentially meaningful English-language sequences with each additional
specified character requirement.
While there is certainly more flexibility for protein-based systems
relative to the English language system, the principle is the same.
Increase either the size or the specificity requirements under
consideration and there will be an exponential decline in the ratio of
potentially useful protein-based systems that meet those
requirements. The best available evidence also suggests that there is
also the same exponential decline in *potentially* beneficial targets
in sequence/structure space at higher and higher levels of minimum
structural threshold requirements.
So what? What does this have to do with anything?
What these facts strongly suggest is that the average distance between
what exists as a starting point or points in a given gene pool of
options and the next closest potentially beneficial system increases
in a linear manner with each increase in the minimum structural
threshold requirements under consideration. A linear increase in the
average distance translates into a linear increase in the minimum
likely distance between any starting point that exists and the next
closest target that is yet to be found in sequence/structure space. A
linear increase in this minimum distance translates into an
exponential increase in the average time it would take for a series of
random mutations or mutational "steps" to find a novel target sequence
or structure in sequence/structure space.
This random walk is truly random at this point. Natural or function-
based selection cannot help guide this walk until the novel target is
actually discovered, to at least some useful level of functionality,
by pure chance.
This method can actually work when the non-beneficial gaps are small -
like only 3 or 4 or steps wide. However, when the minimum gap
distance reaches a few dozen steps wide, the average random walk time
works its way into the trillions upon trillions of years - even for a
colony the size of all the bacteria on Earth (i.e., ~1e30
individuals).
This is a fundamental problem for the ToE. Every living thing
requires many systems that have minimum structural threshold
limitations well beyond the 1000aa mark. A requirement of 1000 fairly
specified amino acid residues, at minimum, produces an average gap
that is two to three hundred residues wide and a likely minimum gap
that is at least 50 mutational changes wide. Such a gap is not
crossable - even given an evolutionary time frame of several billion
years.
There are in fact no examples of evolution at this level or beyond in
all of literature - not one example of evolution in action. There are
only assumptions or stories about how the evolutionary mechanism must
have worked at these higher levels of complexity, but there are no
real observations of the proposed evolutionary mechanism actually
working at such levels - none.
Now, why might that be?
To see a visual representation of existing proteins that show a linear
expansion of the average and minimum gap sizes with increasing size,
see the following link:
http://www.pnas.org/content/vol103/issue38/images/large/zpq0370634700004.jpeg
Sean Pitman
www.DetectingDesign.com
Tony Raymonds
<ee6b4a80-d381-4903...@i72g2000hsd.googlegroups.com>,
Seanpit <seanpi...@naturalselection.0catch.com> writes
>All known language/information systems share a common feature. If
>concepts or ideas or forms of information require a greater number of
>characters or a greater specificity of character arrangement, the
>ratio of potentially meaningful or useful or functional systems
>relative to the number of potential character arrangements drops off
>*exponentially*.
Let's go up a level and see if it still holds true.
Does adding words to a book make in exponentially less likely to hold
meaningful or useful information?
<snip>
>This is a fundamental problem for the ToE. Every living thing
>requires many systems that have minimum structural threshold
>limitations well beyond the 1000aa mark. A requirement of 1000 fairly
>specified amino acid residues, at minimum, produces an average gap
>that is two to three hundred residues wide and a likely minimum gap
>that is at least 50 mutational changes wide. Such a gap is not
>crossable - even given an evolutionary time frame of several billion
>years.
The fundamental problem for your theory is, of course, that you cannot
show that these gaps exist at all. Nor can you show that any apparent
large gap *has* to be crossed in a single step.
The ancestor of any protein may well have crossed the gaps in small
steps over many generations, each small step being either neutral or
advantageous (as the disadvantageous ones will be filtered out by
natural selection).
It is also certain that many different proteins can perform the same
function in life i.e. there is not a unique target which has to be hit
in order for the protein to be of use.
Actually thinking about this it even makes an obvious prediction. Given
that species have split off at different times in the past there should
be numerous examples of proteins that had the same root but which
developed in different ways in different species as different "gaps"
were crossed.
--
to...@wacky.zzn.com
snex
0catch.com> wrote:
> All known language/information systems share a common feature. If
> concepts or ideas or forms of information require a greater number of
> characters or a greater specificity of character arrangement, the
> ratio of potentially meaningful or useful or functional systems
> relative to the number of potential character arrangements drops off
> *exponentially*.
>
this is not the case for systems where all possible combinations of
components form a valid structure, as is the case for mapping DNA to
amino acids. any random string of codons in between a start and stop
codon will generate *something* and that something will always react
to other things in its environment.
the parallel to english languages is simply wrong. not every
combination of english letters or words forms a valid structure within
the language.
Greg G.
0catch.com> wrote:
> All known language/information systems share a common feature. If
> concepts or ideas or forms of information require a greater number of
> characters or a greater specificity of character arrangement, the
> ratio of potentially meaningful or useful or functional systems
> relative to the number of potential character arrangements drops off
> *exponentially*.
>
> This is true of the English language as well as all other spoken or
> written human languages, computer codes and programs, and even of
> genetic information and protein-based biosystems.
>
> Let's start with the English language/information system. What is the
> ratio of potentially meaningful vs. meaningless 2-character sequences
> are there? Well, its around 1 in 7. What about 3-character
> sequences? About 1 in 18. What about 7-character sequences? About 1
> in 250,000.
Wrods do not hvae ot eb sepleld etclxay ceorcrtly ot cevnoy teh
mnaeing fo a sntecene. Yuor non-banciieefl gpas terhoy semes to eb
vrey eaexregtagd. Trehe aer mnay viaorintas taht cna od the jbo
sueciinfltfy, if nto elifictefny.
Wrods do not hvae ot eb slleped etclxay crrcteoly ot cvenoy teh
mnaenig of a snteecne. Yuor onn-beeiciafnl gpas theroy semes ot be
vrey etageaxergd. Trehe are mnay viairtoans taht can od teh jbo
sluincifetfy, fi not elinfectify.
Wdors od not hvae ot be seeplld etalcxy clercorty ot cvenoy the
meianng of a snteecne. Yuor nno-bnaifeceil gpas troehy smees ot eb
vrey eraxgegated. Tehre are mnay vaoaiitrns taht cna do teh jbo
sefnilicfuty, if nto enlfiietcfy.
A given spelling might be correct in more than one language or a word
might be spelled similarly in different languages. A spelling might be
correct in some language but not in others. Who is to say that a word
is misspelled in a language that hasn't been invented yet?
--
Greg G.
In my day, we didn't have a round world. It was flat and traveled on
the back of a turtle!
.
_Arthur
You must demontrate it, Sean, not just handwave a speculation.
> Increase either the size or the specificity requirements under
> consideration and there will be an exponential decline in the ratio of
> potentially useful protein-based systems that meet those
> requirements.
Who is increasing the size and specificity requirements ? Certainly
not me.
> The best available evidence also suggests that there is
> also the same exponential decline in *potentially* beneficial targets
> in sequence/structure space at higher and higher levels of minimum
> structural threshold requirements.
WHAT "best available evidence", Sean ?
The only evidence you have trolled in concerns a SINGLE protein
family with respect to a SINGLE functionality.
You have generalized the estimated Cytochrome C functionality curve to
ALL possible protein of ALL sizes, towards ALL possible
functionalities, known or unknown. That is a profundly dishonest
shell game, Sean.
Basically, you're arguing that since you know your birth date, every
single human must have the same birthday.
> So what? What does this have to do with anything?
Yes, SFW, Sean ?
> What these facts strongly suggest is that the average distance between
> what exists as a starting point or points in a given gene pool of
> options and the next closest potentially beneficial system increases
> in a linear manner with each increase in the minimum structural
> threshold requirements under consideration.
What facts ? you haven't shown any.
The rules for words in human languages cannot possibly offer any
insight on the rules for biological activity of proteins. Your analogy
is so deeply flawed it is not even funny, Sean.
> A linear increase in the
> average distance translates into a linear increase in the minimum
> likely distance between any starting point that exists and the next
> closest target that is yet to be found in sequence/structure space.
--Proof ?
> A linear increase in this minimum distance translates into an
> exponential increase in the average time it would take for a series of
> random mutations or mutational "steps" to find a novel target sequence
> or structure in sequence/structure space.
Proteins, mutated or not, have no "target sequence".
> This random walk is truly random at this point. Natural or function-
> based selection cannot help guide this walk until the novel target is
> actually discovered, to at least some useful level of functionality,
> by pure chance.
--unless an useful *secondary* biological functionality was already
present in the initial protein.
Funny didn't think of that, Sean. You know, (or maybe you dont), most
proteins do not have an unique active site.
> This method can actually work when the non-beneficial gaps are small -
> like only 3 or 4 or steps wide.
--or 0 wide.
> However, when the minimum gap
> distance reaches a few dozen steps wide, the average random walk time
> works its way into the trillions upon trillions of years - even for a
> colony the size of all the bacteria on Earth (i.e., ~1e30
> individuals).
Who gets to set the "minimum gap distance" ?? Certainly not you,
Sean.
One can find any number of proteins where the minimum gap size is 0.
Any protein that have several binding sites or active sites has an
effective gap of 0. A 1 codon mutation that increase that *secondary*
functionality becomes the starting point for natural selection to
favor "exploring" that (working) sequence, and at some point, abandon
the original functionality. Your strawman falls apart at the 0th gap,
Sean.
> This is a fundamental problem for the ToE.
No, only for the Piman strawman model ofToE, indeed. It has been
pointed to you a zillion times already. You're impervious to any
rebuttal.
> Every living thing
> requires many systems that have minimum structural threshold
> limitations well beyond the 1000aa mark.
Groundless assertion, magic number, numerology.
> A requirement of 1000 fairly
> specified amino acid residues,
-what is a "fairly specificied amino acid residue" ? You have never
provided an usable definition.
> at minimum, produces an average gap
> that is two to three hundred residues wide
How so? Your calculations have been shown entirely fraudulent, and are
entirely based on Cytochrome C respective to a single funtionality.
They wouldn't be true for CytC, and are certainly meaningless when
applied to an unknown protein respective to an *UNKNOWN* biological
functionality.
By the way, the method to calculate an average is to take all values,
tally them, and average them.
Since the lowest values of the "gap" are unknown to you, and the
highest are as long as the whole sequence. any average of you come up
with is fraudulent. In fact, you have taken the most conserved part
of Cytochrome C, and called it the "average" "gap" for all possible
proteins of all lenghts. That's pure delirium.
> and a likely minimum gap
> that is at least 50 mutational changes wide.
You have told me that your way to estimate the "likely minium gap" was
to take your flawed 300 number, which isn't an average, and applied a
Poisson distribution over it. You calling the resulting number the
resulting number the "likely minimum gap" is, once again pure fantasy.
In a school class, the average score is 76. Now, Sean, tell me: what
is the minimum score ?
No way to tell from the raw average number, Poisson or no Poisson.
Your calculation is most Fishy.
> Such a gap is not
> crossable - even given an evolutionary time frame of several billion
> years.
We're so fortunate that such a gap is the product of your numerology.
> There are in fact no examples of evolution at this level or beyond in
> all of literature - not one example of evolution in action.
There are plenty of counterexamples, tho. Any protein with several
identifiable functionalities, active sites or binding points already
demolish your fancy theory. So does any protein with a dual biological
use, say, as a neurotransmitter in the brain, and as a digestive
enzyme in the gut. Also, any two different proteins with a common
sequence of 50aa or more, but with 2 different identifiable biological
uses.
Any such example would torpedo your theory. Do you assert no such
example can ever be found, or will you assert you meant to say
otherwise in your theory ?
Such examples would show there are no 50aa gaps, "likely minimums" and
all that farrago.
Do you deny it, Sean ?
You would also have to show me "gap proteins", that are 1 aa away from
a known useful protein, but now utterly devoid of any *POSSIBLE*
biological usefulness. The Pitman Theory imply that there are an
infinite number of such "Neutral Gap Pitman proteins", surrounding
every known proteins in living things. Now show us one, Sean.
> There are
> only assumptions or stories about how the evolutionary mechanism must
> have worked at these higher levels of complexity, but there are no
> real observations of the proposed evolutionary mechanism actually
> working at such levels - none.
Yes, plenty of assumptions, assertions, handwaving, known-faulty
"computations" of your part, and not a single ovservation. Fancy that,
heh, Sean ?
We're still talking about a single proten, are we not, Sean ?
That's the point were you always generalize your busted "Pitman Gap"
for single proteins for whole, undefined "systems"
> Now, why might that be?
That one is easy. There is no "be" in Pitman's speculation and
numerology.
> To see a visual representation of existing proteins that show a linear
> expansion of the average and minimum gap sizes with increasing size,
> see the following link:
>
> http://www.pnas.org/content/vol103/issue38/images/large/zpq0370634700...
"Page not found" is a poor argument
_Arthur
_Arthur
> http://www.pnas.org/content/vol103/issue38/images/large/zpq0370634700...
Your URL doesn't resolve, but at: http://www.pnas.org/cgi/content/full/103/38/14050
(hurray for Open Access!!!)
I see: Ancestral reconstruction of the ligand-binding pocket of
Family C G protein-coupled receptors
Donghui Kuang, Yi Yao, David MacLean, Minghua Wang, David R.
Hampson,,, and Belinda S. W. Chang
Abstract:
"The metabotropic glutamate receptors (mGluRs) within the Family C
subclass of G protein-coupled receptors are crucial modulators of
synaptic transmission. However, their closest relatives include a
diverse group of sensory receptors whose biological functions are not
associated with neurotransmission, raising the question of the
evolutionary origin of amino acid-binding Family C receptors. A common
feature of most, if not all, functional Family C receptors is the
presence of an amino acid-binding site localized within the large
extracellular Venus flytrap domain. Here, we used maximum likelihood
methods to infer the ancestral state of key residues in the amino acid-
binding pocket of a primordial Family C receptor. These residues were
reconstructed in the background of the fish 5.24 chemosensory
receptor, a broad-spectrum amino acid-activated receptor. Unlike the
WT 5.24 receptor, which was not activated by mGluR agonists and
displayed low sensitivity toward L-glutamate, the reconstructed
ancestral receptor possessed a pharmacological profile characterized
by high affinity for both L-glutamate and selective Group I mGluR
agonists. This pharmacological phenotype could be largely
recapitulated by mutating only two residues in the 5.24 receptor-
binding pocket. Our results suggest that this primordial Family C
receptor may have arisen early in metazoan evolution and that it
already was preadapted as a glutamate receptor for its later use at
excitatory synapses in glutamate-mediated neurotransmission."
Nothing it the Abstract supports Pitman's Neurtal Gap Speculation.
Au contraire.
I see: http://www.pnas.org/cgi/content/full/103/38/14050/F2
with figure http://www.pnas.org/content/vol103/issue38/images/large/zpq0370634950002.jpeg
which I interpret as invalidating the Pitman Speculation.
In the same issue I see:
A phosphoryl transfer intermediate in the GTPase reaction of Ras in
complex with its GTPase-activating protein
Abstract:
The hydrolysis of nucleoside triphosphates by enzymes is used as a
regulation mechanism in key biological processes. Here, the GTP
hydrolysis of the protein complex of Ras with its GTPase-activating
protein is monitored at atomic resolution in a noncrystalline state by
time-resolved FTIR spectroscopy. At 900 ms, after the attack of water
at the -phosphate, there appears a H2PO4- intermediate that is shown
to be hydrogen-bonded in an eclipsed conformation to the -phosphate of
GDP. The H2PO4- intermediate is in a position where it can either
reform GTP or be released from the protein in 7 s in the rate-limiting
step of the GTPase reaction. We propose that such an intermediate also
occurs in other GTPases and ATPases.
No support for Pitman either there.
is it in
Combinations of biomarkers predictive of later life mortality
or in
Admixture mapping identifies 8q24 as a prostate cancer risk locus in
African-American men
last chance:
Microbial community in a sediment-hosted CO2 lake of the southern
Okinawa Trough hydrothermal system
Where is that figure that support your flight of fancy, Sean ?
Ron O
Let's say that this is all true (a false assumption), put forward a
single example where some evolutionary step required an organism to
jump a gap of more than 3 or 4 (wasn't it more like 10 or 20 in some
earlier incarnation?) all at once. Just one example and you can make
your case if the rest is true. So where is this example? What is
your evidence that such a gap ever had to be crossed in a single
evolutionary event? You know for a fact that you can't just claim
that a bunch of mutations had to happen to get a certain function
because you don't know the evolutionary pathway and you don't have a
clue how that functional character evolved. Just take your example of
the flagellum. You claim lots of gaps had to be crossed to pass your
1000 aa whatever. Don't you have to figure out the path taken before
you make any bogus claims that it couldn't have happened? What were
the protein sequences and what changes had to occur at any given step?
Why run and pretend? What good do bogus arguments like this do you
when you know for a fact that your own junk is so bad that you are
embarassed to even tell us what it is? What is your alternative to
common descent and the evidence you claimed to have for it that was
just as good as the evidence that you claim isn't good enough for
common descent? Where is the science or ID that you claimed to have
to teach to school children? No alternative, no evidence, no science,
so what do you think that you are doing?
You made these claims, so why not make good on them. Why play these
bogus games if you have to run from your own junk.
Ron Okimoto
_Arthur
Ron, about the flagellum, the Pitman Magik Number was 10,000 only 2
weeks ago:
"Specific examples of high-level systems include the famous flagellar
motility system. This system, in particular, requires a minimum of
over 10,000 fairly specified amino acid residues working together at
the same time (coded by over 10,000 fairly specified codons of
genetic
real estate). "
When Challenged over the Flagellum and Fairly Specified Residues,
Pitman decided that discretion is the best (fairly specified) part of
valor, and ran away from the sub-thread.
wf3h
that is true. they are properties of brains and brains are material
and obey the laws of nature...a fact you ignore.
>
> This is a fundamental problem for the ToE.
the fundamental problem with creationism is that it cherry picks its
observations. seanpit insists a non material supernatural intelligence
exists.
has he ever seen one? nope. yet he insists it's real. can he tell us
how such an intelligence would work?
nope. yet he insists its real.
thus creationism...a religious fraud that pushes ignorance and is
based on cherry picking its observations.
>
> There are in fact no examples of evolution at this level or beyond in
> all of literature - not one example of evolution in action.
ah. but we have examples of evolution as you admit
yet even YOU cherrypick your observations to fit your argument.
that's dishonest.
>
> Sean Pitmanwww.DetectingDesign.com
a website that is the equivalent of snake oil.
Ron O
>
> "Specific examples of high-level systems include the famous flagellar
> motility system. This system, in particular, requires a minimum of
> over 10,000 fairly specified amino acid residues working together at
> the same time (coded by over 10,000 fairly specified codons of
> genetic
> real estate). "
>
> When Challenged over the Flagellum and Fairly Specified Residues,
> Pitman decided that discretion is the best (fairly specified) part of
>
> - Show quoted text -
It is sort of gap inflation, but these are gaps that aren't gaps until
Sean wants them to be gaps.
Ron Okimoto
_Arthur
> It is sort of gap inflation, but these are gaps that aren't gaps until
> Sean wants them to be gaps.
>
> Ron Okimoto
Huge gaping gap in his theory ? A gaping pit, man ?
_Arthur
0catch.com> wrote:
> All known language/information systems share a common feature. If
> concepts or ideas or forms of information require a greater number of
> characters or a greater specificity of character arrangement, the
> ratio of potentially meaningful or useful or functional systems
> relative to the number of potential character arrangements drops off
> *exponentially*.
>
> This is true of the English language as well as all other spoken or
> written human languages, computer codes and programs, and even of
> genetic information and protein-based biosystems.
>
> Let's start with the English language/information system. What is the
> ratio of potentially meaningful vs. meaningless 2-character sequences
> are there? Well, its around 1 in 7. What about 3-character
> sequences? About 1 in 18. What about 7-character sequences? About 1
> in 250,000.
>
Your analogy is weak; as nay Scrabble player knows, there are of often
several 7-letter "scrabble" words posible with a given set of 7
letters. Words have multiple meanings, homonyms; sometimes a 1-letter
typo or letter reversion confers a whole new meaning to a word. A word
that means nothing in one language may have a meaning in another
tongue.
Nothing from that words analogy has any relevance to the molecular
biology of proteins or their DNA encoding.
R. Baldwin
news:ee6b4a80-d381-4903...@i72g2000hsd.googlegroups.com...
> All known language/information systems share a common feature. If
> concepts or ideas or forms of information require a greater number of
> characters or a greater specificity of character arrangement, the
> ratio of potentially meaningful or useful or functional systems
> relative to the number of potential character arrangements drops off
> *exponentially*.
Wrong. In a terrain data information system, every possible data value for
elevation is potentially meaningful or useful. Every possible sequence of
elevation values is potentially meaningful or useful.
>
> This is true of the English language as well as all other spoken or
> written human languages, computer codes and programs, and even of
> genetic information and protein-based biosystems.
Prove it. Let's take the APL programming language. Demonstrate this
exponential drop-off for APL, please.
>
> Let's start with the English language/information system. What is the
> ratio of potentially meaningful vs. meaningless 2-character sequences
> are there? Well, its around 1 in 7. What about 3-character
> sequences? About 1 in 18. What about 7-character sequences? About 1
> in 250,000.
Extrapolating from a single analogy, eh?
>
> Exactly the same pattern is present in computer codes and programs.
And just how many computer codes and programs did you research in order to
reach this dubious conclusion, Sean? Not many, I'll bet. At the assembly
language level, for example, you are quite wrong. I've programmed in
FORTRAN, Basic, Pascal, C, APL, custom script languages, dozens of assembly
languages, direct machine language, bit slice, PLDs, and custom machine
languages of my own design for custom machines. The simpler the language
structure, the less likely that increasing sequence length produces anything
like the kind of ratios you describe.
[snip rest of unfounded assertions]
The Enigmatic One
seanpi...@naturalselection.0catch.com says...
>This method can actually work when the non-beneficial gaps are small -
>like only 3 or 4 or steps wide. However, when the minimum gap
>distance reaches a few dozen steps wide, the average random walk time
>works its way into the trillions upon trillions of years - even for a
>colony the size of all the bacteria on Earth (i.e., ~1e30
>individuals).
>
Wow.
You're amazingly dumb.
-Tim
richardal...@googlemail.com
>
> Sean Pitmanwww.DetectingDesign.com
Sean, you keep posting this nonsense here.
Every time you do so it is thoroughly demolished by other posters.
If you think that your ideas have any merit why not present them to
people who understand them.
Of course, your continued evasion of the question of just who you
think *is* capable of understanding them implies that you know
perfectly well that they are a load of bull, and that you post them
here in the facile pretence that they have scientific merit in order
to impress creationists. Each time you post them this conclusion is
reinforced.
By the way, this is Question 9 on the list of your unanswered
questions. Just to remind you, here it is again.
9)
> Again, as I've mentioned to you several times now, this isn't about
> intellectual ability so much as it is about bias. Mainstream
> scientists aren't stupid. But, they are very biased. They are human
> and prone to bias just like anyone else - even you.
So who do you think *is* capable of understanding your "theories",
Sean?
RF
hersheyh
get called to testify at the next 'Dover' trial. And that it would be
interesting, rather than to leave him with the open-ended questions
one might ask to *real* scientists, trained as they are in presenting
evidence as honestly as they can, to take a more legalistic tack.
[snip]
> > Richard, if you get a straight answer from Sean about anything at all, my
> > hat will be off to you.
>
> The point of the question is as much to demonstrate how evasive and
> dishonest he is rather than any real expectation of a clear answer.
> After all, as I frequently say, one of my reasons for posting here is
> to expose the intellectual and moral vacuum of creationism. Sean is
> very helpful in this respect.
[snip]
Perhaps a more judicial/prosecutorial/courtroom approach is needed.
Open-ended questions appear to let Sean avoid answering questions.
But although "numbers don't lie", it is certainly also true that liars
regularly use numbers. They do so by claiming that the numbers
represent something they don't. But since "numbers don't lie", one
can usually clearly spot where the liars change the meanings of
numbers.
In the following exercise I will let Sean assume that he has been
called before "the" ultimate Judge to attest to and account for his
conduct on Earth. [Obviously creationists do not fear 'earthly'
judges as at Dover some creationist schoolboard dupes showed
themselves more than willing to perjure themselves.] I am, in this
case, the 'angelic' lawyer (call me Thomas the Doubter, patron saint
of scientists) claiming, for the prosecution, that Sean has engaged in
dishonesty, dissimulation, and untruthfulness in his conduct on earth
and deserves an appropriate fate in the hereafter. It is my turn to
interrogate him.
I am making extensive use of asking "Yes or no" questions. And, like
a good lawyer, I am asking questions I usually know the answer to
*and* how Sean has replied to them in the past. Sean will undoubtedly
add a whining addition with a 'but'. But the *real* answer will
always be the 'yes' or 'no', not the excuses following the 'but'.
Thomas: "Sean, do you understand the importance of complete
truthfulness and accuracy in the analysis and reporting of scientific
findings? Yes or no?
If Sean (or Glenn or JAlexander or any other of Sean ass-kissers)
wishes to reply, they, like Sean, can only give a "Yes or no." answer
to the questions except where indicated. [There will be ample
opportunity to explain, justify, whine, or present oneself as a victim
of a zealous prosecutor later.]
Sean's answer (Yes or no):
Thomas: "Do you understand the penalties for lying to or for God? All
*good* Christians, from St. Aquinas on, know that lying *for* God by
claiming that reality is not what it really is brings Him into
disrepute and disrespect. And the penalty for lying to God is quite
severe."
Sean's answer (Yes or no.):
Thomas: "Do you understand the importance of clearly stating one's
working assumptions and hypotheses or models in scientific analyses
and calculations? Yes or no?"
Sean's answer (Yes or no.):
Thomas: "Do you understand the difference between a mathematical
calculation and a crude hand-waving guess or estimation and why it is
important to explicitly state which is which? Yes or no?"
Sean's answer (Yes or no):
Thomas would then ask Sean to read the following statement:
"Well, first we have to calculate the likely gap size. Using an
average between the calculations of Yockey and Sauer, the ratio of
potential beneficial vs. non-beneficial for 100aa systems is about
1e-40. This creates a ratio for a 1,000aa system of about
1e-40^(1000/100) = 1e-400. So, the average gap size between
potentially beneficial sequences at this level would be about 308
residue differences - i.e., 20^308 = 1e400."
Thomas: "Did you write and post this in your web site? Yes or no."
Sean's reply (yes or no):
Thomas: "Do you use this paragraph to claim that you can and have
mathematically *calculated* a number you call "average gap size" or
"likely gap size". Yes or no?"
Sean's reply (yes or no):
Thomas: "Does this paragraph tell the viewer how to calculate the
value you call "average gap size? Yes or no?"
Sean's reply (yes or no):
Thomas: "Do you not claim, in this paragraph, that Yockey's ratio of
1e-40 is "the ratio of potential beneficial vs. non-beneficial
[sequences] for 100aa systems"? Yes or no?"
Sean's reply (yes or no):
Thomas: "Is, in fact, Yockey's ratio of 1e-40 *actually* "the ratio
of potential beneficial vs. non-beneficial [sequences] for 100aa
systems"? Yes or no?"
Sean's reply (yes or no):
Thomas: "Would it not be accurate to say that Yockey's ratio is an
"estimate of the number of sequences that have modern cytochrome c
function (i.e., a single *specified* function) divided by (roughly,
given the assumption that total sequence space at the 100aa level and
total sequence space minus the sequences that have cytochrome c
activity are about the same number) the number of sequences that lack
modern cytochrome c function? Yes or no?"
Sean's reply (yes or no):
Thomas (assuming that Sean answered the previous question honestly):
"Why, then, are you using and insisting on using an inaccurate
description rather than an accurate one to describe Yockey's ratio?
[Note to Sean: This is where you can blather on about how you *want*
people reading your paragraph to be misled into thinking the number
means one thing when it actually means something else.]
Sean's blather about why his lying about what Yockey's ratio means is
valid here:
Thomas: "Is not your calculation of "average gap size" merely the
taking of the 20th root of the inverse of Yockey's ratio or its
extrapolation to larger proteins? Yes or no?"
Sean's answer (yes or no):
Thomas: "Isn't the inverse of the Yockey ratio the number of
sequences that lack cytochrome c function per each sequence that has
cytochrome c function? Yes or no?"
Sean's answer (yes or no):
Thomas: "Isn't the Yockey ratio a measure of "sequence specificity"
for the particular specified function (cytochrome c in this case)?
That is, the greater the sequence stricture for the specified
function, the smaller the fraction of total sequence space (for a
given length) that would have that function. Yes or no?"
Sean's answer (yes or no):
Thomas: "Since Yockey's ratio or its inverse is a measure of
"sequence specificity" and taking the 20th root of a number is simply
a mathematical transformation, is not the 20th root also just a
measure of the degree of "sequence specificity" of modern cytochrome
c's (the specified function that Yockey examined)? Yes or no?"
Sean's answer (yes or no):
Thomas (assuming that Sean answers the previous question honestly, or
is able to understand his math): "Specifically, is not the 20th root
of the inverse of Yockey's ratio *really* a measure of the 'effective
number of invariant aa residues required for a modern cytochrome c
function', which is mathematically the same as the number of invariant
sites in cytochrome c if one assumes that there are only invariant and
freely variant sites? Yes or no?"
Sean's answer (yes or no):
Thomas: "There are two standard meanings of the the word "average".
When you use the word "average" in the phrase "average gap size",
which of the following meanings are you using?: 1) In math, "average"
is the sum of a series of actual measurements divided by the number of
trials in the series? 2) "Average" can also mean, colloquially,
'typical' and, in this case, might imply that the "gap size" has been
determined for a 'typical' or 'average' protein, namely cytochrome c.
3) Some private non-standard meaning."
Sean's answer (1, 2, or 3):
Depending on Sean's answer to the above, a follow-up question will
allow him to explain his reasoning.
Thomas: "If you answered 1) above, could you please present the
evidence, the series of trials, that produced that "average"? And
explain how an "average" can be computed from the 20th root of the
inverse of Yockey's ratio?"
Sean's answer here:
Thomas: "If you answered 2) above, could you please present the
evidence that cytochrome c is an "average" protein wrt the degree of
sequence specificity as measured by "effective number of invariant
sites"?"
Sean's answer here:
Thomas: "If you answered 3) above, could you explain why you chose to
use the word "average" when you did not mean any of the standard
meanings of "average". Did you do it because it sounded good? Did
you do it because you thought it might fool some innumerate people,
possibly including yourself, into thinking you had actually calculated
an "average"?"
Sean's answer here:
Thomas: "Since the only relevant biological meaning of the 20th root
of the inverse of Yockey's ratio is that it is the "effective number
of invariant aa sites in cytochrome c", isn't saying that this number
is the "gap size" *really* mean that the "gap" that must be crossed
is one that includes *all* and *each* of the effectively invariant
sites in this protein? IOW, rather than an "average" gap size,
doesn't this number represent the *maximum* possible gap size,
representing, as it does, all the aa sites that are relevant to the
specified function? Yes or no?"
Sean's answer here (yes or no):
If Sean answers dishonestly by saying "No.", a follow-up question will
be asked.
Thomas: "Explain why you think this number is not the 'maximum' gap
size -- the largest number of aa's that must be fully specified to
generate the function. All the other aa's are, of course, free to be
any aa."
Sean's answer here (if needed):
Thomas: "Is it not the case that the only models of evolution in
which there is a gap size that is the same as the "total number of
effectively invariant sites" away from a specified function models
where the starting point is either no sequence at all (the sequence
must be built from scratch) or a sequence which differs from the
specified end function at each and every effectively invariant site.
And is it not true, further, that these models assume that the
sequences are built by chance alone either _ab nihilo_ or from a
starting point which is maximally distant from any sequence with the
specified function? Yes or no?"
Sean's answer here (yes or no):
Thomas: "Have you not, elsewhere in your writings, claimed,
specifically, that you recognize that these models do not represent
standard evolutionary models? Yes or no?"
Sean's answer here (yes or no):
Thomas: "So which should we believe, Sean? Your math or your words?"
Sean's answer here (math or words):
Thomas: "I rest my case. But God is a forgiving God who believes in
the personal redemption of sinners and the power that comes from
people who honestly face the reality that He is ultimately responsible
for and the mechanisms He really uses rather than putting their blind
faith in mere words written by men. So He is willing to give Sean a
second chance and send him back to correct his errors if he so
chooses. So Sean, what are you going to do to correct the above
paragraph and your other writings about "average gap size" so that you
are not claiming one thing with your math and another with your
words?"
Sean's answer here:
Seanpit
You evidently don't know much about protein-based systems. Not every
arrangement of amino acid residues will produce a functional much less
beneficial protein system from the perspective of a given life form.
In fact, only a tiny minority of potential arrangements will be
beneficial in a given life form. This fraction (potential beneficial
vs. non-beneficial) shrinks in an exponential manner with each
increase in the minimum structural threshold requirements under
consideration for higher and higher level systems.
Sean Pitman
www.DetectingDesign.com
snex
why are you lying? present any sequence of DNA base pairs in between a
start and stop codon that will have no function whatsoever once
translated into chained amino acids. go on, do it.
>
> Sean Pitmanwww.DetectingDesign.com
Seanpit
>
> > Let's start with the English language/information system. What is the
> > ratio of potentially meaningful vs. meaningless 2-character sequences
> > are there? Well, its around 1 in 7. What about 3-character
> > sequences? About 1 in 18. What about 7-character sequences? About 1
> > in 250,000.
>
> Wrods do not hvae ot eb sepleld etclxay ceorcrtly ot cevnoy teh
> mnaeing fo a sntecene. Yuor non-banciieefl gpas terhoy semes to eb
> vrey eaexregtagd. Trehe aer mnay viaorintas taht cna od the jbo
> sueciinfltfy, if nto elifictefny.
>
> Wrods do not hvae ot eb slleped etclxay crrcteoly ot cvenoy teh
> mnaenig of a snteecne. Yuor onn-beeiciafnl gpas theroy semes ot be
> vrey etageaxergd. Trehe are mnay viairtoans taht can od teh jbo
> sluincifetfy, fi not elinfectify.
>
> Wdors od not hvae ot be seeplld etalcxy clercorty ot cvenoy the
> meianng of a snteecne. Yuor nno-bnaifeceil gpas troehy smees ot eb
> vrey eraxgegated. Tehre are mnay vaoaiitrns taht cna do teh jbo
> sefnilicfuty, if nto enlfiietcfy.
>
> A given spelling might be correct in more than one language or a word
> might be spelled similarly in different languages. A spelling might be
> correct in some language but not in others. Who is to say that a word
> is misspelled in a language that hasn't been invented yet?
I get this a lot . . .
Of course there is a certain flexibility to the English language
system - quite true. The same thing is true of protein-based
systems. A certain degree of change to the "spelling" of the protein
sequence(s) can be tolerated without a complete loss of beneficial
function. This flexibility produces an "island" in sequence/structure
space that can perform a given function in a given life from to at
least some degree of useful benefit.
However, there is a limit to this degree of flexibility beyond which
the beneficial function of the system in question will be lost
completely. This limitation defines the edges of the island.
All an evolving organism really has to do then is find the edge of one
of these novel potentially beneficial islands in sequence/structure
space via random mutation. The real question is then, what happens to
the number and relative size of these islands with an increase in the
minimum structural threshold requirements of potentially beneficial
target island functional systems?
As with the English language system, the greater the minimum size or
specificity requirement for a given system, the exponentially rarer it
will be in sequence/structure space. That's a non-arguable fact.
The argument that a nonsense sequence may make sense in a different
langauge, other than English, is not a good argument because the novel
sequence must make sense to the one trying to use it. In other words,
it has to make sense in the language/information system of the life
form in question. It doesn't matter if a different kind of life form
might find the sequence in question useful. All that matter is if the
particular life form in question finds it useful in its own particular
environment right now.
Quiziligook might make perfect beneficial sense to some alien from
Zorg, but what good is it from the perspective of the English language
system? The same thing is true of a particular type of bacteria that
happens to evolve a particular genetic sequence in a particular
environment. It doesn't matter if that sequence happens to be useful
to some other kind of bacteria in the same or different environment.
All that matters is if the sequence is or is not beneficial to the
bacteria in question in its current environment.
> Greg G.
>
> In my day, we didn't have a round world. It was flat and traveled on
> the back of a turtle!
Time to get off the turtle . . .
Sean Pitman
www.DetectingDesign.com
hersheyh
[reposted]
Seanpit
wrote:
> "Seanpit" <seanpitnos...@naturalselection.0catch.com> wrote in message
>
> news:ee6b4a80-d381-4903...@i72g2000hsd.googlegroups.com...
>
> > All known language/information systems share a common feature. If
> > concepts or ideas or forms of information require a greater number of
> > characters or a greater specificity of character arrangement, the
> > ratio of potentially meaningful or useful or functional systems
> > relative to the number of potential character arrangements drops off
> > *exponentially*.
>
> Wrong. In a terrain data information system, every possible data value for
> elevation is potentially meaningful or useful. Every possible sequence of
> elevation values is potentially meaningful or useful.
Not from a given perspective of a particular life form in a particular
environment.
When a mutation produces a novel genetic sequence in a particular
living thing in a particular environment, the vast majority of
potential mutations will not be beneficial. Even when it comes to
producing low-level single protein systems (<1000aa), most mutations
will be functionally neutral. Of those that do produce a functional
change (about 1%) most will be detrimental by a ratio of at least
1000:1. As one considers higher-level systems, systems that require a
greater minimum structural threshold, the ratio of non-beneficial vs.
beneficial declines even further - in an exponential manner.
< snip rest >
Sean Pitman
www.DetectingDesign.com
Seanpit
>
> > > the parallel to english languages is simply wrong. not every
> > > combination of english letters or words forms a valid structure within
> > > the language.
>
> > You evidently don't know much about protein-based systems. Not every
> > arrangement of amino acid residues will produce a functional much less
> > beneficial protein system from the perspective of a given life form.
> > In fact, only a tiny minority of potential arrangements will be
> > beneficial in a given life form. This fraction (potential beneficial
> > vs. non-beneficial) shrinks in an exponential manner with each
> > increase in the minimum structural threshold requirements under
> > consideration for higher and higher level systems.
>
> why are you lying? present any sequence of DNA base pairs in between a
> start and stop codon that will have no function whatsoever once
> translated into chained amino acids. go on, do it.
The vast majority of potential DNA sequences of a given length, if
transcribed and translated into amino acid sequences, would produce
completely non-viable proteins - not to mention non-beneficial
proteins from the perspective of a given life form. If you don't
believe me, look it up an try to prove me wrong. Or, ask someone in
this forum. Even someone like Howard Hershey could straighten you out
on this very elementry fact.
Sean Pitman
www.DetectingDesign.com
Seanpit
> In article
> <ee6b4a80-d381-4903-b489-5e49ad105...@i72g2000hsd.googlegroups.com>,
> Seanpit <seanpitnos...@naturalselection.0catch.com> writes
> >All known language/information systems share a common feature. If
> >concepts or ideas or forms of information require a greater number of
> >characters or a greater specificity of character arrangement, the
> >ratio of potentially meaningful or useful or functional systems
> >relative to the number of potential character arrangements drops off
> >*exponentially*.
>
> Let's go up a level and see if it still holds true.
>
> Does adding words to a book make in exponentially less likely to hold
> meaningful or useful information?
What is exponentially less likely is that by adding characters to a
book, at random, you will improve its meaning in a novel way
beneficial way significantly beyond where you started. That is why
novels and computer programs cannot be written via random mutation and
function-based selection. They require intelligent input in order to
cross over non-beneficial gaps.
> >This is a fundamental problem for the ToE. Every living thing
> >requires many systems that have minimum structural threshold
> >limitations well beyond the 1000aa mark. A requirement of 1000 fairly
> >specified amino acid residues, at minimum, produces an average gap
> >that is two to three hundred residues wide and a likely minimum gap
> >that is at least 50 mutational changes wide. Such a gap is not
> >crossable - even given an evolutionary time frame of several billion
> >years.
>
> The fundamental problem for your theory is, of course, that you cannot
> show that these gaps exist at all. Nor can you show that any apparent
> large gap *has* to be crossed in a single step.
The gaps do exist. Even between low-level systems requiring only a
few hundred fairly specified amino acid residues at minimum the averge
and minimum gap sizes can be demonstrated to at least a useful
degree.
Beyond this, no one said that the gaps had to be crossed in a single
step. That's not at all true. The gaps can be crossed by a single
step or a series of random walk steps. The problem is that until the
gap is crossed, natural selection is blind and cannot help in the
process. Therefore, the larger the gap the exponentially more steps
are required to cross it - on average.
> The ancestor of any protein may well have crossed the gaps in small
> steps over many generations, each small step being either neutral or
> advantageous (as the disadvantageous ones will be filtered out by
> natural selection).
If a small step is functionally neutral, it is beyond the powers of
natural selection to guide it. If the small step is advantageous,
then it has only crossed a small gap. Gaps are defined by being non-
advantageous - i.e., either neutral or detrimental or both. As
minimum structural threshold requirements for higher-level systems
increase, so do the non-beneficial gap sizes - in a linear manner.
Crossing a linearly larger gap size requires a exponential increase in
the average number of mutational steps.
> It is also certain that many different proteins can perform the same
> function in life i.e. there is not a unique target which has to be hit
> in order for the protein to be of use.
There is not a unique target, but there most certainly is a very
limited number of unique targets, each of which is quite limited in
relative size. Hitting any of these targets is very difficult
relative to the vast majority of non-targets out there in sequence/
structure space.
> Actually thinking about this it even makes an obvious prediction. Given
> that species have split off at different times in the past there should
> be numerous examples of proteins that had the same root but which
> developed in different ways in different species as different "gaps"
> were crossed.
Different uses of the same basic structure can also be equally
explained by conservation of design. Human designers use this feature
all the time. Why reinvent the wheel each time a wheel-like
structure, with a few modifications, might be useful?
Sean Pitman
www.DetectingDesign.com
Seanpit
0catch.com> wrote:
>
> > why are you lying? present any sequence of DNA base pairs in between a
> > start and stop codon that will have no function whatsoever once
> > translated into chained amino acids. go on, do it.
>
> The vast majority of potential DNA sequences of a given length, if
> transcribed and translated into amino acid sequences, would produce
> completely non-viable proteins - not to mention non-beneficial
> proteins from the perspective of a given life form. If you don't
> believe me, look it up an try to prove me wrong. Or, ask someone in
> this forum. Even someone like Howard Hershey could straighten you out
> on this very elementry fact.
"As described above, sequence space is a highly dimensional
space. The majority of possible sequences represent non-viable
proteins, with no accessible and stable folded state. We can imagine
that there are regions in this space that do correspond to viable
proteins with a stability sufficient to avoid proteolysis and
aggregation. The boundary between this viable region and the
surrounding unviable region then represents the boundary between
stable and unstable native states."
E. I. Shakhnovich, R. A. Broglia, G. Tiana, "Protein Folding,
Evolution And Design", 2001. ISBN 1586031694, pp. 201, 202
http://books.google.com/books?id=Jwiz7S7UP_IC
Notice that the authors of this book explicitly point out that the
majority of possible protein sequences are "non-vaible". This doesn't
even deal with the fact that even among those protein sequences that
are viable, most are non-beneficial from the perspective of a
particular life form in a particular environment.
Hope this helps clarify the nature of sequence space just a bit for
you.
Sean Pitman
www.DetectingDesign.com
snex
what is a "non-viable" protein? if it doesnt fold, it still engages in
chemical reactions. every single chain of amino acids will engage in
chemical reactions. since we have no idea what reactions these would
be, there is no way to say whether or not they would be beneficial.
R. Baldwin
> On Feb 1, 12:25 am, "R. Baldwin" <res0k...@nozirevBACKWARDS.net>
> wrote:
>> "Seanpit" <seanpitnos...@naturalselection.0catch.com> wrote in message
>>
>> news:ee6b4a80-d381-4903...@i72g2000hsd.googlegroups.com...
>>
>> > All known language/information systems share a common feature. If
>> > concepts or ideas or forms of information require a greater number of
>> > characters or a greater specificity of character arrangement, the
>> > ratio of potentially meaningful or useful or functional systems
>> > relative to the number of potential character arrangements drops off
>> > *exponentially*.
>>
>> Wrong. In a terrain data information system, every possible data value
>> for
>> elevation is potentially meaningful or useful. Every possible sequence of
>> elevation values is potentially meaningful or useful.
>
> Not from a given perspective of a particular life form in a particular
> environment.
If you are going to restrict your view to "a given perspective of a
particular life form in a particular environment" then you should not begin
your argument with "All known language/information systems share a common
feature." I was pointing out that you were starting from a flawed premise
about the nature of known language/information systems, so life forms and
environments are not relevant.
>
> When a mutation produces a novel genetic sequence in a particular
> living thing in a particular environment, the vast majority of
> potential mutations will not be beneficial. Even when it comes to
> producing low-level single protein systems (<1000aa), most mutations
> will be functionally neutral. Of those that do produce a functional
> change (about 1%) most will be detrimental by a ratio of at least
> 1000:1. As one considers higher-level systems, systems that require a
> greater minimum structural threshold, the ratio of non-beneficial vs.
> beneficial declines even further - in an exponential manner.
>
You can go on making these unfounded assertions as long as you like, Sean.
That does not make these falsehoods any more correct. In any case, it has
nothing to do with my previous post, which was challenging your broad
assertions about languages and information processing *in general* and *not*
in the context of Biology.
Now how about addressing the snipped challenge? I'll restore the text for
your convenience below:
Tony Raymonds
<0da0bf86-b5f0-4ca2...@l16g2000hsh.googlegroups.com>,
Seanpit <seanpi...@naturalselection.0catch.com> writes
>On Jan 31, 12:57 pm, Tony Raymonds <to...@wacky.zzn.com> wrote:
>> In article
>> <ee6b4a80-d381-4903-b489-5e49ad105...@i72g2000hsd.googlegroups.com>,
>> Seanpit <seanpitnos...@naturalselection.0catch.com> writes
>> >All known language/information systems share a common feature. If
>> >concepts or ideas or forms of information require a greater number of
>> >characters or a greater specificity of character arrangement, the
>> >ratio of potentially meaningful or useful or functional systems
>> >relative to the number of potential character arrangements drops off
>> >*exponentially*.
>>
>> Let's go up a level and see if it still holds true.
>>
>> Does adding words to a book make in exponentially less likely to hold
>> meaningful or useful information?
>
>What is exponentially less likely is that by adding characters to a
>book, at random, you will improve its meaning in a novel way
>beneficial way significantly beyond where you started.
So adding a random letter or character to a long book is more likely to
damage it than adding a character or letter to a short book is it?
>That is why
>novels and computer programs cannot be written via random mutation and
>function-based selection. They require intelligent input in order to
>cross over non-beneficial gaps.
Assertion with no absolutely evidence to back it up. Actually computer
programs written using random mutations can be written and work very
well. Ever heard of genetic algorithms?
>> >This is a fundamental problem for the ToE. Every living thing
>> >requires many systems that have minimum structural threshold
>> >limitations well beyond the 1000aa mark. A requirement of 1000 fairly
>> >specified amino acid residues, at minimum, produces an average gap
>> >that is two to three hundred residues wide and a likely minimum gap
>> >that is at least 50 mutational changes wide. Such a gap is not
>> >crossable - even given an evolutionary time frame of several billion
>> >years.
>>
>> The fundamental problem for your theory is, of course, that you cannot
>> show that these gaps exist at all. Nor can you show that any apparent
>> large gap *has* to be crossed in a single step.
>
>The gaps do exist.
Show me some then. Give me a list of proteins that cannot have a a
single amino acid deleted, added or changed without it having no
biological function.
> Even between low-level systems requiring only a
>few hundred fairly specified amino acid residues at minimum the averge
>and minimum gap sizes can be demonstrated to at least a useful
>degree.
>
>Beyond this, no one said that the gaps had to be crossed in a single
>step. That's not at all true. The gaps can be crossed by a single
>step or a series of random walk steps. The problem is that until the
>gap is crossed, natural selection is blind and cannot help in the
>process.
Yes, exactly. It also doesn't have a target either though and that is
the bit you are missing. You are doing the equivalent of saying a hand
of cards is impossible because of the odds of getting that particular
collection of cards is incredibly unlikely.
>Therefore, the larger the gap the exponentially more steps
>are required to cross it - on average.
In reality there are actually no gaps because it's a continuum of useful
proteins. All that natural selection says is that all the stages have
to be useful or at least neutral. You haven't shown a single real
example of a real gap.
>> The ancestor of any protein may well have crossed the gaps in small
>> steps over many generations, each small step being either neutral or
>> advantageous (as the disadvantageous ones will be filtered out by
>> natural selection).
>
>If a small step is functionally neutral, it is beyond the powers of
>natural selection to guide it.
Absolutely, there is no guiding going on. Having said that a neutral or
even a detrimental mutation can take the protein to a different
functional space. How can it have a detrimental mutation and not be
selected out I hear you ask?
If section of DNA which produces a protein is duplicated then the
duplicate can mutate freely (and even lose it's original function)
without disrupting the production of the original protein.
Haemoglobin is a very good example of where this appears to have
happened multiple times:
http://en.wikipedia.org/wiki/Hemoglobin
>If the small step is advantageous,
>then it has only crossed a small gap. Gaps are defined by being non-
>advantageous - i.e., either neutral or detrimental or both.
Give me a list of proteins in which you can show that adding, removing
or replacing a single amino acid anywhere along it has no useful
biological function.
> As
>minimum structural threshold requirements for higher-level systems
>increase, so do the non-beneficial gap sizes - in a linear manner.
>Crossing a linearly larger gap size requires a exponential increase in
>the average number of mutational steps.
Give us a list of these large gaps rather than just asserting that they
exist.
I think that this is the crucial point. All of your calculations rely
on large gaps but you haven't shown that these large gaps exist,
therefore all of your calculations are theoretical at best and pointless
at worst.
>> It is also certain that many different proteins can perform the same
>> function in life i.e. there is not a unique target which has to be hit
>> in order for the protein to be of use.
>
>There is not a unique target, but there most certainly is a very
>limited number of unique targets, each of which is quite limited in
>relative size.
I will agree that the number of combinations of DNA for a particular
length is finite, and that the number of combinations that produce a
biologically neutral or useful protein is also finite - but they are
also both *very* large numbers for any significant length of DNA.
It's known that there are large numbers of different proteins that
perform exactly the same function since large numbers of SNP and other
mutations have already been mapped.
>Hitting any of these targets is very difficult
>relative to the vast majority of non-targets out there in sequence/
>structure space.
>
>> Actually thinking about this it even makes an obvious prediction. Given
>> that species have split off at different times in the past there should
>> be numerous examples of proteins that had the same root but which
>> developed in different ways in different species as different "gaps"
>> were crossed.
>
>Different uses of the same basic structure can also be equally
>explained by conservation of design. Human designers use this feature
>all the time. Why reinvent the wheel each time a wheel-like
>structure, with a few modifications, might be useful?
Don't you think that it's odd that your designer re-used the functions
in a nested hierarchy which looks *exactly* as predicted by evolution
right down to the molecular DNA level.
>
>> to...@wacky.zzn.com
>
>Sean Pitman
>www.DetectingDesign.com
>
richardal...@googlemail.com
0catch.com> wrote:
)
[SP]
> You also know that I wasn't talking about "concentration" of
carnivore
> remains in the passages you reference from my website. This is a
> deliberate mischaracterization and strawman building on your part.
> What I was talking about are layers in which dinosaurs are found
> without much to each - like the Morrison formation.
What on earth do you mean "without much to each"? That doesn't even
make sense as English! Do you mean that small numbers of individuals
of each species are found in each location?
2)
"You say "For example, the fossils of some layers consist primarily of
large meat eating dinosaurs." Well, I know that some sites contain
concentrations of meat-eating dinosaurs, but don't know of any
horizons (which I presume is what you mean by "layers" in this
context) which cover large areas and contain an abundance of meat-
eating dinosaurs.
So if you are not referring to the sites which are known as predator
traps, what exactly *do* you mean by "The fossils of some layers
consist primarily of large meat eating dinosaurs", and what evidence
can you provide to support your assertions? "
3)
"> The evidence isn't based on just a single quarry, but millions of
data
> from across the globe.
So how does this explain the fact that we have different current
orientations in
the same stratigraphic sequence separated by many meters of sediment?
"
4)
From here: http://wyomingpaleo.org/references/Turner-Peterson_synthesis.pdf
"Plant material preserved as megaflora is generally scarce throughout
the Morrison Formation. About
32 leaf form species of megaflora have been reported in the Morrison
(Parrish et al., this volume), whereas
over 225 fossil pollen and spore types have been recovered (Litwin et
al., 1998). The appreciable
difference between the quantity of plant life recorded by the abundant
palynomorph flora compared to the
relatively meager amount of megaplant remains is intriguing. Some of
the palynomorphs undoubtedly
came from the uplands; however, many of the palynomorphs likely came
from herbaceous plants, many
of which do not leave a megaplant fossil record (Parrish et al., this
volume). Ferns account for many
of the taxa in the palynological record of the Morrison Formation
(Litwin et al., 1998). The scarcity of megaplant
remains, limited occurrences of fossil wood, small shallow root
impressions (even on well-developed
paleosols), and the high ratio of palynomorph types to megafloral taxa
throughout the Morrison are a
strong indication that the entire Morrison flora was dominated by
herbaceous plants and small-statured woody plants (Parrish et al.,
this volume)."
So are you still asserting that the Morrison Formation is "essentially
barren of the "palynomorphs""?
And perhaps you can read this paper and identify where and how the
conclusions of the authors are influenced by their "long-age
paradigm". By "identify" I mean identify specific conclusions reached
by the authors, and what alternative testable explanation you can
provide which shows that they have been misled by a priori
assumptions.
Has it never occurred to you that an education in the subject might
make you less prone to put yourself into the situation in which you
look both evasive and dishonest?
5)
> Again, there is the problem of constant bioturbation that
> prevents fossilization and crisp layer formation without fairly rapid
> and deep burial.
What "problem of bioturbation"? Your problem, which is that massive
floods cause massive amounts of turbation. The papers whose abstracts
I have posted go into detail on the taphonomy of deposits in the
Morrison. For example, we find deposits of jumbled bones which have
been trampled over and broken covered with a layer of volcanic ash,
and buried under many meters of later sediment. How is that compatible
with a single massive flood?
6)
> Relative to
> other forms of plant fossils in the Morrison formation pollen and
> spore fossils may indeed be relatively abundant. That doesn't mean
> that they were abundant enough to explain the plant life needed to
> support millions of very large dinosaurs.
So what is wrong with the model which has been proposed, i.e. a semi-
arid seasonal environment similar to the savannahs of modern Africa?
7)
> Even recently published papers note that the lack of plant fossils in
> the Morrison formation would make it rather difficult to support the
> huge populations of large dinosaurs found in this region.
...and they provide a testable hypothesis which explain the relative
lack of abundance of plant fossils.
What is wrong with that explanation?
8)
Sean, even if Roth is correct, and these structures are not termite
mounds - and the reference you provide is hardly convincing - in what
possible way does "catastrophism" lead to the creation of large,
complex concretionary structures? How long do you think it would take
a structure like this to form?
9)
> Again, as I've mentioned to you several times now, this isn't about
> intellectual ability so much as it is about bias. Mainstream
> scientists aren't stupid. But, they are very biased. They are human
> and prone to bias just like anyone else - even you.
So who do you think *is* capable of understanding your "theories",
Sean?
10)
> Bretz already had enough evidence to strongly suggest that
> catastrophic flooding was responsible for the main features of the
> Scablands.
...which he presented in the form of numerous scientific papers.
Where is your evidence, Sean?
And from John Harshman:
11. Why would an intelligent designer produce a nested hierarchy of
just
the sort that would happen automatically from common descent?
Anyone else have a few more to add?
RF
Rodjk #613
0catch.com> wrote:
> All known language/information systems share a common feature. If
> concepts or ideas or forms of information require a greater number of
> characters or a greater specificity of character arrangement, the
> ratio of potentially meaningful or useful or functional systems
> relative to the number of potential character arrangements drops off
> *exponentially*.
>
<SNIP>
>
> Now, why might that be?
>
> To see a visual representation of existing proteins that show a linear
> expansion of the average and minimum gap sizes with increasing size,
> see the following link:
>
> http://www.pnas.org/content/vol103/issue38/images/large/zpq0370634700...
>
> Sean Pitmanwww.DetectingDesign.com
You use so many words to say such silly things...
Rodjk #613
Tony Raymonds
<2c86683c-4255-4295...@s8g2000prg.googlegroups.com>,
Seanpit <seanpi...@naturalselection.0catch.com> writes
So what is the average ratio of non-viable proteins compared to viable
proteins for any length of DNA after a single nucleotide mutation?
I'm assuming you have worked this out since you keep making statements
about how unlikely it is for viable proteins to be produced.
For example if I have a protein 100 amino acid residues long and either
add, remove or change an amino acid from it then, on average, what
percentage of the resulting proteins would have no biological function?
Don't forget that proteins come in families and those proteins with
successful viable small roots will have far larger families than those
which have non-viable roots.
For example, say we had a theoretical organism that mutated by adding
one codon per generation (unrealistic I know, but it's a simplified
example). Say that it started out with a single codon:
AAA
Then at the next generation generated this sequence which was fatal:
AAA CTC
Then the *entire* sequence space starting AACTC would be selected out
immediately. On the other hand if this sequence in an offspring was
useful:
AAA CCC
Then the next generation could then try things like:
AAA CCC CCA
AAA CCC GTA
AAA CCC TTT
If the first two of those were non-viable but the third one was useful
or neutral then the next generation could then try things like:
AAA CCC TTT GTC
AAA CCC TTT ACA
AAA CCC TTT GTT
and so on.
Notice how the viable branch is followed generation by generation but
the non-viable branch is cut off almost immediate. The whole sequence
space isn't searched, only the viable branches will pass on to the next
generation which then uses them as it's *starting* point.
There is *no* exponential increase in the unlikelyhood of each step.
That is why your calculations giving exponential decrease of
probabilities are nonsense and, given that you have not shown that there
the large gaps that you keep talking about exist, it means your
assertions are groundless.
Here is question for you. What is the probability of these two
sequences appearing at the fifth generation of our hypothetical beastie:
AAA CCC TTT GTT AAT
AAA CTC ACT GTC TAT
--
to...@wacky.zzn.com
hersheyh
Even without reading the source, I have a couple of points of
disagreement. Proteins are assembled by a stepwise mechanism and the
protein 'folds' (and that includes re-folding) as it is being
synthesized. Since folding is merely the process of finding the
lowest energy state at that temperature, the claim that most sequences
do not find the set of 3-D structures that have the lowest energy
state but simply flounder around in a perpetual state of structural
flux is clearly nonsense that no physicist worth his or her salt
should be claiming. *That* would be a violation of the laws of
thermodynamics. *Most* sequences will form one or a few stable or
quasi-stable structures (or stable substructures linked by flexible
linkers) because of spontaneous folding to minimum thermodynamic
structures (hydrophobic structures on the inside; hydrophilic on the
outside). Temperature obviously can affect the relative stability as
can other environmental conditions. That is why all proteins denature
at some temperature. Some sequences (functional or not) would be
structurally unstable in the conditions the particular organism lives
in (e.g., hydrothermal pools as opposed to arctic ice lakes). Natural
selection simply excludes such sequences from being searched.
That said, it *is* possible for the same sequence to fold several
different ways into a *few* stable or quasi-stable (at certain
temperatures) structures. [Prions, for example.] It is also possible
for a protein to, instead of folding on itself, to attach to and
aggregate to other proteins. When one *denatures* (disrupts) the
structure of proteins (by heat, acid, or base extremes) and then goes
rapidly back to the normal conditions, the protein, even those with
known function and structure, will not typically fold back properly
but will aggregate with other proteins and fold back in ways that
disrupt function. [There are some interesting exceptions. RNase A
function, for example, is very hard to remove precisely because the
small protein, over time, will, in a fraction of the proteins, re-fold
in such a way to form a functional peptide after denaturation. A slow
renaturation favors such spontaneous re-folding.]
Unfortunately for Sean, even *if* there are regions of sequence space
that cannot form a stable (or a few stable -- as in prions)
structures, all that would do is reduce the size of total sequence
space that is searchable by natural mechanisms. Any mutation that
entered such a space would quickly be removed from the population (if
it were deleterious), just like any other lethal or functionless (if
such lack of function were deleterious rather than beneficial -- there
are instances where "loss-of-function" mutations are beneficial). If
Sean wants to claim that some specific search algorithm that produced
some actual real protein sequence *must* have crossed a series of
sequences that lack any structure, he has to produce real evidence
rather than bogus math based on a strawman model of evolution that
calls the *maximum gap size* assuming random synthesis of sequences
from scratch or from a *maximally* distant sequence the "average gap
size".
>
> Sean Pitmanwww.DetectingDesign.com
mur...@tntech.edu
[...]
>
> Anyone else have a few more to add?
(To SP): Robert Gentry, a young-earth Creationist member of your
church (and a man you've probably met) sent his work in for
publication. He had at least two articles published in two completely
different fields (geology and cosmology). Both have now been refuted
pretty convincingly but the point is that in spite of the Creationist
motivation he was able to stick to science in these articles, and they
were published.
What's stopping *you*?
---DPM
>
> RF
Tony Raymonds
<0da0bf86-b5f0-4ca2...@l16g2000hsh.googlegroups.com>,
Seanpit <seanpi...@naturalselection.0catch.com> writes
>> that species have split off at different times in the past there should
>> be numerous examples of proteins that had the same root but which
>> developed in different ways in different species as different "gaps"
>> were crossed.
>
>Different uses of the same basic structure can also be equally
>explained by conservation of design. Human designers use this feature
>all the time. Why reinvent the wheel each time a wheel-like
>structure, with a few modifications, might be useful?
Re-reading this I realised that you completely mis-answered my
prediction. You pulled one of the stock creationist answers out at the
wrong time.
I was not saying that the same sequences would be present in multiple
organisms here, in fact I'm saying almost the opposite. What I was
saying is that if there is the "gap" between primitive proteins and
modern ones then examples of the gap being crossed in stages should
exist in different species as they split off at different times in the
past.
Can you give us some examples of these large gaps you keep talking
about? Maybe after you do that we could look at the related species to
see whether the "gap" was crossed in slightly different ways in
different species giving *different* but functional protein end results.
Give us an example of these gaps from humans since both we and
(theoretically) closely related species have been sequenced so the data
is readily available for all to look at.
If evolution happened then we should see the DNA sequence for your
example large gap being crossed as we go back through the species
towards what we consider more primitive forms (although this is slightly
complicated by the fact that they will have been evolving for exactly
the same time as we have, but the basic principle should hold true)
--
to...@wacky.zzn.com
hersheyh
0catch.com> wrote:
> On Jan 31, 1:20 pm, snex <s...@comcast.net> wrote:
>
>
>
> > On Jan 31, 1:18 pm, Seanpit <seanpitnos...@naturalselection.
>
> > 0catch.com> wrote:
> > > All known language/information systems share a common feature. If
> > > concepts or ideas or forms of information require a greater number of
> > > characters or a greater specificity of character arrangement, the
> > > ratio of potentially meaningful or useful or functional systems
> > > relative to the number of potential character arrangements drops off
> > > *exponentially*.
>
> > this is not the case for systems where all possible combinations of
> > components form a valid structure, as is the case for mapping DNA to
> > amino acids. any random string of codons in between a start and stop
> > codon will generate *something* and that something will always react
> > to other things in its environment.
>
> > the parallel to english languages is simply wrong. not every
> > combination of english letters or words forms a valid structure within
> > the language.
>
> You evidently don't know much about protein-based systems.
I sure as hell know that *you* don't.
> Not every
> arrangement of amino acid residues will produce a functional
How do you determine what sequences *can* produce a "function"? One
reasonable definition of "function" is that the sequence produces a
product that interacts with other biological materials. *All*
sequences can do that. Perhaps you want to define "function" as a
sequence that interacts with some *specific* biological material
rather than any biological materials. But how 'specific' is
'specific'? If the sequence cleaves *all* peptide bonds, is that
specific enough to be called a "function"? If the sequence binds to
a specific HLA protein, is that a "function"?
> much less
> beneficial protein system from the perspective of a given life form.
"Beneficial" is highly conditional. In some cases, loss-of-function
mutations are 'beneficial'. The same protein sequence can be
'beneficial' in one context, 'detrimental' in another context, and
'neutral' in a third. And that is in the *same* given life form.
[Look up 'frequency-dependent' selection for an example.]
> In fact, only a tiny minority of potential arrangements will be
> beneficial in a given life form. This fraction (potential beneficial
> vs. non-beneficial) shrinks in an exponential manner with each
> increase in the minimum structural threshold requirements under
> consideration for higher and higher level systems.
And, as I have pointed out, your math is nothing but bullshit
numerology based on bogus strawman models of evolution working by
starting each protein from scratch or from the *maximally* distant
sequence (one which as the wrong aa at each and every functionally
relevant site).
>
> Sean Pitmanwww.DetectingDesign.com
Seanpit
>
> > "As described above, sequence space is a highly dimensional
> > space. The majority of possible sequences represent non-viable
> > proteins, with no accessible and stable folded state. We can imagine
> > that there are regions in this space that do correspond to viable
> > proteins with a stability sufficient to avoid proteolysis and
> > aggregation. The boundary between this viable region and the
> > surrounding unviable region then represents the boundary between
> > stable and unstable native states."
>
> > E. I. Shakhnovich, R. A. Broglia, G. Tiana, "Protein Folding,
> > Evolution And Design", 2001. ISBN 1586031694, pp. 201, 202
>
> >http://books.google.com/books?id=Jwiz7S7UP_IC
>
> > Notice that the authors of this book explicitly point out that the
> > even deal with the fact that even among those protein sequences that
> > are viable, most are non-beneficial from the perspective of a
> > particular life form in a particular environment.
>
> > Hope this helps clarify the nature of sequence space just a bit for
> > you.
>
> Even without reading the source, I have a couple of points of
> disagreement.
Oh, so you don't have to read the article to know that the authors are
mistaken?
> Proteins are assembled by a stepwise mechanism and the
> protein 'folds' (and that includes re-folding) as it is being
> synthesized. Since folding is merely the process of finding the
> lowest energy state at that temperature, the claim that most sequences
> do not find the set of 3-D structures that have the lowest energy
> state but simply flounder around in a perpetual state of structural
> flux is clearly nonsense that no physicist worth his or her salt
> should be claiming. *That* would be a violation of the laws of
> thermodynamics. *Most* sequences will form one or a few stable or
> quasi-stable structures (or stable substructures linked by flexible
> linkers) because of spontaneous folding to minimum thermodynamic
> structures (hydrophobic structures on the inside; hydrophilic on the
> outside). Temperature obviously can affect the relative stability as
> can other environmental conditions. That is why all proteins denature
> at some temperature. Some sequences (functional or not) would be
> structurally unstable in the conditions the particular organism lives
> in (e.g., hydrothermal pools as opposed to arctic ice lakes). Natural
> selection simply excludes such sequences from being searched.
You don't seem to understand the concept of protein viability.
Protein viability is determined by a protein's ability to successfully
avoid rapid proteolysis by proteolytic enzymes and/or non-specific
aggregation as well as the ability to be able to form stable folds.
Beyond this, natural selection does not exclude such sequences from
being searched because natural selection cannot select until after the
sequence is produced. Random mutations produce novel sequences before
selection takes place. And, therefore, random mutations most
certainly can search regions of non-viable protein sequence space.
> That said, it *is* possible for the same sequence to fold several
> different ways into a *few* stable or quasi-stable (at certain
> temperatures) structures. [Prions, for example.] It is also possible
> for a protein to, instead of folding on itself, to attach to and
> aggregate to other proteins. When one *denatures* (disrupts) the
> structure of proteins (by heat, acid, or base extremes) and then goes
> rapidly back to the normal conditions, the protein, even those with
> known function and structure, will not typically fold back properly
> but will aggregate with other proteins and fold back in ways that
> disrupt function. [There are some interesting exceptions. RNase A
> function, for example, is very hard to remove precisely because the
> small protein, over time, will, in a fraction of the proteins, re-fold
> in such a way to form a functional peptide after denaturation. A slow
> renaturation favors such spontaneous re-folding.]
This has nothing to do with the fact that the majority of potential
proteins in sequence space are not viable from the perspective of a
given life form in a given environment.
> Unfortunately for Sean, even *if* there are regions of sequence space
> that cannot form a stable (or a few stable -- as in prions)
> structures, all that would do is reduce the size of total sequence
> space that is searchable by natural mechanisms.
Unfortunately for Howard, this notion is mistaken. All of sequence
space can be searched via random mutations.
> Any mutation that
> entered such a space would quickly be removed from the population (if
> it were deleterious), just like any other lethal or functionless (if
> such lack of function were deleterious rather than beneficial -- there
> are instances where "loss-of-function" mutations are beneficial).
Now you are talking about natural selection. Again, natural selection
cannot remove something until it is already there - i.e., until the
random search has actually hit upon it and brought it into the gene
pool. In other words, just because natural selection removes
something from a gene pool doesn't mean it was therefore non-
searchable. Nature has nothing to do with the search until after the
search is performed. Natural selection only selects among the options
that the random search produced - and then only between those
sequences/structures that are actually functionally unique (i.e.,
functionally non-neutral).
> If
> Sean wants to claim that some specific search algorithm that produced
> some actual real protein sequence *must* have crossed a series of
> sequences that lack any structure, he has to produce real evidence
> rather than bogus math based on a strawman model of evolution that
> calls the *maximum gap size* assuming random synthesis of sequences
> from scratch or from a *maximally* distant sequence the "average gap
> size".
The evidence for non-beneficial gaps is obvious. Look at any protein-
based system that exists and compare it to all other known protein-
based systems. If you do this, you will notice a pattern. Those
systems that require a greater number of amino acid "characters", at
minimum, will have a greater number of minimum differences between
themselves and the next closest viable, potentially beneficial protein-
based system.
The very same thing is true in all language/information systems.
Sean Pitman
www.DetectingDesign.com
Seanpit
> > The vast majority of potential DNA sequences of a given length, if
> > transcribed and translated into amino acid sequences, would produce
> > completely non-viable proteins - not to mention non-beneficial
> > proteins from the perspective of a given life form. If you don't
> > believe me, look it up an try to prove me wrong. Or, ask someone in
> > this forum. Even someone like Howard Hershey could straighten you out
> > on this very elementry fact.
>
> what is a "non-viable" protein?
Did your read the quote from the article I referenced for you? A non-
viable protein is an amino acid sequence that is subject to rapid
proteolysis or non-specific aggregation or a lack of ability to take
on any particular stable folded state.
> if it doesnt fold, it still engages in
> chemical reactions.
Not to any useful degree.
> every single chain of amino acids will engage in
> chemical reactions.
Not in a useful manner.
> since we have no idea what reactions these would
> be, there is no way to say whether or not they would be beneficial.
Yes, there is. Experimental results clearly demonstrate that the
majority of "non-viable" proteins do not produce any useful/beneficial
functions in any living thing.
You need to go back a read up a bit on "non-viable" proteins. The
link I gave you above is a decent place to start.
Sean Pitman
www.DetectingDesign.com
snex
0catch.com> wrote:
> On Feb 13, 5:03 pm, snex <s...@comcast.net> wrote:
>
> > > The vast majority of potential DNA sequences of a given length, if
> > > transcribed and translated into amino acid sequences, would produce
> > > completely non-viable proteins - not to mention non-beneficial
> > > proteins from the perspective of a given life form. If you don't
> > > believe me, look it up an try to prove me wrong. Or, ask someone in
> > > this forum. Even someone like Howard Hershey could straighten you out
> > > on this very elementry fact.
>
> > what is a "non-viable" protein?
>
> Did your read the quote from the article I referenced for you? A non-
> viable protein is an amino acid sequence that is subject to rapid
> proteolysis or non-specific aggregation or a lack of ability to take
> on any particular stable folded state.
and how is this relevant when determining if its beneficial? you dont
know what kinds of effects these reactions will have.
>
> > if it doesnt fold, it still engages in
> > chemical reactions.
>
> Not to any useful degree.
and how is this relevant when determining if its beneficial? you dont
know what kinds of effects these reactions will have.
>
> > every single chain of amino acids will engage in
> > chemical reactions.
>
> Not in a useful manner.
and how is this relevant when determining if its beneficial? you dont
know what kinds of effects these reactions will have.
>
> > since we have no idea what reactions these would
> > be, there is no way to say whether or not they would be beneficial.
>
> Yes, there is. Experimental results clearly demonstrate that the
> majority of "non-viable" proteins do not produce any useful/beneficial
> functions in any living thing.
no such experiment has ever been performed. as you yourself note, the
sequence space of these so-called "non-viable" proteins may be very
large. nobody has searched even 1% of them.
_Arthur
http://groups.google.ca/group/talk.origins/browse_frm/thread/258b143a2018a09d/c9ddc14dafb46f3c?hl=en&lnk=raot#c9ddc14dafb46f3c
You assert blithely:
> Chadwick is a believer in a very limited form of evolution and
> speciation - as am I. This does not mean that he believes in high-
> level evolution. There are very clear limits in terms of functional
> complexity beyond which evolution does not go and cannot go this side
> of trillions of years of time (i.e., beyond those functional systems
> that require at least 1000 fairly specified amino acid residues
> working together at the same time).
I have a couple of question for you:
1) How many aa differences is there between the allele for blue eyes
and brown eyes ?
2) How many aa differences do you estimate between your DNA and my
DNA ?
3) Are we of different species, did goddidit ?
Seanpit
>
> So what is the average ratio of non-viable proteins compared to viable
> proteins for any length of DNA after a single nucleotide mutation?
> I'm assuming you have worked this out since you keep making statements
> about how unlikely it is for viable proteins to be produced.
"For a 100-dimensional space (corresponding to a 100-residue protein),
99% of the sequence volume would be in the outer 1% of the
hypersphere. If the region inside the hypersphere represents viable
proteins - foldable and stable - and the region outside the
hypersphere represents non-viable proteins - unfoldable and unstable -
this suggests that the vast majority of viable proteins are barely
viable."
http://www.beilstein-institut.de/bozen2004/proceedings/Goldstein/Goldstein.htm
Of course, as you increase the size of sequence space, the number of
non-viable protein options outpaces the viable options exponentially.
Among those that are viable, the vast majority of them are marginally
viable . In fact, most useful proteins are marginally stable so that
they have at least a fair degree of flexibility and adaptability.
However, the fact that a protein sequence is viable, does not mean
that it is therefore useful or "beneficial" from the perspective of a
particular life form in a particular environment. Obviously, the
number of proteins that are both viable and potentially useful will be
far less than the number that are just viable. This means that the
ratio of proteins that are actually beneficial vs. non-beneficial will
decrease at an even greater exponential rate with an increase in the
size of the overall sequence space.
You forget that the odds of the next closest potentially beneficial
sequence will be just 3-character differences away drops exponentially
as the overall ratio of potentially beneficial vs. non-beneficial
targets drops in the overall sequence space. Pretty soon the odds
that an addition of any 3-character sequence will produce any novel
beneficial change reaches quite close to zero. Now, on average, 5 or
6 additional characters or character changes are needed to reach the
next closest potentially beneficial target sequence.
Beyond this little problem, you don't seem to realize that mutations
can affect the entire sequence, from beginning to end. Sure, natural
selection can maintain a particular starting sequence, like AAA CCC
TTT (or whatever), but mutations come in all kinds of varieties.
Point mutations could affect any character in the sequence to produce
something like TAA CCC TTT. Multicharacter or "indel" mutations could
also affect any portion of the starting sequence, and even replace
most or all of it - to include something like AAG TTC CCT TTG. You
also forget about neutral random walks where natural selection does
not infer. In fact, most mutations are considered to be essentially
neutral with respect to function.
> Here is question for you. What is the probability of these two
> sequences appearing at the fifth generation of our hypothetical beastie:
>
> AAA CCC TTT GTT AAT
> AAA CTC ACT GTC TAT
It depends upon the ability of natural selection to guide each
individual mutation - - the odds of which drop exponentially with each
additional character requirement.
Sean Pitman
www.DetectingDesign.com
Seanpit
> Hey, Pitt, in the threadhttp://groups.google.ca/group/talk.origins/browse_frm/thread/258b143a...
>
> You assert blithely:
>
> > Chadwick is a believer in a very limited form of evolution and
> > speciation - as am I. This does not mean that he believes in high-
> > level evolution. There are very clear limits in terms of functional
> > complexity beyond which evolution does not go and cannot go this side
> > of trillions of years of time (i.e., beyond those functional systems
> > that require at least 1000 fairly specified amino acid residues
> > working together at the same time).
>
> I have a couple of question for you:
>
> 1) How many aa differences is there between the allele for blue eyes
> and brown eyes ?
The mutations needed to produce blue eyes involve the OCA2 gene that
produces a P-protein. Various numbers of mutations in different
locations of the OCA2 gene can inhibit the production of melanin
pigment to varying degrees. Complete disruption of P-protein
production produces a condition known as albinism. Such mutations are
relatively easy to produce in short order because they involve the
disruption of a pre-existing functional system. Many different
mutations have the potential to disrupt this system and produce
varying degrees of blue eyes.
This is also the basic mechanism for many forms of antibiotic
resistance. Most forms of antibiotic resistance work by using random
mutations to disrupt the pre-established antibiotic target
interaction. Many different mutations can result in at least some
disruption of this interaction and thereby produce varying degrees of
antibiotic resistance for the mutant bacterium. Since there are so
many potential options for success, antibiotic resistance is rapidly
achieved to the vast majority of antibiotics in short order in a
decent sized colony of bacteria given sublethal levels of exposure.
Remember, Humpty Dumpty. It is easy to break something because there
are so many ways to do it. It is quite another thing to make
something entirely new that is not dependent upon the disruption of
some pre-existing system or interaction (i.e., to put Humpty Dumpty
back together again).
This is also the basis for various cancerous conditions, such as
chronic myelogenous leukemia (CML). CML is based on a mutation that
produces a genetic translocation between specific regions of
chromosomes 9 and 22. The result is a link up between portions of
proteins BCR and ABL. This link up prevents the tyrosine kinase
activity of ABL from being turned off. In other words, the mutation
results in disruption of a pre-established functional system. The
constant turned-on state of ABL results in an inability of the cell to
go into apoptosis and cell death. And, a survival advantage is gained
for that cell and its offspring - but not for the host of course.
Such examples of evolution in action, though quite real, are very low
level examples. Even examples of the evolution of novel single
protein enzymes, like lactase or nylonase, are much higher-level
examples of evolution in action since they actually produce something
new without the need to destroy or disrupt some pre-existing system or
interaction.
> 2) How many aa differences do you estimate between your DNA and my
> DNA ?
Quite a few actually. Each child experiences around 200 to 300
mutations in each generation. Fortunately though, the majority of
these are functionally neutral. Of those that are functional, the
vast majority are detrimental.
> 3) Are we of different species, did goddidit ?
Intelligent design is not required for all genetic differences.
However, certain functional differences (like those with minimum
structural requirements beyond 1000aa) are clearly beyond the powers
of any non-deliberate mindless non-directed process of nature.
Sean Pitman
www.DetectingDesign.com
Seanpit
< snip >
> no such experiment has ever been performed. as you yourself note, the
> sequence space of these so-called "non-viable" proteins may be very
> large. nobody has searched even 1% of them.
A great many have been produced via random generation. None that have
been produced have proved to be beneficial. Now, you may argue that
there is always a chance that others which have not been produced
might prove to be beneficial - to a majority, but that is highly
unlikely given the evidence that is currently available.
Did you actually read the reference I gave you?
Sean Pitman
www.DetectingDesign.com
Seanpit
wrote:
>
> >> Wrong. In a terrain data information system, every possible data value
> >> for
> >> elevation is potentially meaningful or useful. Every possible sequence of
> >> elevation values is potentially meaningful or useful.
>
> > Not from a given perspective of a particular life form in a particular
> > environment.
>
> If you are going to restrict your view to "a given perspective of a
> particular life form in a particular environment" then you should not begin
> your argument with "All known language/information systems share a common
> feature." I was pointing out that you were starting from a flawed premise
> about the nature of known language/information systems, so life forms and
> environments are not relevant.
All known language/information systems depend upon being viewed from a
particular perspective/environment. Character sequences, by
themselves, are meaningless without a particular context or
environment - like the English lanuage *system*. The same thing is
true of DNA sequences. A DNA sequence means nothing outside of the
context of a particular organism and environment. That is what is
meant by a language "system".
> > When a mutation produces a novel genetic sequence in a particular
> > living thing in a particular environment, the vast majority of
> > potential mutations will not be beneficial. Even when it comes to
> > producing low-level single protein systems (<1000aa), most mutations
> > will be functionally neutral. Of those that do produce a functional
> > change (about 1%) most will be detrimental by a ratio of at least
> > 1000:1. As one considers higher-level systems, systems that require a
> > greater minimum structural threshold, the ratio of non-beneficial vs.
> > beneficial declines even further - in an exponential manner.
>
> You can go on making these unfounded assertions as long as you like, Sean.
> That does not make these falsehoods any more correct. In any case, it has
> nothing to do with my previous post, which was challenging your broad
> assertions about languages and information processing *in general* and *not*
> in the context of Biology.
All languages and information processing are done in context - the
same as biosystems.
> Now how about addressing the snipped challenge? I'll restore the text for
> your convenience below:
>
> > This is true of the English language as well as all other spoken or
> > written human languages, computer codes and programs, and even of
> > genetic information and protein-based biosystems.
>
> Prove it. Let's take the APL programming language. Demonstrate this
> exponential drop-off for APL, please.
Prove me wrong using any language/information system you want.
> > Let's start with the English language/information system. What is the
> > ratio of potentially meaningful vs. meaningless 2-character sequences
> > are there? Well, its around 1 in 7. What about 3-character
> > sequences? About 1 in 18. What about 7-character sequences? About 1
> > in 250,000.
>
> Extrapolating from a single analogy, eh?
It works exactly the same way with any meaningful language/information
you choose. There is no fundamental difference.
> > Exactly the same pattern is present in computer codes and programs.
>
> And just how many computer codes and programs did you research in order to
> reach this dubious conclusion, Sean? Not many, I'll bet. At the assembly
> language level, for example, you are quite wrong. I've programmed in
> FORTRAN, Basic, Pascal, C, APL,
> custom script languages, dozens of assembly
> languages, direct machine language, bit slice, PLDs, and custom machine
> languages of my own design for custom machines. The simpler the language
> structure, the less likely that increasing sequence length produces anything
> like the kind of ratios you describe.
Systems of meaningful/beneficial function that require an increased
sequence length and/or specificity will be exponentially less common
in sequence space regardless of the coding language system you are
using. It is true of English, Spanish, Dutch, Russian, all the
computer languages you've listed, Morse Code, all biosystems, etc.
They are all essentially the same. They all code for useful
information with various character sequences. They all also have
essentially the same ratio and distribution of potential targets at
different minimum size and specificity requirements in sequence
space.
If you think I'm wrong to any significant degree for any existing
language system you know of, then by all means, prove me wrong.
Sean Pitman
www.DetectingDesign.com
Seanpit
> Seanpit <seanpitnos...@naturalselection.0catch.com> writes
>
> >> Actually thinking about this it even makes an obvious prediction. Given
> >> that species have split off at different times in the past there should
> >> be numerous examples of proteins that had the same root but which
> >> developed in different ways in different species as different "gaps"
> >> were crossed.
>
> >Different uses of the same basic structure can also be equally
> >explained by conservation of design. Human designers use this feature
> >all the time. Why reinvent the wheel each time a wheel-like
> >structure, with a few modifications, might be useful?
>
> Re-reading this I realised that you completely mis-answered my
> prediction. You pulled one of the stock creationist answers out at the
> wrong time.
>
> I was not saying that the same sequences would be present in multiple
> organisms here, in fact I'm saying almost the opposite. What I was
> saying is that if there is the "gap" between primitive proteins and
> modern ones then examples of the gap being crossed in stages should
> exist in different species as they split off at different times in the
> past.
I know. That is the nested hierarchy argument. In short, the closer
the evolutionary relationship, the more similar the genetic sequence.
Again, this pattern, while certainly explainable via common ancestry,
is also explainable via common design.
Herein is the basis of the design-only hypothesis. This hypothesis
can be falsified if it can be shown that the nested differences can in
fact be produced via any non-deliberate non-intelligent process of
nature.
> Can you give us some examples of these large gaps you keep talking
> about? Maybe after you do that we could look at the related species to
> see whether the "gap" was crossed in slightly different ways in
> different species giving *different* but functional protein end results.
Look at any higher-level system, like the flagellar motility system.
Now, try to find the next closest uniquely functional beneficial
system. How many character differences are there at minimum?
Hmmmmmm? That minimum difference constitutes the minimum gap size.
For the flagellar system, requiring around 10,000 fairly specified
codons of genetic real estate, the minimum gap size is dozens of
character difference wide. This is an uncrossable gap this side of
trillions upon trillions of years of time - even given a colony the
size of all the bacteria on Earth (i.e., ~1e30 or so).
> Give us an example of these gaps from humans since both we and
> (theoretically) closely related species have been sequenced so the data
> is readily available for all to look at.
Actually, even though our genome has been sequenced, the functional
elements of our genome, compared with say, apes, are still poorly
understood. It is much easier to consider functional differences of
lower-level creatures, like bacteria, where the functional features
and differences are much better known in much greater detail.
> If evolution happened then we should see the DNA sequence for your
> example large gap being crossed as we go back through the species
> towards what we consider more primitive forms (although this is slightly
> complicated by the fact that they will have been evolving for exactly
> the same time as we have, but the basic principle should hold true)
> --
> to...@wacky.zzn.com
Sean Pitman
www.DetectingDesign.com
hersheyh
0catch.com> wrote:
> On Feb 14, 7:19 am, hersheyh <hershe...@yahoo.com> wrote:
>
>
>
>
>
> > > "As described above, sequence space is a highly dimensional
> > > space. The majority of possible sequences represent non-viable
> > > proteins, with no accessible and stable folded state. We can imagine
> > > that there are regions in this space that do correspond to viable
> > > proteins with a stability sufficient to avoid proteolysis and
> > > aggregation. The boundary between this viable region and the
> > > surrounding unviable region then represents the boundary between
> > > stable and unstable native states."
>
> > > E. I. Shakhnovich, R. A. Broglia, G. Tiana, "Protein Folding,
> > > Evolution And Design", 2001. ISBN 1586031694, pp. 201, 202
>
> > >http://books.google.com/books?id=Jwiz7S7UP_IC
>
> > > Notice that the authors of this book explicitly point out that the
> > > majority of possible protein sequences are "non-viable". This doesn't
> > > even deal with the fact that even among those protein sequences that
> > > are viable, most are non-beneficial from the perspective of a
> > > particular life form in a particular environment.
>
> > > Hope this helps clarify the nature of sequence space just a bit for
> > > you.
>
> > Even without reading the source, I have a couple of points of
> > disagreement.
>
> Oh, so you don't have to read the article to know that the authors are
> mistaken?
>
>
> > Proteins are assembled by a stepwise mechanism and the
> > protein 'folds' (and that includes re-folding) as it is being
> > synthesized. Since folding is merely the process of finding the
> > lowest energy state at that temperature, the claim that most sequences
> > do not find the set of 3-D structures that have the lowest energy
> > state but simply flounder around in a perpetual state of structural
> > flux is clearly nonsense that no physicist worth his or her salt
> > should be claiming. *That* would be a violation of the laws of
> > thermodynamics. *Most* sequences will form one or a few stable or
> > quasi-stable structures (or stable substructures linked by flexible
> > linkers) because of spontaneous folding to minimum thermodynamic
> > structures (hydrophobic structures on the inside; hydrophilic on the
> > outside). Temperature obviously can affect the relative stability as
> > can other environmental conditions. That is why all proteins denature
> > at some temperature. Some sequences (functional or not) would be
> > structurally unstable in the conditions the particular organism lives
> > in (e.g., hydrothermal pools as opposed to arctic ice lakes). Natural
> > selection simply excludes such sequences from being searched.
>
> You don't seem to understand the concept of protein viability.
Proteins cannot exhibit "viability". They can exhibit "stability".
They can exhibit differential rates of degradibility by proteases.
But they are not "alive".
> Protein viability is determined by a protein's ability to successfully
> avoid rapid proteolysis by proteolytic enzymes and/or non-specific
> aggregation as well as the ability to be able to form stable folds.
That is not "viability". But I certainly agree that some proteins are
more stable and less susceptible to degradation than others.
Including 'functional' proteins.
BTW, globular proteins are more stable.
> Beyond this, natural selection does not exclude such sequences from
> being searched because natural selection cannot select until after the
> sequence is produced. Random mutations produce novel sequences before
> selection takes place. And, therefore, random mutations most
> certainly can search regions of non-viable protein sequence space.
That means only that mutation can continually test the waters of
stability, not cross it. You seem to be claiming that in order to
produce a new 'functional' protein from the "maximally distant"
sequence you always start with that it *must* cross a space in which
it goes from being unstable to being more unstable. You are claiming
that there cannot *even in principle* be a pathway that does not
involve crossing such gaps. Yet you cannot produce a single example
to support that claim.
>
> > That said, it *is* possible for the same sequence to fold several
> > different ways into a *few* stable or quasi-stable (at certain
> > temperatures) structures. [Prions, for example.] It is also possible
> > for a protein to, instead of folding on itself, to attach to and
> > aggregate to other proteins. When one *denatures* (disrupts) the
> > structure of proteins (by heat, acid, or base extremes) and then goes
> > rapidly back to the normal conditions, the protein, even those with
> > known function and structure, will not typically fold back properly
> > but will aggregate with other proteins and fold back in ways that
> > disrupt function. [There are some interesting exceptions. RNase A
> > function, for example, is very hard to remove precisely because the
> > small protein, over time, will, in a fraction of the proteins, re-fold
> > in such a way to form a functional peptide after denaturation. A slow
> > renaturation favors such spontaneous re-folding.]
>
> This has nothing to do with the fact that the majority of potential
> proteins in sequence space are not viable from the perspective of a
> given life form in a given environment.
SFW? No evolutionary biologist claims that new proteins evolve by
entering in and crossing such "unstable" sequence space.
>
> > Unfortunately for Sean, even *if* there are regions of sequence space
> > that cannot form a stable (or a few stable -- as in prions)
> > structures, all that would do is reduce the size of total sequence
> > space that is searchable by natural mechanisms.
>
> Unfortunately for Howard, this notion is mistaken. All of sequence
> space can be searched via random mutations.
No, I am not mistaken. Your claim would only be true if all of
sequence space can be reached by a single mutation from some pre-
existing functional sequence. If there are sequence spaces that can
only be reached by mutation first to one of your "inviable" sequences
and then having second, third, or fourth mutations to carry it deeper
into the heart of darkness, all the subsequent changes after the first
will be irrelevant. Selection (be it for or against) will have
already occurred *after* the first mutation.
You are still under the delusion that somehow evolution proceeds by
crossing long *functionless* gaps. It doesn't. No one (beside you)
claims it does. Specifically, *your* math claims that the starting
point for any protein of any size is either no sequence at all (the
protein is constructed aa by aa completely by chance) and just happens
to plug in the right aa's in the right sites or, what is essentially
the same thing, starts with a protein of the right length but one that
has the wrong aa at each and every functionally relevant site which
must be changed to the correct aa by chance alone. And, in both
cases, you assume that NONE of the sequences except the teleologically
determined end set of sequences (having the right aa's at the
functionally relevant sites, not the irrelevant filler sites) can have
ANY function at all. This despite the fact that many other functional
proteins of that same size may exist.
> > Any mutation that
> > entered such a space would quickly be removed from the population (if
> > it were deleterious), just like any other lethal or functionless (if
> > such lack of function were deleterious rather than beneficial -- there
> > are instances where "loss-of-function" mutations are beneficial).
>
> Now you are talking about natural selection.
Well, duh. Glad you could recognize it.
> Again, natural selection
> cannot remove something until it is already there - i.e., until the
> random search has actually hit upon it and brought it into the gene
> pool.
And, effectively, in the large population, a strongly deleterious
mutation won't be there in any significant numbers. The waters can be
tested, but unless the change is beneficial, the odds are that it will
never be significant.
> In other words, just because natural selection removes
> something from a gene pool doesn't mean it was therefore non-
> searchable. Nature has nothing to do with the search until after the
> search is performed. Natural selection only selects among the options
> that the random search produced - and then only between those
> sequences/structures that are actually functionally unique (i.e.,
> functionally non-neutral).
I certainly agree that natural selection only works on variants that
actually appear. Which is why new genes are so very, very often due
to modification of pre-existing genes and recombinations of functional
moieties. IOW, you keep trying to pretend (or lie) that evolution
works by crossing these large functionless *gaps*. I am telling you
that, when a mutation to functionlessness (if that is detrimental)
occurs, it is selected against. Further changes to a functionless
gene may occur, and it might happen that some later such change
produces a new function, but that is not the usual pathway for
evolution of a new protein function. New protein functions arise by
modification of pre-existing proteins (as evidenced by sequence
homology) or by chimera formation. Typically this occurs by changes
that produce a functional protein at each and every step.
>
> > If
> > Sean wants to claim that some specific search algorithm that produced
> > some actual real protein sequence *must* have crossed a series of
> > sequences that lack any structure, he has to produce real evidence
> > rather than bogus math based on a strawman model of evolution that
> > calls the *maximum gap size* assuming random synthesis of sequences
> > from scratch or from a *maximally* distant sequence the "average gap
> > size".
>
> The evidence for non-beneficial gaps is obvious.
It is not obvious. And your math is still bogus numerology. You
continually use the dishonest term "average" gap, when you have not
ever presented an "average", but only a *maximum*.
> Look at any protein-
> based system that exists and compare it to all other known protein-
> based systems. If you do this, you will notice a pattern.
Yes. A pattern of sequence homology and derivation from ancestral
sequences. And a pattern of selectively neutral changes that is
easily explained by historical branching patterns.
> Those
> systems that require a greater number of amino acid "characters", at
> minimum, will have a greater number of minimum differences between
> themselves and the next closest viable, potentially beneficial protein-
> based system.
That is not a pattern I see. Nor have you presented a shred of
evidence for it. In fact, you yourself have presented evidence
against this pattern in that you give examples of systems where
evolution has occurred and shown that the number of mutational steps
required to produce these changes are quite small. Of course, you
always make 'excuses' for why these examples of evolution don't meet
your criteria.
R. Baldwin
> On Feb 13, 6:46 pm, "R. Baldwin" <res0k...@nozirevBACKWARDS.net>
> wrote:
>>
>> >> Wrong. In a terrain data information system, every possible data value
>> >> for
>> >> elevation is potentially meaningful or useful. Every possible sequence
>> >> of
>> >> elevation values is potentially meaningful or useful.
>>
>> > Not from a given perspective of a particular life form in a particular
>> > environment.
>>
>> If you are going to restrict your view to "a given perspective of a
>> particular life form in a particular environment" then you should not
>> begin
>> your argument with "All known language/information systems share a common
>> feature." I was pointing out that you were starting from a flawed premise
>> about the nature of known language/information systems, so life forms and
>> environments are not relevant.
>
> All known language/information systems depend upon being viewed from a
> particular perspective/environment. Character sequences, by
> themselves, are meaningless without a particular context or
> environment - like the English lanuage *system*. The same thing is
> true of DNA sequences. A DNA sequence means nothing outside of the
> context of a particular organism and environment. That is what is
> meant by a language "system".
Irrelevent. You still started with a flawed premise, namely:
> > All known language/information systems share a common feature. If
> > concepts or ideas or forms of information require a greater number of
> > characters or a greater specificity of character arrangement, the
> > ratio of potentially meaningful or useful or functional systems
> > relative to the number of potential character arrangements drops off
> > *exponentially*.
Within this flawed premise we see nothing about "being viewed from a
particular perspective/environment." You are making a strict claim about a
ratio, and assert (without evidence) that this applies to "all known
language/information systems." Not "all known lanugage systems," but "all
known language/information systems." I gave an example where your claim
clearly doesn't hold, so we at the very least must withdraw the word "all."
>
>> > When a mutation produces a novel genetic sequence in a particular
>> > living thing in a particular environment, the vast majority of
>> > potential mutations will not be beneficial. Even when it comes to
>> > producing low-level single protein systems (<1000aa), most mutations
>> > will be functionally neutral. Of those that do produce a functional
>> > change (about 1%) most will be detrimental by a ratio of at least
>> > 1000:1. As one considers higher-level systems, systems that require a
>> > greater minimum structural threshold, the ratio of non-beneficial vs.
>> > beneficial declines even further - in an exponential manner.
>>
>> You can go on making these unfounded assertions as long as you like,
>> Sean.
>> That does not make these falsehoods any more correct. In any case, it has
>> nothing to do with my previous post, which was challenging your broad
>> assertions about languages and information processing *in general* and
>> *not*
>> in the context of Biology.
>
> All languages and information processing are done in context - the
> same as biosystems.
So what?
>
>> Now how about addressing the snipped challenge? I'll restore the text for
>> your convenience below:
>>
>> > This is true of the English language as well as all other spoken or
>> > written human languages, computer codes and programs, and even of
>> > genetic information and protein-based biosystems.
>>
>> Prove it. Let's take the APL programming language. Demonstrate this
>> exponential drop-off for APL, please.
>
> Prove me wrong using any language/information system you want.
I didn't make any claim about languages. You did. Back up your assertion, or
withdraw it. I don't think you can. I think you pulled it out of nothing,
having no background knowledge, because it sounded nice to you and you
thought it supported your argument.
HOW MANY computer codes and programs have you evaluated for this exponential
ratio that you claim exists, Sean? I would be astounded if that number is as
large as one. What method did you use to establish this ratio? Where are
your statistical results?
>
>> > Let's start with the English language/information system. What is the
>> > ratio of potentially meaningful vs. meaningless 2-character sequences
>> > are there? Well, its around 1 in 7. What about 3-character
>> > sequences? About 1 in 18. What about 7-character sequences? About 1
>> > in 250,000.
>>
>> Extrapolating from a single analogy, eh?
>
> It works exactly the same way with any meaningful language/information
> you choose. There is no fundamental difference.
Demonstrate this. I think you are lying. I don't think you have any data to
back this assertion up.
>
>> > Exactly the same pattern is present in computer codes and programs.
>>
>> And just how many computer codes and programs did you research in order
>> to
>> reach this dubious conclusion, Sean? Not many, I'll bet. At the assembly
>> language level, for example, you are quite wrong. I've programmed in
>> FORTRAN, Basic, Pascal, C, APL,
>> custom script languages, dozens of assembly
>> languages, direct machine language, bit slice, PLDs, and custom machine
>> languages of my own design for custom machines. The simpler the language
>> structure, the less likely that increasing sequence length produces
>> anything
>> like the kind of ratios you describe.
>
> Systems of meaningful/beneficial function that require an increased
> sequence length and/or specificity will be exponentially less common
> in sequence space regardless of the coding language system you are
> using. It is true of English, Spanish, Dutch, Russian, all the
> computer languages you've listed, Morse Code, all biosystems, etc.
Where is your data, Sean? How have you gone about determining this ration
for such a broad array of situations?
>
> They are all essentially the same. They all code for useful
> information with various character sequences. They all also have
> essentially the same ratio and distribution of potential targets at
> different minimum size and specificity requirements in sequence
> space.
How do you know this? What analytical method gave you data on the
"distribution of potential targets" for all languages, all computer codes,
and all programs?
>
> If you think I'm wrong to any significant degree for any existing
> language system you know of, then by all means, prove me wrong.
>
The burden is on the person making the claim, Sean. That is you.
snex
0catch.com> wrote:
> On Feb 14, 5:43 pm, snex <s...@comcast.net> wrote:
>
> < snip >
>
> > no such experiment has ever been performed. as you yourself note, the
> > sequence space of these so-called "non-viable" proteins may be very
> > large. nobody has searched even 1% of them.
>
> A great many have been produced via random generation. None that have
> been produced have proved to be beneficial. Now, you may argue that
> there is always a chance that others which have not been produced
> might prove to be beneficial - to a majority, but that is highly
> unlikely given the evidence that is currently available.
*none* that have been produced have proven so? come on, nobody is dumb
enough to believe that. references of beneficial mutations are
everywhere.
snex
>
> > Now how about addressing the snipped challenge? I'll restore the text for
> > your convenience below:
>
> > > This is true of the English language as well as all other spoken or
> > > written human languages, computer codes and programs, and even of
> > > genetic information and protein-based biosystems.
>
> > Prove it. Let's take the APL programming language. Demonstrate this
> > exponential drop-off for APL, please.
>
> Prove me wrong using any language/information system you want.
brainfuck without looping structures. every single string of
characters in the language produces a viable program. therefore, any
mutation will result in a viable program.
just like the way the genetic code maps to amino acids. every single
string of nucleotides codes for some molecule that reacts with other
molecules in its environment.
<snip>
Tony Raymonds
<76640160-ba7b-4fe2...@d5g2000hsc.googlegroups.com>,
Seanpit <seanpi...@naturalselection.0catch.com> writes
>> Can you give us some examples of these large gaps you keep talking
>> about? Maybe after you do that we could look at the related species to
>> see whether the "gap" was crossed in slightly different ways in
>> different species giving *different* but functional protein end results.
>
>Look at any higher-level system, like the flagellar motility system.
Is that the *only* example you people have? I specifically asked for an
example in humans.
It's also an example that has been shown to be false as the various
parts have been shown to have functions outside of the flagella system
*and* it appears that there are at least two different flagellum system
- which means that there was not a unique target that had to be hit.
That last point means that it is probable that there are many more
flagellum system that are possible.
http://en.wikipedia.org/wiki/Evolution_of_flagella
http://en.wikipedia.org/wiki/Flagellum
>Now, try to find the next closest uniquely functional beneficial
>system.
Actually we would only need to find a system which is very slightly
worse than the current flagellum system, and that is probably only a few
base changes away.
>How many character differences are there at minimum?
>Hmmmmmm? That minimum difference constitutes the minimum gap size.
>For the flagellar system, requiring around 10,000 fairly specified
>codons of genetic real estate, the minimum gap size is dozens of
>character difference wide. This is an uncrossable gap this side of
>trillions upon trillions of years of time - even given a colony the
>size of all the bacteria on Earth (i.e., ~1e30 or so).
You are back to saying that any hand of cards is impossible because the
odds of the particular cards ending up in it is infinitesimally small.
To show that it is "uncrossable gap" you have to show that you cannot
add, remove or change any part of the DNA sequence without turning the
resulting proteins into something that has no biological function.
You haven't shown that it is an uncrossable gap other than by assertion
so your conclusion fails.
Note that in adding, removing or changing bases you would be going
*backwards* in time and reversing the evolutionary process so the
changes would probably make the flagella *worse* at each step.
>> Give us an example of these gaps from humans since both we and
>> (theoretically) closely related species have been sequenced so the data
>> is readily available for all to look at.
>
>Actually, even though our genome has been sequenced, the functional
>elements of our genome, compared with say, apes, are still poorly
>understood. It is much easier to consider functional differences of
>lower-level creatures, like bacteria, where the functional features
>and differences are much better known in much greater detail.
So you don't actually have any example of the gaps that you base all
your calculations on? Why should we just take your word for it that
these large gaps are there at all?
--
to...@wacky.zzn.com
Tony Raymonds
<a43365cf-90da-4810...@i29g2000prf.googlegroups.com>,
Seanpit <seanpi...@naturalselection.0catch.com> writes
>Beyond this, natural selection does not exclude such sequences from
>being searched because natural selection cannot select until after the
>sequence is produced. Random mutations produce novel sequences before
>selection takes place. And, therefore, random mutations most
>certainly can search regions of non-viable protein sequence space.
Yes, but very little of the non-viable protein space will be searched
compared to non-viable space and that is the bit you are ignoring.
Proteins come in families which all have the same root. If the root
protein was not viable then none of the related family of proteins will
not be searched. In effect natural selection optimises the search to
only viable families of proteins so very little of the non-viable
protein space will be searched.
This will dramatically reduce the odds of new non-viable proteins being
produced after a mutation, and is why your calculations are wrong.
--
to...@wacky.zzn.com
Tony Raymonds
<d390fa86-d185-40ff...@e6g2000prf.googlegroups.com>,
Seanpit <seanpi...@naturalselection.0catch.com> writes
>On Feb 14, 5:30 am, Tony Raymonds <to...@wacky.zzn.com> wrote:
>>
>> So what is the average ratio of non-viable proteins compared to viable
>> proteins for any length of DNA after a single nucleotide mutation?
>> I'm assuming you have worked this out since you keep making statements
>> about how unlikely it is for viable proteins to be produced.
>
>"For a 100-dimensional space (corresponding to a 100-residue protein),
>99% of the sequence volume would be in the outer 1% of the
>hypersphere. If the region inside the hypersphere represents viable
>proteins - foldable and stable - and the region outside the
>hypersphere represents non-viable proteins - unfoldable and unstable -
>this suggests that the vast majority of viable proteins are barely
>viable."
You didn't answer the question. I asked:
>> So what is the average ratio of non-viable proteins compared to viable
>> proteins for any length of DNA after a single nucleotide mutation?
What you did was give me the size of the entire search space. The odds
of a viable protein (i.e. one that does not make the whole organism
non-viable) being a single base pair change away from an existing viable
sequence is vastly higher than generating a complete 100 base pair
sequence completely at random.
Evolution does not do that so your answer giving the size of the entire
search space is irrelevant.
If I asked you the distance to my nearest shop would you answer that the
average distance from me to all shops on the planet is 20,000km so I
should book a flight to buy my groceries?
<snip>
>This means that the
>ratio of proteins that are actually beneficial vs. non-beneficial will
>decrease at an even greater exponential rate with an increase in the
>size of the overall sequence space.
But the space isn't searched randomly, it starts from a beneficial root
and explores out along neutral and beneficial pathways. Beneficial
mutations will quickly spread through the whole population whereas
neutral mutations will allow the population to drift into new search
spaces.
<snip>
>> There is *no* exponential increase in the unlikelyhood of each step.
>> That is why your calculations giving exponential decrease of
>> probabilities are nonsense and, given that you have not shown that there
>> the large gaps that you keep talking about exist, it means your
>> assertions are groundless.
>
>You forget that the odds of the next closest potentially beneficial
>sequence will be just 3-character differences away drops exponentially
>as the overall ratio of potentially beneficial vs. non-beneficial
>targets drops in the overall sequence space.
I didn't forget it, I just don't accept your groundless assertion.
If I'm crossing an ocean by sailing from island to island and have got
half way across then is it exponentially more unlikely that I will find
the next island compared to me finding the first island when I started?
All it needs is that the next codon added be either neutral or
beneficial, as long as it doesn't harm the organism. In our
hypothetical example all in needs is that at least 1 in 64 possible next
codon steps must not be harmful to the organism.
I will agree that if *all* 64 possible next steps are non-viable then it
is stuck, but you haven't shown anything like that happens in reality.
The only time exponential numbers are involved is if you think there is
a pre-defined target at the end which you are trying to reach by a
random walk, but that is not how evolution works. There are no targets.
> Pretty soon the odds
>that an addition of any 3-character sequence will produce any novel
>beneficial change reaches quite close to zero. Now, on average, 5 or
>6 additional characters or character changes are needed to reach the
>next closest potentially beneficial target sequence.
Ah, at last we have some interesting numbers. How did you calculate that
"5 or 6" additional changes are needed for the next beneficial sequence?
Actually even if it were true then that kind of gap could be hopped over
quite easily assuming that there were some non-viable search paths which
could be weeded out early.
>Beyond this little problem, you don't seem to realize that mutations
>can affect the entire sequence, from beginning to end.
What makes you think I don't know that? I simplified my example to
avoid that complication not because I didn't know about it but because
it makes it easier to show the principle of what is going on.
>Sure, natural
>selection can maintain a particular starting sequence, like AAA CCC
>TTT (or whatever), but mutations come in all kinds of varieties.
I explained that I limited mutations to adding a codon at the end to
make a point, which you appear to have missed completely. I know full
well that mutations do not normally happen like that. That is why I
wrote:
> (unrealistic I know, but it's a simplified example)
<snip>
>> Here is question for you. What is the probability of these two
>> sequences appearing at the fifth generation of our hypothetical beastie:
>>
>> AAA CCC TTT GTT AAT
>> AAA CTC ACT GTC TAT
>
>It depends upon the ability of natural selection to guide each
>individual mutation - - the odds of which drop exponentially with each
>additional character requirement.
So you won't do any calculations on my simplified example but you want
us to accept your calculations about the probability of crossing your
theoretical gaps in real life DNA sequences when even scientists working
in the field admit that there is much they don't understand yet?
Note that natural selection does not guide mutations, it can only choose
from the available mutations. In addition the odds only drop off
exponentially if you have a *known* target that you are trying to reach
randomly. There are no targets in evolution. That's why your
calculations do not reflect reality.
I'll ask you a simpler question about my hypothetical organism in the
previous post. What are the odds of the non-viable sequence below
appearing at the fifth generation if all sequences starting with "AAA
CTC" are lethal at the second generation?
AAA CTC ACT GTC TAT
_Arthur
New functionalities happening "at very low level" in a very short
time, much less than 100 years. That should be a clue to you, Sean.
> > 2) How many aa differences do you estimate between your DNA and my
> > DNA ?
>
> Quite a few actually. Each child experiences around 200 to 300
> mutations in each generation. Fortunately though, the majority of
> these are functionally neutral. Of those that are functional, the
> vast majority are detrimental.
"Of those that are functional, the vast majority are detrimental."
Do you have a cite for this ? PubMed reference, please.
You'll notice that none of those mutations are attributed to a protein
falling into a Neutral Gap, in any of the peer-reviewed litterature.
"200 to 300" mutations ??? The last number I heard was 3, 0 to 9
mutations between parents and child being a normal range.
So, You and me can differ in hundres of alleles, totalizing more than
your voodo number "1000 aa".
> > 3) Are we of different species, did goddidit ?
>
> Intelligent design is not required for all genetic differences.
> However, certain functional differences (like those with minimum
> structural requirements beyond 1000aa) are clearly beyond the powers
> of any non-deliberate mindless non-directed process of nature.
Huh ? Which functional differences have such "minimum structural
requirements" ?
Please compute the structural requirement of the elephant trunk and
the penguin flipper for me, Sean.
No handwaving, use only numbers from scientific publications.
Ron O
>
> > 3) Are we of different species, did goddidit ?
>
> Intelligent design is not required for all genetic differences.
> However, certain functional differences (like those with minimum
> structural requirements beyond 1000aa) are clearly beyond the powers
> of any non-deliberate mindless non-directed process of nature.
Give an example in nature. One verifiable 1000aa whatever. Why can't
you do that? Doesn't prevaricating and lying get to you?
They really need you in Florida right now. There are plenty of rubes
that fell for the teach ID scam, but for some reason they can't find
anything to teach. They don't need this obfuscation bull pucky, they
need something real. Why do they have to take the switch scam like
you had to? Why isn't there any science of intelligent design worth
teaching. Doesn't that make the name of your web site some kind of
dishonest scam? Why still try to run the scam when the perps that ran
it have a new scam that doesn't even mention that ID ever existed?
Why do the Florida rubes have to settle for some dishonest switch scam
if ID were all it was cracked up to be?
Why run and pretend? You made the claims that you had science to
teach to school kids about intelligent design, so where is this
science? You claimed that you had an alternative to common descent
that had evidence for it that was just as good as the evidence that
real science has, so why run? Why not make good on your claims? Why
are you stuck running an obfuscation scam?
Without the science, and without a vaild alternative all you can do is
blow smoke. How honest could that possibly be?
Why do you think that running and pretending is a valid means of
settling your bogus claims? We aren't just talking about a few posts,
but years of dishonest evasion.
Sean is an example of one of the principle reasons why so may
creationist rubes had to have the bait and switch scam run on them in
Florida by the guys that they trusted to support their views. The
science side didn't have to run a dishonest scam on them. It was
their own side. Sean knows this for a fact. Sean is the type of
person responsible for such a dishonest boondoggle.
Hey, Sean, whose fault was it that the Florida creationist rubes
didn't get the memo that the switch was in and that ID was just a
dishonest political ploy. They didn't get it from guys like you, with
Design in your web page name. Guys that never came up with any
intelligent design science worth teaching. Guys that keep running and
pretending.
Ron Okimoto
>
> Sean Pitmanwww.DetectingDesign.com-
Ron O
It is a common expectation. Just look up any molecular paper that
deals with what types of mutations are not seen in the coding regions
of genes. The vast majority of mutations in the coding regions that
are observed (after selection) fixed or nearly fixed withing a species
are found at the redundant positions of the codons. The mutations
that are missing (not observed after selection) should outnumber the
observed ones by around 2:1. This is only for closely related
species. The more divergent the taxa the more the ratio slips back to
what would be expected because replacement subsitutions build up over
time as the "neutral" ones or the tolerated ones increase in number.
Ask Sean how long it would take to skew the ratio back like that. He
knows that the mutations that are selected against really happen all
the time, so how long would it take to accumulate all the replacment
substitutions that we see between distantly related species, but that
we do not see between more closely related species like chimps and
humans?
>
> "200 to 300" mutations ??? The last number I heard was 3, 0 to 9
> mutations between parents and child being a normal range.
> So, You and me can differ in hundres of alleles, totalizing more than
> your voodo number "1000 aa".
The new estimates within the last decade have gone to around 200
mutations inherited from your parents. Look up papers by Nachman in
PubMed and go to related papers to find the references.
>
> > > 3) Are we of different species, did goddidit ?
>
> > Intelligent design is not required for all genetic differences.
> > However, certain functional differences (like those with minimum
> > structural requirements beyond 1000aa) are clearly beyond the powers
> > of any non-deliberate mindless non-directed process of nature.
>
> Huh ? Which functional differences have such "minimum structural
> requirements" ?
> Please compute the structural requirement of the elephant trunk and
> the penguin flipper for me, Sean.
> No handwaving, use only numbers from scientific publications.-
Prevarication is a way of life for Sean. For some reason he thinks
that if he just shades the truth or forgets to mention certain things
that it isn't lying.
Ron Okimoto
hersheyh
> On Feb 15, 6:40 am, _Arthur <Arth...@sympatico.ca> wrote:
>
>
>
> > Seanpit wrote:
[snip]
>
> Prevarication is a way of life for Sean. For some reason he thinks
> that if he just shades the truth or forgets to mention certain things
> that it isn't lying.
You are too kind to Sean. His major form of prevarication is simply
to name numbers either as something they are not ("average gap size"
for example is not an "average" at all in the mathematical sense -- he
has no average of actual trials measuring gap sizes) or to make
grandiose claims (the ratio of sequences with modern cytochrome c
function to a number which is close to the number of sequences without
modern cytochrome c function becomes the "ratio of functional to non-
functional sequences for proteins 100 aa long" -- it isn't).
Sean, but only when pressed in this forum and *not* at all on his web
site, admits that he cannot actually produce the values he is claiming
to present. This is a classic bait-and-switch con. He falsely
advertises that he has a brand new Lexus for $10,000, but when he
actually presents something, we observe that it is a rusty AMC Gremlin
that doesn't run that he has put a lexus symbol on. In his case, he
presents bogus numerology based on a strawman model of evolution that
he knows is false. He claims that this is the best he can do, so we
should be satisfied with his results.
His bogus numerology is pure con game designed to dupe innumerate
idiots and HE KNOWS IT. There will be a special place in hell....
>
> Ron Okimoto
Seanpit
> In article
> <a43365cf-90da-4810-b65b-f53529473...@i29g2000prf.googlegroups.com>,
> Seanpit <seanpitnos...@naturalselection.0catch.com> writes
>
> >Beyond this, natural selection does not exclude such sequences from
> >being searched because natural selection cannot select until after the
> >sequence is produced. Random mutations produce novel sequences before
> >selection takes place. And, therefore, random mutations most
> >certainly can search regions of non-viable protein sequence space.
>
> Yes, but very little of the non-viable protein space will be searched
> compared to non-viable space and that is the bit you are ignoring.
>
> Proteins come in families which all have the same root. If the root
> protein was not viable then none of the related family of proteins will
> only viable families of proteins so very little of the non-viable
> protein space will be searched.
>
> This will dramatically reduce the odds of new non-viable proteins being
> produced after a mutation, and is why your calculations are wrong.
You are mistaken. The majority of functionally unique mutations are
detrimental, not beneficial. Also, there are many different kinds of
mutations, to include multicharacter indel type mutations, insertions,
and deletions, that can take very large steps in any direction within
hyperdimensional sequence space. Natural selection plays no part in
these types of mutations until after the random step is taken. While
it is true that multicharacter mutations are less common than single
character mutations, like point mutations, the fact remains that all
of sequence space is open to search.
Beyond this, the real problem here is in finding novel functional
systems beyond the starting points. You say that it isn't a problem
because the protein families are so clustered. It is true that there
is a clustering effect in sequence space where potentially beneficial
sequence islands are somewhat clustered together. However, this
clustering effect becomes less and less clustered at higher and higher
levels of functional complexity. That's the real problem with your
notions here.
Sean Pitman
www.DetectingDesign.com
Seanpit
LOL - right . . .
This "wording" is used quite commonly in literature. These authors
aren't the only ones. I'm afraid your "wording" is a bit
aberrant . . .
> > > Proteins are assembled by a stepwise mechanism and the
> > > protein 'folds' (and that includes re-folding) as it is being
> > > synthesized. Since folding is merely the process of finding the
> > > lowest energy state at that temperature, the claim that most sequences
> > > do not find the set of 3-D structures that have the lowest energy
> > > state but simply flounder around in a perpetual state of structural
> > > flux is clearly nonsense that no physicist worth his or her salt
> > > should be claiming. *That* would be a violation of the laws of
> > > thermodynamics. *Most* sequences will form one or a few stable or
> > > quasi-stable structures (or stable substructures linked by flexible
> > > linkers) because of spontaneous folding to minimum thermodynamic
> > > structures (hydrophobic structures on the inside; hydrophilic on the
> > > outside). Temperature obviously can affect the relative stability as
> > > can other environmental conditions. That is why all proteins denature
> > > at some temperature. Some sequences (functional or not) would be
> > > structurally unstable in the conditions the particular organism lives
> > > in (e.g., hydrothermal pools as opposed to arctic ice lakes). Natural
> > > selection simply excludes such sequences from being searched.
>
> > You don't seem to understand the concept of protein viability.
>
> Proteins cannot exhibit "viability". They can exhibit "stability".
> They can exhibit differential rates of degradibility by proteases.
> But they are not "alive".
You are too much sometimes. The word "viable" doesn't only mean
"alive". It also means "workable", "possible", "doable", etc. Most
potential sequences simply aren't "workable" because of their lack of
enough stability or ability to avoid rapid proteolysis, etc.
> > Protein viability is determined by a protein's ability to successfully
> > avoid rapid proteolysis by proteolytic enzymes and/or non-specific
> > aggregation as well as the ability to be able to form stable folds.
>
> That is not "viability". But I certainly agree that some proteins are
> more stable and less susceptible to degradation than others.
> Including 'functional' proteins.
Most functional proteins are neither highly stable nor unstable.
There is a viability threshold when it comes to stability. Go below
this threshold and the protein sequence is not viable. I know you
don't like that word, but that is your problem. You just don't
understand its meaning in context for some odd reason.
> BTW, globular proteins are more stable.
Not all stable proteins are "viable" or "workable".
> > Beyond this, natural selection does not exclude such sequences from
> > being searched because natural selection cannot select until after the
> > sequence is produced. Random mutations produce novel sequences before
> > selection takes place. And, therefore, random mutations most
> > certainly can search regions of non-viable protein sequence space.
>
> That means only that mutation can continually test the waters of
> stability, not cross it. You seem to be claiming that in order to
> produce a new 'functional' protein from the "maximally distant"
> sequence you always start with that it *must* cross a space in which
> it goes from being unstable to being more unstable. You are claiming
> that there cannot *even in principle* be a pathway that does not
> involve crossing such gaps. Yet you cannot produce a single example
> to support that claim.
You continually present this mischaracterization despite my repeated
corrections of this very same strawman of yours. As I've always
pointed out to you, the starting point is never "maximally distant".
How many times have I explained to you that the average gap distance
is always smaller than the minimum size requirement and the minimum
likely gap distance is always smaller than the average gap distance?
I must have explained this to you dozens of times by now. And you
still can't remember?
Your notion that the minimum likely distance is always the minimum
possible distance of one mutation, regardless of the minimum
structural threshold requirements, is what is unsupported and
downright ludicrous here. Yes, "in principle" the minimum gap
distance could always be just one character change wide - just like
you like to suggest. However, in practice, the odds that this will
actually be the case in reality drop dramatically with each increase
in the minimum structural threshold requirements - along a Poisson
distribution.
I've also explained that concept to you dozens of times as well - -
yet you evidently don't remember any of those explanations either. A
goldfish could do better.
Your notions are simply way off base. You clearly don't understand
the nature of sequence space or how it is searched. Your statement
that non-viable sequence are beyond the search is clearly wrong and
your notion of a likely one step gap regardless of the level of
functional complexity is even more inane.
< snip >
> > In other words, just because natural selection removes
> > something from a gene pool doesn't mean it was therefore non-
> > searchable. Nature has nothing to do with the search until after the
> > search is performed. Natural selection only selects among the options
> > that the random search produced - and then only between those
> > sequences/structures that are actually functionally unique (i.e.,
> > functionally non-neutral).
>
> I certainly agree that natural selection only works on variants that
> actually appear. Which is why new genes are so very, very often due
> to modification of pre-existing genes and recombinations of functional
> moieties. IOW, you keep trying to pretend (or lie) that evolution
> works by crossing these large functionless *gaps*.
I never said that evolution could only work by crossing large gaps. I
said that evolution could work in this manner. Clearly, small steps
are much more common than large steps. But, contrary to your
assertion, large steps are not impossible. They happen all the time.
Also, there are large sections of DNA that are essentially free of the
influence of natural selection and can sustain many mutations without
hindrance along a long random walk. Such sections can then be cut and
pasted elsewhere in the genome to produce large random walk steps.
In short, you are the one trying to limit your own mechanism. I'm
only trying to show you that your proposed mechanism is much more
flexible than you are suggesting. The problem really isn't with the
mechanism per se. It is with the nature of sequence space and the
distribution of potential targets at different levels of functional
complexity. The minimum likely gap distance simply doesn't stay at
the minimum possible distance like you suggest. That notion is pure
nonsense - completely counter to the available data.
< snip rest until you can get at least this much right >
Sean Pitman
www.DetectingDesign.com
Seanpit
Not when it comes to "non-viable" sequences. There are no examples of
a highly unstable beneficial protein.
> > Did you actually read the reference I gave you?
I take that as a no? That figures.
Sean Pitman
www.DetectingDesign.com
richardal...@googlemail.com
0catch.com> wrote:
> On Feb 15, 1:35 am, Tony Raymonds <to...@wacky.zzn.com> wrote:
>
>
>
> > In article
> > <a43365cf-90da-4810-b65b-f53529473...@i29g2000prf.googlegroups.com>,
> > Seanpit <seanpitnos...@naturalselection.0catch.com> writes
>
> > >Beyond this, natural selection does not exclude such sequences from
> > >being searched because natural selection cannot select until after the
> > >sequence is produced. Random mutations produce novel sequences before
> > >selection takes place. And, therefore, random mutations most
> > >certainly can search regions of non-viable protein sequence space.
>
> > Yes, but very little of the non-viable protein space will be searched
> > compared to non-viable space and that is the bit you are ignoring.
>
> > Proteins come in families which all have the same root. If the root
> > protein was not viable then none of the related family of proteins will
> > be searched. In effect natural selection optimises the search to
> > only viable families of proteins so very little of the non-viable
> > protein space will be searched.
>
> > This will dramatically reduce the odds of new non-viable proteins being
> > produced after a mutation, and is why your calculations are wrong.
>
> You are mistaken.
Oh?
> The majority of functionally unique mutations are
> detrimental, not beneficial.
No, the majority of mutations are neutral. About 95%, in fact.
> Also, there are many different kinds of
> mutations, to include multicharacter indel type mutations, insertions,
> and deletions, that can take very large steps in any direction within
> hyperdimensional sequence space.
Nope. Wrong again. Mutations are more common on some parts of the
genome than others.
> Natural selection plays no part in
> these types of mutations until after the random step is taken. While
> it is true that multicharacter mutations are less common than single
> character mutations, like point mutations, the fact remains that all
> of sequence space is open to search.
Nope, wrong again. Only the portions of sequence space which are close
to existing sequences are available.
>
> Beyond this, the real problem here is in finding novel functional
> systems beyond the starting points.
Nope, wrong again. There are no "starting points". Any existing
protein is the outcome of three and a half billion years of evolution.
> You say that it isn't a problem
> because the protein families are so clustered. It is true that there
> is a clustering effect in sequence space where potentially beneficial
> sequence islands are somewhat clustered together.
Nope, wrong again. The proteins are clustered in sequence space
because they share the same evolutionary origin. There may be other
regions in sequence space which contain beneficial proteins, but they
have not been exploited by existing living organisms because those
regions cannot be reached by small incremental modifications of
existing proteins.
> However, this
> clustering effect becomes less and less clustered at higher and higher
> levels of functional complexity.
...which is an unfounded assertion.
> That's the real problem with your
> notions here.
The problem with your notions, Sean, is that they are false
conclusions drawn from unfounded assertions using faulty logic and
rhetoric.
You know this.
I know this.
The other contributors to this forum know it.
Why persist in posting the same old garbage over and over again?
Of course, I have formulated the hypothesis that you do so because
your ego thrives on the fact that you can con some creationists into
thinking that you are providing scientific arguments against
evolution, and every time you post you provide additional evidence to
support that hypothesis.
You could falsify that hypothesis by writing up your "theories" into a
coherent form and submitting them to review by people who you think
capable of understanding them.
The fact that you refuse to tell us who you *do* think is capable of
understanding your "theories" merely supports my hypothesis.
Who do you think you are fooling?
RF
>
> > to...@wacky.zzn.com
>
> Sean Pitmanwww.DetectingDesign.com
Seanpit
New low-level functions evolve much more quickly than 100 years. They
do indeed happen all the time - often within a single bacterial
generation (i.e., 20 minutes or so). What should be a clue to you is
that higher-level examples, such as independent functional systems
requiring a few hundred fairly specified residues, happen much less
commonly. And, examples of systems requiring over 1000aa are non-
existent in literature. That is what should really clue you in.
There is an exponential decline in evolvability with each step up the
ladder of functional complexity.
> > > 2) How many aa differences do you estimate between your DNA and my
> > > DNA ?
>
> > Quite a few actually. Each child experiences around 200 to 300
> > mutations in each generation. Fortunately though, the majority of
> > these are functionally neutral. Of those that are functional, the
> > vast majority are detrimental.
>
> "Of those that are functional, the vast majority are detrimental."
> Do you have a cite for this ? PubMed reference, please.
> You'll notice that none of those mutations are attributed to a protein
> falling into a Neutral Gap, in any of the peer-reviewed litterature.
>
> "200 to 300" mutations ??? The last number I heard was 3, 0 to 9
> mutations between parents and child being a normal range.
> So, You and me can differ in hundres of alleles, totalizing more than
> your voodo number "1000 aa".
Here are a couple of references for you:
The first suggests a mutation rate of around 277 per generation for
humans. The authors of the second article write, "The average
mutation rate was estimated to be ~2.5 x 10^8 mutations per nucleotide
site or 175 mutations per diploid genome per generation" [Based on a
higher diploid genome estimate of 7 billion base pairs].
Sudhir Kumar, Sankar Subramanian, Mutation Rates in Mammalian Genomes,
PNAS, January 22, 2002, Vol. 99, No. 2, p. 803-808. (
www.pnas.org/cgi/doi/10.1073/pnas.022629899 )
Nuchman, Michael W., Crowell, Susan L., Estimate of the Mutation Rate
per Nucleotide in Humans, Genetics, September 2000, 156: 297-304
( http://www.genetics.org/cgi/content/full/156/1/297? )
Your number of "3" is the estimate of some scientists of the
detrimental mutation rate per generation for humans. Some scientists,
like Nachmann and Crowell, favor a detrimental mutation rate (Ud) of
at least 3 per person per generation (see above listed reference).
Other scientist have suggested a Ud of more than 5 or 6.
Beyond this concept, you also don't seem to understand the idea of a
non-beneficial gap. The gap measure isn't the same thing as the
minimum structural threshold requirement. The 1000aa threshold is not
a measure of the gap distance. It is a measure of the minimum
structural threshold requirement for a system before it will work. At
the 1000aa level, the minimum likely gap distance between such a
system and any other system of equivalent complexity will be a smaller
number, like 50 or so character differences. That minimum number of
differences is the non-beneficial gap distance - which is always
smaller than the minimum structural threshold requirement.
> > > 3) Are we of different species, did goddidit ?
>
> > Intelligent design is not required for all genetic differences.
> > However, certain functional differences (like those with minimum
> > structural requirements beyond 1000aa) are clearly beyond the powers
> > of any non-deliberate mindless non-directed process of nature.
>
> Huh ? Which functional differences have such "minimum structural
> requirements" ?
> Please compute the structural requirement of the elephant trunk and
> the penguin flipper for me, Sean.
> No handwaving, use only numbers from scientific publications.
Do you think you can code for a useful elephant trunk or a penguin
flipper with less than 1000 codons of DNA? Every living thing,
including single celled organisms, have functional systems that
require far more than 1000 codons of DNA at minimum to code for them.
The flagellar motility system, for example, requires over 10,000
fairly specified codons to produce the protein-based system where all
the parts are working together at the same time. No such system, or
even parts of such a system, has ever been shown to evolve in real
time. There isn't a single example in all of literature - not one.
Sean Pitman
www.DetectingDesign.com
Tony Raymonds
<c35103d8-edea-41e8...@i12g2000prf.googlegroups.com>,
Seanpit <seanpi...@naturalselection.0catch.com> writes
>On Feb 15, 1:35 am, Tony Raymonds <to...@wacky.zzn.com> wrote:
>> In article
>> <a43365cf-90da-4810-b65b-f53529473...@i29g2000prf.googlegroups.com>,
>> Seanpit <seanpitnos...@naturalselection.0catch.com> writes
>>
>> >Beyond this, natural selection does not exclude such sequences from
>> >being searched because natural selection cannot select until after the
>> >sequence is produced. Random mutations produce novel sequences before
>> >selection takes place. And, therefore, random mutations most
>> >certainly can search regions of non-viable protein sequence space.
>>
>> Yes, but very little of the non-viable protein space will be searched
>> compared to non-viable space and that is the bit you are ignoring.
>>
>> Proteins come in families which all have the same root. If the root
>> protein was not viable then none of the related family of proteins will
>> be searched. In effect natural selection optimises the search to
>> only viable families of proteins so very little of the non-viable
>> protein space will be searched.
>>
>> This will dramatically reduce the odds of new non-viable proteins being
>> produced after a mutation, and is why your calculations are wrong.
>
>You are mistaken.
I am? Please elucidate.
>The majority of functionally unique mutations are
>detrimental, not beneficial.
Agreed, but all evolution needs is a low percentage of those
"functionally unique" mutations to be beneficial. Evolution will still
happen if the vast majority of non-neutral mutations are detrimental or
non-viable.
>Also, there are many different kinds of
>mutations, to include multicharacter indel type mutations, insertions,
>and deletions, that can take very large steps in any direction within
>hyperdimensional sequence space.
Agreed again. However it is also known that non-neutral large steps are
almost always non-viable. Although they have probably played an
occasional role it is unlikely that they are a significant source of
variation.
Having said that some potentially *neutral* large steps such as the
duplication of entire sections of the genetic sequence or even the
duplication of entire chromosomes appear to have been important in
allowing one copy to retain the original function and the other free to
explore new sequence space.
>Natural selection plays no part in
>these types of mutations until after the random step is taken. While
>it is true that multicharacter mutations are less common than single
>character mutations, like point mutations, the fact remains that all
>of sequence space is open to search.
Well technically yes, but life does not explore the entire space equally
- it preferentially searches the space around existing functional
proteins because most viable mutations are small.
It is almost certain that there are wonderful potential proteins that
life has never discovered because their sequences are too far away from
existing proteins so have never been reached. Or are you assuming that
the current set of proteins that life uses is the best possible set? If
you did believe that then it would explain a lot about your
calculations!
Your calculations are all based on the assumption that the sequence
space is search evenly and that is simply not true. Even the paper that
you asked us to read:
http://www.beilstein-institut.de/bozen2004/proceedings/Goldstein/Goldstein.htm
Said:
"For the random sequences, the more stable they are, the more
destabilizing the average mutation. In fact, for every unit of increased
initial stability, there is about an extra unit decrease in stability
resulting from a random mutation. Conversely, for evolved sequences, the
more stable the proteins, the more likely it is that the mutation will
have little or no effect on the stability! Again, population dynamics
work with evolution in order to select sequences that have fit
offspring, that is, have robustness to mutations."
Which is basically stating that evolved sequences are robust and can
take mutations without falling into one of your non-functional gaps.
This means that nearby sequences will be searched first, and most
thoroughly.
Did you actually read the paper?
>Beyond this, the real problem here is in finding novel functional
>systems beyond the starting points. You say that it isn't a problem
>because the protein families are so clustered. It is true that there
>is a clustering effect in sequence space where potentially beneficial
>sequence islands are somewhat clustered together. However, this
>clustering effect becomes less and less clustered at higher and higher
>levels of functional complexity. That's the real problem with your
>notions here.
It's only a problem if you can show that there is no route between
beneficial sequences and you have completely failed to do that.
You have no examples from the real world and your maths erroneously
assumes that all sequence space is searched equally. You have nothing
left but groundless assertions.
--
to...@wacky.zzn.com
Tony Raymonds
<62382f68-25a8-49ea...@s12g2000prg.googlegroups.com>,
hersheyh <hers...@yahoo.com> writes
>On Feb 15, 8:05 am, Ron O <rokim...@cox.net> wrote:
>> On Feb 15, 6:40 am, _Arthur <Arth...@sympatico.ca> wrote:
>>
>>
>>
>> > Seanpit wrote:
>
>[snip]
>>
>> Prevarication is a way of life for Sean. For some reason he thinks
>> that if he just shades the truth or forgets to mention certain things
>> that it isn't lying.
>
>You are too kind to Sean. His major form of prevarication is simply
>to name numbers either as something they are not ("average gap size"
>for example is not an "average" at all in the mathematical sense -- he
>has no average of actual trials measuring gap sizes)
I've never seen him show a single "gap", never mind enough of them to
generate statistics from.
--
to...@wacky.zzn.com
Seanpit
> In article
< snip >
> >You forget that the odds of the next closest potentially beneficial
> >sequence will be just 3-character differences away drops exponentially
> >as the overall ratio of potentially beneficial vs. non-beneficial
> >targets drops in the overall sequence space.
>
> I didn't forget it, I just don't accept your groundless assertion.
>
> If I'm crossing an ocean by sailing from island to island and have got
> half way across then is it exponentially more unlikely that I will find
> the next island compared to me finding the first island when I started?
You aren't sailing across the same ocean. You are trying to sail into
larger and larger oceans. Higher-level systems are part of
exponentially larger sequence spaces. To get to a higher-level
system, you have to sail into a much larger sequence space where the
islands are much farther apart. The average distances between islands
are linearly greater than they were at lower levels. This means that
the likely minimum distance between you and the next closest island is
linearly greater as well. That means that finding a new island will
require a exponentially longer trip - on average.
> All it needs is that the next codon added be either neutral or
> beneficial, as long as it doesn't harm the organism. In our
> hypothetical example all in needs is that at least 1 in 64 possible next
> codon steps must not be harmful to the organism.
You actually need the next codon to be added to be beneficial if you
wish to avoid random walk. Neutral changes require an exponentially
greater search time before success given a linear increase in the
minimum distance to the next island.
> I will agree that if *all* 64 possible next steps are non-viable then it
> is stuck, but you haven't shown anything like that happens in reality.
Name one system that requires a minimum of more than 1000 amino acid
residues working together at the same time (like a flagellar motility
system for example), that is within one residue difference of any
other novel beneficial system with a novel function.
Consider the following sequence: cat-hat-bat-bad-bid-did-dig-dog.
It is easy to link up such sequence of potentially meaningful words
with a single character difference because the minimum likely
character difference between any one 3-letter word and the next
potentially meaningful sequence is usually just one. However, the
odds that a single character difference will still do the job start to
drop dramatically with higher-level minimum requirements. Try doing
the same thing with 7-character sequences, 50-character sequences,
100, 1000, etc. It gets exponentially harder and harder. The likely
minimum gap distance does not stay at one.
You see the problem now?
< snip rest >
Sean Pitman
www.DetectingDesign.com
Seanpit
wrote:
> "Seanpit" <seanpitnos...@naturalselection.0catch.com> wrote in message
You have not given an example of a language or information *system*
that falsifies my view. The concept of a language or information
system requires an actual system - i.e., a particular perspective. At
the very least, you should have grasped this concept considering this
entire discussion is about evolution and the production of the useful
interdependent information within biosystems (i.e., a true "language"
system equivalent to English or Russian or any computer-based coded
language).
> >> > When a mutation produces a novel genetic sequence in a particular
> >> > living thing in a particular environment, the vast majority of
> >> > potential mutations will not be beneficial. Even when it comes to
> >> > producing low-level single protein systems (<1000aa), most mutations
> >> > will be functionally neutral. Of those that do produce a functional
> >> > change (about 1%) most will be detrimental by a ratio of at least
> >> > 1000:1. As one considers higher-level systems, systems that require a
> >> > greater minimum structural threshold, the ratio of non-beneficial vs.
> >> > beneficial declines even further - in an exponential manner.
>
> >> You can go on making these unfounded assertions as long as you like,
> >> Sean.
> >> That does not make these falsehoods any more correct. In any case, it has
> >> nothing to do with my previous post, which was challenging your broad
> >> assertions about languages and information processing *in general* and
> >> *not*
> >> in the context of Biology.
>
> > All languages and information processing are done in context - the
> > same as biosystems.
>
> So what?
So you were wrong . . .
You cannot have a "language" or "information" *system* without context
or perspective.
> >> Now how about addressing the snipped challenge? I'll restore the text for
> >> your convenience below:
>
> >> > This is true of the English language as well as all other spoken or
> >> > written human languages, computer codes and programs, and even of
> >> > genetic information and protein-based biosystems.
>
> >> Prove it. Let's take the APL programming language. Demonstrate this
> >> exponential drop-off for APL, please.
>
> > Prove me wrong using any language/information system you want.
>
> I didn't make any claim about languages. You did. Back up your assertion, or
> withdraw it. I don't think you can. I think you pulled it out of nothing,
> having no background knowledge, because it sounded nice to you and you
> thought it supported your argument.
>
> HOW MANY computer codes and programs have you evaluated for this exponential
> ratio that you claim exists, Sean? I would be astounded if that number is as
> large as one. What method did you use to establish this ratio? Where are
> your statistical results?
If you think I'm so obviously wrong, prove it. Should be easy. Based
on the languages I know about, they all work the same way. I'm
therefore proposing that all lanauge systems, including the ones I
don't know about, also work the same way. If you know of any language/
information system that doesn't work in the same essential way as
English, Russian, BASIC, FORTRAN, Morse Code, etc., please do share it
with me. If you don't know of any real counter, just admit it and
move on.
> >> > Let's start with the English language/information system. What is the
> >> > ratio of potentially meaningful vs. meaningless 2-character sequences
> >> > are there? Well, its around 1 in 7. What about 3-character
> >> > sequences? About 1 in 18. What about 7-character sequences? About 1
> >> > in 250,000.
>
> >> Extrapolating from a single analogy, eh?
>
> > It works exactly the same way with any meaningful language/information
> > you choose. There is no fundamental difference.
>
> Demonstrate this. I think you are lying. I don't think you have any data to
> back this assertion up.
Demonstrate that I'm wrong. You are also making an assertion here
that some language systems exist that do not follow the analogies I've
given. Where is your support for this notion?
< snip repetitive >
Sean Pitman
www.DetectingDesign.com
Tony Raymonds
<d42aa7a3-d33e-408b...@i12g2000prf.googlegroups.com>,
Seanpit <seanpi...@naturalselection.0catch.com> writes
>> > > 3) Are we of different species, did goddidit ?
>>
>> > Intelligent design is not required for all genetic differences.
>> > However, certain functional differences (like those with minimum
>> > structural requirements beyond 1000aa) are clearly beyond the powers
>> > of any non-deliberate mindless non-directed process of nature.
>>
>> Huh ? Which functional differences have such "minimum structural
>> requirements" ?
>> Please compute the structural requirement of the elephant trunk and
>> the penguin flipper for me, Sean.
>> No handwaving, use only numbers from scientific publications.
>
>Do you think you can code for a useful elephant trunk or a penguin
>flipper with less than 1000 codons of DNA? Every living thing,
>including single celled organisms, have functional systems that
>require far more than 1000 codons of DNA at minimum to code for them.
>The flagellar motility system, for example, requires over 10,000
>fairly specified codons to produce the protein-based system where all
>the parts are working together at the same time. No such system, or
>even parts of such a system, has ever been shown to evolve in real
>time. There isn't a single example in all of literature - not one.
That's simply because we haven't been looking for long enough. You
already know that is the answer so why bother stating it?
Evolution on that scale is *slow* and to generate novel sequences of the
length you are talking about will take many millions of years but here
you are saying that not being able to see them in the lab is some kind
of evidence against evolution.
The only changes we will be able to see happening in "real time" are
ones which are only a short distance away from existing sequences. For
example the lengthening of legs in Cane toads in Australia:
http://en.wikipedia.org/wiki/Cane_Toad
If I tell you that I have worked out that it will take 8 hours for my
freezer to turn a glass of water to ice then can you claim that I am
wrong if you open it after 5 minutes and the water is still liquid?
--
to...@wacky.zzn.com
Seanpit
>
> >The majority of functionally unique mutations are
> >detrimental, not beneficial.
>
> Agreed, but all evolution needs is a low percentage of those
> "functionally unique" mutations to be beneficial. Evolution will still
> happen if the vast majority of non-neutral mutations are detrimental or
> non-viable.
Not quite true. The rate of positive mutations must be high enough to
counter-balance the detrimental mutation rate - or extinction will
eventually occur. For rapidly reproducing creatures, like bacteria,
this isn't really a problem. However, for slowing reproducing
creatures, like mammals, it certainly could be a problem. That is why
one tries to avoid radiation and other such mutagens as much as
possible.
The type of "evolution" that usually occurs in such cases comes in the
form of reversion mutations. In other words, a beneficial system is
lost because of mutation by a short distance (one or two character
changes). Reversion mutations can fairly easily restore that system
since the gap distance is so small.
This is not the same type of evolution as coming up with a truly novel
system that was never within the gene pool before.
> >Also, there are many different kinds of
> >mutations, to include multicharacter indel type mutations, insertions,
> >and deletions, that can take very large steps in any direction within
> >hyperdimensional sequence space.
>
> Agreed again. However it is also known that non-neutral large steps are
> almost always non-viable.
Ah - That should tell you something about the nature of sequence
space. The vast majority of that space is non-beneficial from a the
perspective of any given life form in any given environment. The
larger the space that is required (i.e., for higher-level systems) the
exponentially smaller the ratio of potentially beneficial vs. non-
beneficial sequences.
> Although they have probably played an
> occasional role it is unlikely that they are a significant source of
> variation.
>
> Having said that some potentially *neutral* large steps such as the
> duplication of entire sections of the genetic sequence or even the
> duplication of entire chromosomes appear to have been important in
> allowing one copy to retain the original function and the other free to
> explore new sequence space.
That's the story anyway. However, duplication only makes more of the
same starting point. The problem of finding novel island functions
still requires neutral random walk. If the closest island becomes
farther away, in a linear manner, the average random walk time will
increase exponentially. This is in fact what happens with each step
up the ladder of functional complexity.
> >Natural selection plays no part in
> >these types of mutations until after the random step is taken. While
> >it is true that multicharacter mutations are less common than single
> >character mutations, like point mutations, the fact remains that all
> >of sequence space is open to search.
>
> Well technically yes, but life does not explore the entire space equally
> - it preferentially searches the space around existing functional
> proteins because most viable mutations are small.
That's true. But it is actually a problem for the ToE. The reason
for this is that higher-level systems have greater minimum distances
between one island and the next. The fact that most of the search
happens close to the starting island dramatically increases the
average time needed to find a novel island at a higher level.
> It is almost certain that there are wonderful potential proteins that
> life has never discovered because their sequences are too far away from
> existing proteins so have never been reached. Or are you assuming that
> the current set of proteins that life uses is the best possible set? If
> you did believe that then it would explain a lot about your
> calculations!
You are absolutely correct in my view. There certainly exist many
potentially beneficial systems in sequence space that have never been
discovered - at every level of functional complexity. The problem is
that the current set of systems that have been discovered demonstrate
a linear expansion of minimum gap distances with each step up the
ladder of functional complexity under consideration.
> Your calculations are all based on the assumption that the sequence
> space is search evenly and that is simply not true. Even the paper that
> you asked us to read:
>
> http://www.beilstein-institut.de/bozen2004/proceedings/Goldstein/Gold...
>
> Said:
>
> "For the random sequences, the more stable they are, the more
> destabilizing the average mutation. In fact, for every unit of increased
> initial stability, there is about an extra unit decrease in stability
> resulting from a random mutation. Conversely, for evolved sequences, the
> more stable the proteins, the more likely it is that the mutation will
> have little or no effect on the stability! Again, population dynamics
> work with evolution in order to select sequences that have fit
> offspring, that is, have robustness to mutations."
>
> Which is basically stating that evolved sequences are robust and can
> take mutations without falling into one of your non-functional gaps.
> This means that nearby sequences will be searched first, and most
> thoroughly.
>
> Did you actually read the paper?
All the authors are stating here is the obvious. Useful systems are
neither too rigid or too flexible. The same thing is true of the
English language system. Randomly change a single character in this
paragraph and odds are that the overall meaning or function of the
paragraph will not be significantly undermined. In other words, there
is a degree of flexibility to most meaningful sequences in all
language systems - to include biosystems.
All useful protein-based systems have a degree of flexibility before
all beneficial function is lost. This degree of flexibility defines
the size of the island that has a particular type of function in
sequence space. However, all protein-based systems have a flexibility
limit beyond which all beneficial function of the type in question is
lost. In other words, all systems have a degree of "irreducible
complexity" or minimum structural threshold requirements. It is this
minimum requirement, the very edge of the island, that is required to
be found by a random searcher before natural selection will kick in
and optimize the sequence for idea function from the particular
perspective of the particular life form in its particular
environment. Optimization isn't the problem. Finding the edge of the
island is the problem.
> >Beyond this, the real problem here is in finding novel functional
> >systems beyond the starting points. You say that it isn't a problem
> >because the protein families are so clustered. It is true that there
> >is a clustering effect in sequence space where potentially beneficial
> >sequence islands are somewhat clustered together. However, this
> >clustering effect becomes less and less clustered at higher and higher
> >levels of functional complexity. That's the real problem with your
> >notions here.
>
> It's only a problem if you can show that there is no route between
> beneficial sequences and you have completely failed to do that.
>
> You have no examples from the real world and your maths erroneously
> assumes that all sequence space is searched equally. You have nothing
> left but groundless assertions.
There are many examples in every living thing. Take any system of
function that requires a minimum of at least 1000 fairly specified
amino acid residues working together at the same time (like a
flagellar motility system). I challenge you to find any other
uniquely functional system that is within a few dozen required
character differences of such a system.
Good luck.
Sean Pitman
www.DetectingDesign.com
Seanpit
>
> > The majority of functionally unique mutations are
> > detrimental, not beneficial.
>
> No, the majority of mutations are neutral. About 95%, in fact.
Notice that I said that the majority of *functional* mutations are
detrimental. Neutral mutations are not "functional".
> > Also, there are many different kinds of
> > mutations, to include multicharacter indel type mutations, insertions,
> > and deletions, that can take very large steps in any direction within
> > hyperdimensional sequence space.
>
> Nope. Wrong again. Mutations are more common on some parts of the
> genome than others.
While it is true that some parts of a genome are more prone to
mutations than others, this fact doesn't counter what I just said. It
is also a fact that there are many different kinds of mutations - to
include multicharacter indel type mutations, insertions, deletions,
etc.
> > Natural selection plays no part in
> > these types of mutations until after the random step is taken. While
> > it is true that multicharacter mutations are less common than single
> > character mutations, like point mutations, the fact remains that all
> > of sequence space is open to search.
>
> Nope, wrong again. Only the portions of sequence space which are close
> to existing sequences are available.
You are mistaken. Multicharacter mutations, to include multicharacter
insertions and deletions, can and often do cross vast distances of
sequence space in a single bound.
> > Beyond this, the real problem here is in finding novel functional
> > systems beyond the starting points.
>
> Nope, wrong again. There are no "starting points". Any existing
> protein is the outcome of three and a half billion years of evolution.
Any existing sequence is a starting point upon which further searches
into sequence space begin.
> > You say that it isn't a problem
> > because the protein families are so clustered. It is true that there
> > is a clustering effect in sequence space where potentially beneficial
> > sequence islands are somewhat clustered together.
>
> Nope, wrong again. The proteins are clustered in sequence space
> because they share the same evolutionary origin. There may be other
> regions in sequence space which contain beneficial proteins, but they
> have not been exploited by existing living organisms because those
> regions cannot be reached by small incremental modifications of
> existing proteins.
Even the protein-based systems that do exist are less and less
clustered at higher and higher levels of functional complexity.
> > However, this
> > clustering effect becomes less and less clustered at higher and higher
> > levels of functional complexity.
>
> ...which is an unfounded assertion.
It isn't just an assertion, it is a demonstrable fact. All anyone
with a candid mind has to do is go and look at the protein data base
to see that I'm right. Higher-level systems are farther apart in
sequence space. That's a fact. I've already shown you this
demonstration in papers like that written by Choi and Kim. You are
just blind to the obvious.
> > That's the real problem with your
> > notions here.
>
> The problem with your notions, Sean, is that they are false
> conclusions drawn from unfounded assertions using faulty logic and
> rhetoric.
>
> You know this.
> I know this.
> The other contributors to this forum know it.
>
> Why persist in posting the same old garbage over and over again?
>
> Of course, I have formulated the hypothesis that you do so because
> your ego thrives on the fact that you can con some creationists into
> thinking that you are providing scientific arguments against
> evolution, and every time you post you provide additional evidence to
> support that hypothesis.
>
> You could falsify that hypothesis by writing up your "theories" into a
> coherent form and submitting them to review by people who you think
> capable of understanding them.
>
> The fact that you refuse to tell us who you *do* think is capable of
> understanding your "theories" merely supports my hypothesis.
>
> Who do you think you are fooling?
Stick with fossils Richard. At least there you have a remote hope of
coming off as knowing something. When it comes to genetics, you even
more clueless than usual. You feel so forced to disagree with every
little thing I say, that you make ludicrous statements and arguments
all the time - even against statements of mine that are mainstream
facts. Even Tony Raymonds agreed with most of my statements in this
particular post that you said were "wrong".
Give it up already. I do appreciate having such an obviously
ridiculous foil on occasion though. I guess I should be grateful for
that . . .
> RF
Sean Pitman
www.DetectingDesign.com
Seanpit
> In article
> <d42aa7a3-d33e-408b-b6d2-573e1609d...@i12g2000prf.googlegroups.com>,
> Seanpit <seanpitnos...@naturalselection.0catch.com> writes
Yes - - Isn't it interesting that all the available examples of
evolution in action are very low-level functions? This particular
example isn't an example of a producing a truly novel system of
function. It is only an example of modifying a pre-established
function. Modifications of pre-existing functions, like increasing or
decreasing the enzymatic activity of a particular type of enzyme or
increasing or decreasing the size of frog legs, is easy because you
are already on the island.
What is hard is finding the end of a novel island to begin with - at
higher and higher levels of functional complexity.
Novel systems that require no more than a few hundred fairly specified
amino acid residues evolve all the time. However, no novel system
that requires minimum structural threshold of at least 1000aa working
together at the same time has ever been shown to evolve - period.
> If I tell you that I have worked out that it will take 8 hours for my
> freezer to turn a glass of water to ice then can you claim that I am
> wrong if you open it after 5 minutes and the water is still liquid?
> --
> to...@wacky.zzn.com
It doesn't just take a linearly greater time for higher-level systems
to evolve. It takes an exponentially greater time. That's the
problem.
Sean Pitman
www.DetectingDesign.com
Seanpit
> On Feb 14, 8:40 pm, Seanpit <seanpitnos...@naturalselection.0catch.com> wrote:
> > On Feb 14, 5:49 pm, _Arthur <Arth...@sympatico.ca> wrote:
>
> SNIP:
>
>
>
> > > 3) Are we of different species, did goddidit ?
>
> > Intelligent design is not required for all genetic differences.
> > However, certain functional differences (like those with minimum
> > structural requirements beyond 1000aa) are clearly beyond the powers
> > of any non-deliberate mindless non-directed process of nature.
>
> Give an example in nature. One verifiable 1000aa whatever. Why can't
> you do that? Doesn't prevaricating and lying get to you?
I've done this for you dozens of times Ron. You really don't
remember? Why pretend like I've never answered this question for
you? Do you not remember my explaining to you how the flagellar
system requires at least 10,000 fairly specified amino acid residues
(equivalent to a minimum of at least 10,000 codons of genetic real
estate)? What about this did you not understand?
Beyond this, you constantly confuse the minimum structural threshold
requirement with the gap size. They aren't the same thing. The
minimum gap size is *always* smaller than the minimum strucutral
threshold size. If the structural threshold size under consideration
is 1000aa, the likely minimum gap size will be only a few dozen
character differences wide. The gap size is a measure of the minimum
number of character differences between the system in question and the
next closest potentially beneficial system in sequence space. That is
not the same thing as the minimum structure requirements needed for
system function. These are related but distinctly different
concepts.
It isn't that hard if you actually try to understand instead of just
blowing smoke.
< snip >
Sean Pitman
www.DetectingDesign.com
snex
0catch.com> wrote:
> On Feb 14, 10:32 pm, snex <s...@comcast.net> wrote:
>
>
>
> > On Feb 14, 8:43 pm, Seanpit <seanpitnos...@naturalselection.
>
> > 0catch.com> wrote:
> > > On Feb 14, 5:43 pm, snex <s...@comcast.net> wrote:
>
> > > < snip >
>
> > > > no such experiment has ever been performed. as you yourself note, the
> > > > sequence space of these so-called "non-viable" proteins may be very
> > > > large. nobody has searched even 1% of them.
>
> > > A great many have been produced via random generation. None that have
> > > been produced have proved to be beneficial. Now, you may argue that
> > > there is always a chance that others which have not been produced
> > > might prove to be beneficial - to a majority, but that is highly
> > > unlikely given the evidence that is currently available.
>
> > *none* that have been produced have proven so? come on, nobody is dumb
> > enough to believe that. references of beneficial mutations are
> > everywhere.
>
> Not when it comes to "non-viable" sequences. There are no examples of
> a highly unstable beneficial protein.
thats probably because the protein has degenerated before anybody can
find it. isnt it you IDers that hope and pray that youll find a
function for "junk-DNA" some day? maybe this is exactly the kind of
thing you should be looking for.
Seanpit
> Seanpit <seanpitnos...@naturalselection.0catch.com> writes
>
> >> Can you give us some examples of these large gaps you keep talking
> >> about? Maybe after you do that we could look at the related species to
> >> see whether the "gap" was crossed in slightly different ways in
> >> different species giving *different* but functional protein end results.
>
> >Look at any higher-level system, like the flagellar motility system.
>
> Is that the *only* example you people have? I specifically asked for an
> example in humans.
Don't you know that humans do have flagella (i.e., human men). Beyond
this, there are a lot of other examples as well. The system for DNA
transcription, RNA translation, pinocytosis, exocytosis, intracellular
vesicle transport, mitochondrial motility, ATPase, mitosis, meiosis,
etc, are all examples of systems requiring thousand of codons of
genetic real estate at minimum.
> It's also an example that has been shown to be false as the various
> parts have been shown to have functions outside of the flagella system
There are a lot of subsystem functions within the overall flagellar
system - besides the usually references TTSS system. Not one of these
is within a handful of required residue changes or differences from
the overall flagellar system. You do realize, of course, that the
minimum TTSS system requirement is no more than 10 proteins (averaging
around 300aa each) while the overall flagellar system requires around
30 structural proteins at minimum? That's a huge gap. Beyond this,
all the other proposed gaps that are smaller than this all have dozens
of minimum sequence differences relative to the next higher proposed
step in the proposed pathway.
Beyond this, you do realize that even mainstream scientist have
suggested that the TTSS system evolved from the fully formed flagellar
system - not the other way round?
http://www.detectingdesign.com/flagellum.html
> *and* it appears that there are at least two different flagellum system
> - which means that there was not a unique target that had to be hit.
There are more than two. There are actually quite a number of
uniquely different flagellar motility systems.
> That last point means that it is probable that there are many more
> flagellum system that are possible.
Certainly true. And, they are all widely separated by non-beneficial
gaps from each other and from every other system and subsystem that
might be beneficial as a steppingstone.
> http://en.wikipedia.org/wiki/Evolution_of_flagellahttp://en.wikipedia.org/wiki/Flagellum
>
> >Now, try to find the next closest uniquely functional beneficial
> >system.
>
> Actually we would only need to find a system which is very slightly
> worse than the current flagellum system, and that is probably only a few
> base changes away.
You are only moving around on the same island here. The question is
how to get to the edge of the island with a particular type of
function to begin with. Modifications and refinements to a system
once it is realized to a least some useful degree isn't a problem.
Getting to at least the edge of the island is the problem.
> >How many character differences are there at minimum?
> >Hmmmmmm? That minimum difference constitutes the minimum gap size.
> >For the flagellar system, requiring around 10,000 fairly specified
> >codons of genetic real estate, the minimum gap size is dozens of
> >character difference wide. This is an uncrossable gap this side of
> >trillions upon trillions of years of time - even given a colony the
> >size of all the bacteria on Earth (i.e., ~1e30 or so).
>
> You are back to saying that any hand of cards is impossible because the
> odds of the particular cards ending up in it is infinitesimally small.
Not true. I'm saying that getting to any "beneficial" hand of cards
is essentially impossible this side of trillion upon trillions of
years of the next closest hand is just a few dozen card differences
away.
> To show that it is "uncrossable gap" you have to show that you cannot
> add, remove or change any part of the DNA sequence without turning the
> resulting proteins into something that has no biological function.
That's also not true. It is easy to remove parts and still keep the
function of subsystems, like TTSS, intact. It is quite a different
story to start with a TTSS system that requires only 10 proteins at
minimum and get the flagellar motility system. That's a whole
different ball game. It is like breaking Humpty Dumpty vs. putting
him back together again.
> You haven't shown that it is an uncrossable gap other than by assertion
> so your conclusion fails.
Show me anything that is remotely close to any novel system beyond the
1000aa threshold.
> Note that in adding, removing or changing bases you would be going
> *backwards* in time and reversing the evolutionary process so the
> changes would probably make the flagella *worse* at each step.
Exactly - - to the point at which the motility function, in
particular, would disappear entirely well before you could realize any
other novel beneficial functional system at the same level or even at
a higher or lower level.
> >> Give us an example of these gaps from humans since both we and
> >> (theoretically) closely related species have been sequenced so the data
> >> is readily available for all to look at.
>
> >Actually, even though our genome has been sequenced, the functional
> >elements of our genome, compared with say, apes, are still poorly
> >understood. It is much easier to consider functional differences of
> >lower-level creatures, like bacteria, where the functional features
> >and differences are much better known in much greater detail.
>
> So you don't actually have any example of the gaps that you base all
> your calculations on? Why should we just take your word for it that
> these large gaps are there at all?
I've just given you an example. You haven't shown anything to
counter.
Sean Pitman
www.DetectingDesign.com
Tony Raymonds
<e461d5a5-76bc-475a...@i12g2000prf.googlegroups.com>,
Seanpit <seanpi...@naturalselection.0catch.com> writes
>> > However, this
>> > clustering effect becomes less and less clustered at higher and higher
>> > levels of functional complexity.
>>
>> ...which is an unfounded assertion.
>
>It isn't just an assertion, it is a demonstrable fact. All anyone
>with a candid mind has to do is go and look at the protein data base
>to see that I'm right. Higher-level systems are farther apart in
>sequence space. That's a fact. I've already shown you this
>demonstration in papers like that written by Choi and Kim. You are
>just blind to the obvious.
You don't define what you mean by "higher -level" but I will assume you
mean longer and more complicated. What do you mean by "farther apart"
though. From what?
For your argument to hold true you would have to mean the "gap" between
a functional protein and the next "improved" one it evolves into is
proportional to the length and complexity of the protein.
You would also have to be claiming that none of the intervening
sequences were beneficial because (by definition) that would be the end
of the gap.
I can't see how you can clam either of those though, given that you have
not shown us any gaps at all, even though you have been asked many
times. You have not produced a single one.
I'll try again, give us an example of proteins at either side of a gap
(you can use an analogous sequences between two species to do this) and
demonstrate that there is no neutral or beneficial mutation path between
the two sequences.
I'm fascinated to see you do this as I can't see how you could possibly
predict what how the intervening sequences would behave nor can I see
how can demonstrate that none of them would be beneficial.
--
to...@wacky.zzn.com
Seanpit
> Seanpit <seanpitnos...@naturalselection.0catch.com> writes
>
> >> > However, this
> >> > clustering effect becomes less and less clustered at higher and higher
> >> > levels of functional complexity.
>
> >> ...which is an unfounded assertion.
>
> >It isn't just an assertion, it is a demonstrable fact. All anyone
> >with a candid mind has to do is go and look at the protein data base
> >to see that I'm right. Higher-level systems are farther apart in
> >sequence space. That's a fact. I've already shown you this
> >demonstration in papers like that written by Choi and Kim. You are
> >just blind to the obvious.
>
> You don't define what you mean by "higher -level" but I will assume you
> mean longer and more complicated.
I have defined what I mean by higher-level many times in this forum,
but you seem to be new.
In short, a system that has a larger minimum part requirement or
greater specificity of part arrangement is a higher-level system
compared to one with fewer structural threshold requirements. So,
yes, size is part of the equation to determine what "level" of
functional complexity one is talking about.
> What do you mean by "farther apart"
> though. From what?
From other unique or novel systems of function - not just
modifications of the same system. All the sequences that carry
essentially the same function but with varying degrees of
functionality are part of the same functional "island". Getting to
different points on this island isn't a problem. Getting to an
entirely new island with a uniquely different function is a problem.
> For your argument to hold true you would have to mean the "gap" between
> a functional protein and the next "improved" one it evolves into is
> proportional to the length and complexity of the protein.
Not just "improved", but improved *and* novel with regard to
functionality. Different levels of the same function don't count.
> You would also have to be claiming that none of the intervening
> sequences were beneficial because (by definition) that would be the end
> of the gap.
That's correct . . .
> I can't see how you can clam either of those though, given that you have
> not shown us any gaps at all, even though you have been asked many
> times. You have not produced a single one.
What do you call the example of the flagellar motility system? The
minimum gap between this system and the next closest beneficial system
of any kind is more than a few dozen residue differences. The same
thing is true of practically all of the proposed steppingstones in the
proposed evolutionary pathway of flagellar evolution. All of them are
all separated by dozens of required residue differences from the
previous proposed steppingstone system. Those required residue
differences defined the gap distance.
> I'll try again, give us an example of proteins at either side of a gap
> (you can use an analogous sequences between two species to do this) and
> demonstrate that there is no neutral or beneficial mutation path between
> the two sequences.
>
> I'm fascinated to see you do this as I can't see how you could possibly
> predict what how the intervening sequences would behave nor can I see
> how can demonstrate that none of them would be beneficial.
It is impossible to prove the gap absolutely. However, it is possible
to falsify the gap idea absolutely. If only you had evidence of
intervening steppingstones beyond the 1000aa threshold. I'm telling
you, there are no closely spaced steppingstones that have very been
found beyond the 1000aa threshold level. You can look up the
sequences if you wish to try and find a closely spaced system to some
higher level system. You won't be able to do it. Beyond this, there
is no experimental evidence either. There isn't a single example of
evolution producing a novel system of function that requires at least
1000 fairly specified amino acid residues working together at the same
time. That fact is very interesting since low-level examples,
requiring only a few hundred residues, are quite common.
Sean Pitman
www.DetectingDesign.com
_Arthur
You're handwaving again. You have no idea how many "aa" mutations are
involved for a penguin's flipper or an elephant trunk, but you are
assuming that they can be safely attributed to a god tampering with a
seagull genes or an hyrax genes.
"No such system, or even parts of such a system, has ever been shown
to evolve in real time."
That offers no support for your pet speculation that it would either
take trillions of years, or that one or several gods are involved.
Seanpit
>
> > > *none* that have been produced have proven so? come on, nobody is dumb
> > > enough to believe that. references of beneficial mutations are
> > > everywhere.
>
> > Not when it comes to "non-viable" sequences. There are no examples of
> > a highly unstable beneficial protein.
>
> thats probably because the protein has degenerated before anybody can
> find it. isnt it you IDers that hope and pray that youll find a
> function for "junk-DNA" some day? maybe this is exactly the kind of
> thing you should be looking for.
Read the link I gave you . . . You obviously haven't done much reading
on this topic.
Sean Pitman
www.DetectingDesign.com
Seanpit
> On Feb 15, 11:20 am, Seanpit <seanpitnos...@naturalselection.
>
>
>
>
>
> 0catch.com> wrote:
> > On Feb 15, 4:40 am, _Arthur <Arth...@sympatico.ca> wrote:
> > > Please compute the structural requirement of the elephant trunk and
> > > the penguin flipper for me,Sean.
> > > No handwaving, use only numbers from scientific publications.
>
> > Do you think you can code for a useful elephant trunk or a penguin
> > flipper with less than 1000 codons of DNA? Every living thing,
> > including single celled organisms, have functional systems that
> > require far more than 1000 codons of DNA at minimum to code for them.
> > The flagellar motility system, for example, requires over 10,000
> > fairly specified codons to produce the protein-based system where all
> > the parts are working together at the same time. No such system, or
> > even parts of such a system, has ever been shown to evolve in real
> > time. There isn't a single example in all of literature - not one.
>
> >SeanPitmanwww.DetectingDesign.com
>
> You're handwaving again. You have no idea how many "aa" mutations are
> involved for a penguin's flipper or an elephant trunk, but you are
> assuming that they can be safely attributed to a god tampering with a
> seagull genes or an hyrax genes.
I have a very good idea that the minimum number of codons of genetic
real estate neede is well over 1000. If you think you can counter, by
all means do so.
> "No such system, or even parts of such a system, has ever been shown
> to evolve in real time."
> That offers no support for your pet speculation that it would either
> take trillions of years, or that one or several gods are involved.
A decent rough estimate of the likely minimum gap distance for
functions with minimum structural threshold requirements of at least
1000 fairly specified amino acids can be achieved. It is dozens of
character changes wide, at a likely minimum at this level.
Statistically, such a gap would indeed require trillions of years to
cross.
If you think otherwise, please do provide your reasoning. I've seen
absolutely no statistical analysis coming from you or any other
evolutionist for that matter when it comes to predicting the average
time needed to evolve novel functional systems at different levels of
complexity.
Sean Pitman
www.DetectingDesign.com
snex
assuming the book restates your assertion, it is still just a position
of ignorance. you have absolutely no idea what kinds of reactions
unstable proteins engage in.
>
> Sean Pitmanwww.DetectingDesign.com
_Arthur
0catch.com> wrote:
> Beyond this concept, you also don't seem to understand the idea of a
> non-beneficial gap. The gap measure isn't the same thing as the
> minimum structural threshold requirement. The 1000aa threshold is not
> a measure of the gap distance. It is a measure of the minimum
> structural threshold requirement for a system before it will work. At
> the 1000aa level, the minimum likely gap distance between such a
> system and any other system of equivalent complexity will be a smaller
> number, like 50 or so character differences. That minimum number of
> differences is the non-beneficial gap distance - which is always
> smaller than the minimum structural threshold requirement.
" The 1000aa threshold is not structural threshold requirement for a
system before it will work. "
That is another Pitmanism. You are saying that every "system"
whatsoever has a 1000aa "structural requirement".
Note that I already challenged you to provide the exact number of
aas, and the *exact* number of fairly specified aas in the bacterial
flagella, and you fled the thread.
"At the 1000aa level, the minimum likely gap distance between such a
number, like 50 or so character differences."
Your numbers are pulled out of thin air, or from your nether body
parts. The CytochromeC estimates, upon which you base all your voodo,
do not provide any information of the distance between Cytochrome C
and other possible protein functionalities, and leastways, say
absolutely *nothing* about the distance between an unknown "system"
and another unknown "system". You're making it up, all of it.
"That minimum number of differences is the non-beneficial gap distance
- which is always smaller than the minimum structural threshold
requirement."
Poppyycock. Do you acknowledge that there are many known proteins
for which the *known* "beneficial gap distance" is 0 (as in ZERO,
zilch and squat) ?
Any such protein makes mincemeat of your fancy sandcastle.
Glenn
> On Feb 15, 3:34 pm, Seanpit <seanpitnos...@naturalselection.
>
> > The majority of functionally unique mutations are
> > detrimental, not beneficial.
>
> No, the majority of mutations are neutral. About 95%, in fact.
>
Neutral mutations are not functional, Richard.
snip
_Arthur
Glenn, neutral mutations, (those which happen within an active genes),
do not hamper the functionality of the encoded protein.
See http://en.wikipedia.org/wiki/Neutral_mutation
For example, if a mutation would give you yellow eyes, that mutation
might be neutral.
Seanpit
>
> >> Does adding words to a book make in exponentially less likely to hold
> >> meaningful or useful information?
>
> >What is exponentially less likely is that by adding characters to a
> >book, at random, you will improve its meaning in a novel way
> >beneficial way significantly beyond where you started.
>
> So adding a random letter or character to a long book is more likely to
> damage it than adding a character or letter to a short book is it?
No, that's not true. What is more unlikely, however, is that by
adding or changing characters to system that requires a larger minimum
number of fairly specified characters one will be able to hit upon a
novel system with a novel function or meaning that also requires a
larger number of fairly specified characters at minimum.
> >That is why
> >novels and computer programs cannot be written via random mutation and
> >function-based selection. They require intelligent input in order to
> >cross over non-beneficial gaps.
>
> Assertion with no absolutely evidence to back it up. Actually computer
> programs written using random mutations can be written and work very
> well. Ever heard of genetic algorithms?
Yes, but they do not produce novel systems of function that require
significantly greater minimums than what they started with. That is
why computer programmers will never be out of work. The ability of
genetic algorithms to search out sequence spaces is actually quite
limited - despite the blazing fast search speeds of computers these
days.
> >> >This is a fundamental problem for the ToE. Every living thing
> >> >requires many systems that have minimum structural threshold
> >> >limitations well beyond the 1000aa mark. A requirement of 1000 fairly
> >> >specified amino acid residues, at minimum, produces an average gap
> >> >that is two to three hundred residues wide and a likely minimum gap
> >> >that is at least 50 mutational changes wide. Such a gap is not
> >> >crossable - even given an evolutionary time frame of several billion
> >> >years.
>
> >> The fundamental problem for your theory is, of course, that you cannot
> >> show that these gaps exist at all. Nor can you show that any apparent
> >> large gap *has* to be crossed in a single step.
>
> >The gaps do exist.
>
> Show me some then. Give me a list of proteins that cannot have a
> single amino acid deleted, added or changed without it having no
> biological function.
That's not the definition of a gap. The definition of a gap is the
number of amino acid changes or additions that are required, at
minimum, to realize a novel system of function.
> > Even between low-level systems requiring only a
> >few hundred fairly specified amino acid residues at minimum the average
> >and minimum gap sizes can be demonstrated to at least a useful
> >degree.
>
> >Beyond this, no one said that the gaps had to be crossed in a single
> >step. That's not at all true. The gaps can be crossed by a single
> >step or a series of random walk steps. The problem is that until the
> >gap is crossed, natural selection is blind and cannot help in the
> >process.
>
> Yes, exactly. It also doesn't have a target either though and that is
> the bit you are missing. You are doing the equivalent of saying a hand
> of cards is impossible because of the odds of getting that particular
> collection of cards is incredibly unlikely.
There most certainly are "target hands" - so the speak. A target hand
is a sequence that is potentially beneficial in sequence space. There
are many potential target hands. It is just that the vast majority of
possible hands are not "targets" because they would not produce any
functional benefit if they were dealt. This ratio of targets vs. non-
targets drops exponentially with each increase in the minimum size and/
or specificity requirements under consideration for novel systems of
function.
> >Therefore, the larger the gap the exponentially more steps
> >are required to cross it - on average.
>
> In reality there are actually no gaps because it's a continuum of useful
> proteins. All that natural selection says is that all the stages have
> to be useful or at least neutral. You haven't shown a single real
> example of a real gap.
Neutral differences are indeed gaps because nature is blind to such
differences. Neutral gaps can only be crossed via purely random
walk. A linear increase in even a neutral gap therefore requires an
exponential increase in the average random walk time.
There are many examples of real gaps in the available data. I've
already shown you the gaps that exist between the various proposed
steppingstones of the flagellar system. None of them are just a
handful of required residue differences - neutral or detrimental. All
of them require dozens of non-beneficial character differences. The
same thing is true for every other higher-level system beyond the
1000aa threshold limitation.
> >> The ancestor of any protein may well have crossed the gaps in small
> >> steps over many generations, each small step being either neutral or
> >> advantageous (as the disadvantageous ones will be filtered out by
> >> natural selection).
>
> >If a small step is functionally neutral, it is beyond the powers of
> >natural selection to guide it.
>
> Absolutely, there is no guiding going on. Having said that a neutral or
> even a detrimental mutation can take the protein to a different
> functional space. How can it have a detrimental mutation and not be
> selected out I hear you ask?
>
> If section of DNA which produces a protein is duplicated then the
> duplicate can mutate freely (and even lose it's original function)
> without disrupting the production of the original protein.
Then that isn't a "detrimental" mutation now is it? What you are
suggesting is a sequence that is open to neutral evolution. The
problem with neutral evolution is that it doesn't help find novel
beneficial islands any faster. Statistically there simply is no
benefit to the average time needed to find a novel beneficial island
target.
> Haemoglobin is a very good example of where this appears to have
> happened multiple times:
>
> http://en.wikipedia.org/wiki/Hemoglobin
Hemoglobin is a single protein with a minimum structural threshold
requirement of only a few hundred residues. It isn't a high-level
system. Also, none of these "stories" for various forms of the globin
molecule as parts of higher-level systems (like muscle activity vs.
oxygen transport and usage) has been demonstrated in real life. It is
imply assumed that the evolutionary mechanism produced these higher
level systems because of the similarities of some of the subparts of
the system - like hemoglobin, myoglobin, etc.
> >If the small step is advantageous,
> >then it has only crossed a small gap. Gaps are defined by being non-
> >advantageous - i.e., either neutral or detrimental or both.
>
> Give me a list of proteins in which you can show that adding, removing
> or replacing a single amino acid anywhere along it has no useful
> biological function.
Again, that's not the definition of a gap. A gap is between novel
systems of function, but between variations of functionality of the
same type of functional system. Different levels of lactase activity,
for example, do not qualify as different types of functional systems.
The difference between lactase and nylonase, on the other hand, would
qualify because these are two systems have uniquely different
functionalities.
< snip rest, repetitive >
Sean Pitman
www.DetectingDesign.com
richardal...@googlemail.com
0catch.com> wrote:
> On Feb 15, 8:14 am, richardalanforr...@googlemail.com wrote:
>
>
>
> > > The majority of functionally unique mutations are
> > > detrimental, not beneficial.
>
> > No, the majority of mutations are neutral. About 95%, in fact.
>
> Notice that I said that the majority of *functional* mutations are
> detrimental. Neutral mutations are not "functional".
Neutral mutations change the proteins which the gene expresses. The
change in the protein may not affect the functioning of the organism,
but it is nevertheless a functional change.
>
> > > Also, there are many different kinds of
> > > mutations, to include multicharacter indel type mutations, insertions,
> > > and deletions, that can take very large steps in any direction within
> > > hyperdimensional sequence space.
>
> > Nope. Wrong again. Mutations are more common on some parts of the
> > genome than others.
>
> While it is true that some parts of a genome are more prone to
> mutations than others, this fact doesn't counter what I just said.
Emm.. .yes it does.
> It
> is also a fact that there are many different kinds of mutations - to
> include multicharacter indel type mutations, insertions, deletions,
> etc.
And it is also a fact that these mutations are more common in some
parts of the genome than others, and that the incidence varies between
different organisms.
>
> > > Natural selection plays no part in
> > > these types of mutations until after the random step is taken. While
> > > it is true that multicharacter mutations are less common than single
> > > character mutations, like point mutations, the fact remains that all
> > > of sequence space is open to search.
>
> > Nope, wrong again. Only the portions of sequence space which are close
> > to existing sequences are available.
>
> You are mistaken. Multicharacter mutations, to include multicharacter
> insertions and deletions, can and often do cross vast distances of
> sequence space in a single bound.
If we are talking about the sequence space as described by protein
function, we aren't. Duplicating sections of a genome or inserting
fragments from other genomes does not mean that the proteins expressed
by those genes are changed.
>
> > > Beyond this, the real problem here is in finding novel functional
> > > systems beyond the starting points.
>
> > Nope, wrong again. There are no "starting points". Any existing
> > protein is the outcome of three and a half billion years of evolution.
>
> Any existing sequence is a starting point upon which further searches
> into sequence space begin.
And when mutations shift the "starting point", you exactly the same
applies.
> > > You say that it isn't a problem
> > > because the protein families are so clustered. It is true that there
> > > is a clustering effect in sequence space where potentially beneficial
> > > sequence islands are somewhat clustered together.
>
> > Nope, wrong again. The proteins are clustered in sequence space
> > because they share the same evolutionary origin. There may be other
> > regions in sequence space which contain beneficial proteins, but they
> > have not been exploited by existing living organisms because those
> > regions cannot be reached by small incremental modifications of
> > existing proteins.
>
> Even the protein-based systems that do exist are less and less
> clustered at higher and higher levels of functional complexity.
That's an unfounded assertion, Sean.
One of the questions you refuse to answer is how to calculate
"functional complexity".
>
> > > However, this
> > > clustering effect becomes less and less clustered at higher and higher
> > > levels of functional complexity.
>
> > ...which is an unfounded assertion.
>
> It isn't just an assertion, it is a demonstrable fact.
No, it's an unfounded assertion, because you have provided no way of
calculating functional complexity. Pulling numbers out of the air is
not calculation.
> All anyone
> with a candid mind has to do is go and look at the protein data base
> to see that I'm right.
The scientists who study the proteins and contribute to the protein
database say that you are wrong.
What do you know that they don't?
> Higher-level systems are farther apart in
> sequence space.
You have not provided any way of establishing what a "higher-level
system" is, so this is just another unfounded assertion.
> That's a fact.
No, it's an unfounded assertion.
> I've already shown you this
> demonstration in papers like that written by Choi and Kim. You are
> just blind to the obvious.
The Choi and Kim paper makes no mention of "higher-level systems".
Mind you, as you claim that this paper supports assertions which Choi
and Kim specifically state their data cannot show, I wonder if you
have read it at all.
Oh? Such as?
> Even Tony Raymonds agreed with most of my statements in this
> particular post that you said were "wrong".
>
I think that Tony Raymond is confusing genetic mutations, which can
produce large morphological and biochemical changes with the proteins
expressed by the genes which can only change by small incremental
steps.
> Give it up already. I do appreciate having such an obviously
> ridiculous foil on occasion though. I guess I should be grateful for
> that . . .
So why not prove how ignorant and silly I and all your other critics
on this forum for that matter by writing up your "theory" in a
coherent form and submitting it to people who *are* capable of
understanding them?
Of course, you won't because you know perfectly well that all you have
is a handful of unsubstantiated assertions and some numbers you have
pulled out of the air.
>
> > RF
>
> Sean Pitmanwww.DetectingDesign.com
So tell me, Sean. Why do you post the same unfounded assertions over
and over again? It's evident that you are not convincing anyone here,
so why persist? Why not write up your "theory" and present it to
people who are capable of understanding it?
Who *do* you think is capable of understanding your "theories"?
Of course, I have formulated the hypothesis that you do so because
your ego thrives on the fact that you can con some creationists into
thinking that you are providing scientific arguments against
evolution, and every time you post you provide additional evidence to
support that hypothesis.
You could falsify that hypothesis by writing up your "theories" into a
coherent form and submitting them to review by people who you think
capable of understanding them.
The fact that you refuse to tell us who you *do* think is capable of
understanding your "theories" merely supports my hypothesis.
Who do you think you are fooling?
RF
Seanpit
It is a mainstream publication by well-known well-respected
scientist. In fact, these scientist wrote this book from an
evolutionary perspective - in support of evolution.
Sean Pitman
www.DetectingDesign.com
_Arthur
Which you have repeatedly failed to do. Your "rough estimate" is an
utter sham.
>
> If you think otherwise, please do provide your reasoning. I've seen
> absolutely no statistical analysis coming from you or any other
> evolutionist for that matter when it comes to predicting the average
> time needed to evolve novel functional systems at different levels of
> complexity.
"Evolutionists" consider that partial and new partial biological
activities in proteins manifest from new point mutations of already
fonctional protein. The slightly better protein is selected for,
increases in numbers thru the population, and will eventually be the
target of other mutations, which may increase the new biological
activity. At some point, the new functionality may become more
important than the old, so the old functionality may be lost, or
continue in a different gene, thru gene duplication. The sequence
needs not to be monotonally increasing in functionality, and may even
go thru sharply reduced functionality, you would call them "gaps".
Such "gaps" are not expected to be a major point, most proteins are
expected to have a gap-less path. In other words, a protein can go
from one known biological usefulness, to a new biological usefulness,
of "function" in Pitmanese, in a single mutation, NO GAPS.
Human DNA carry many pseudogenes, functionless genes, which would be
tantamount to Pitman's "gap proteins", but are not considered by
scientist to be part of the Pitman bogus evolutionary mechanism.
If most of the human DNA was made of pseudogenes, desperately flailing
around trying to come up with "new functionalities" for no
functionality at all, then we would have the Pitman models. But
evolutionary scientists don't consider pseudogenes to be a driver of
protein evolution. Functioning genes are, and their evolution to even
better proteins or to new functionalities does not entail long
functionless periods as the base mechanism, as in Pitman's straman
model.
Seanpit
> On Feb 15, 5:20 pm, Seanpit <seanpitnos...@naturalselection.
>
> 0catch.com> wrote:
> > On Feb 15, 8:14 am, richardalanforr...@googlemail.com wrote:
>
> > > > The majority of functionally unique mutations are
> > > > detrimental, not beneficial.
>
> > > No, the majority of mutations are neutral. About 95%, in fact.
>
> > Notice that I said that the majority of *functional* mutations are
> > detrimental. Neutral mutations are not "functional".
>
> Neutral mutations change the proteins which the gene expresses. The
> change in the protein may not affect the functioning of the organism,
> but it is nevertheless a functional change.
A genetic mutation can occur without any change in protein sequence or
function. Also, many changes in protein sequence produce no
significant change in protein functionality. Such changes are
functionally neutral. Of those changes that do affect protein
function, the vast majority are detrimental. The same thing goes for
those changes that affect the overall organism. The vast majority of
such mutations are also detrimental. If a change in happens to produce
a change in protein function that does not affect the overall function
of the organism, such a change would be beyond the powers of natural
selection and would therefore be "neutral".
Again, all non-neutral changes, regardless how you define the term,
are largely negative.
< snip rest of nonsense >
Sean Pitman
Seanpit
>
> 0catch.com> wrote:
> > On Feb 15, 8:14 am, richardalanforr...@googlemail.com wrote:
>
> > > > The majority of functionally unique mutations are
> > > > detrimental, not beneficial.
>
> > > No, the majority of mutations are neutral. About 95%, in fact.
>
> > Notice that I said that the majority of *functional* mutations are
> > detrimental. Neutral mutations are not "functional".
>
> Neutral mutations change the proteins which the gene expresses. The
> change in the protein may not affect the functioning of the organism,
> but it is nevertheless a functional change.
"Here we consider the realistic situation in which all alleles are
subject to drift, some are neutral, and of the remainder, the vast
majority are detrimental."
http://nitro.biosci.arizona.edu/courses/EEB600A-2003/handouts/ECOL600ALectureHandout3.pdf
Sean Pitman
www.DetectingDesign.com
richardal...@googlemail.com
0catch.com> wrote:
> On Feb 15, 11:29 am, richardalanforr...@googlemail.com wrote:
>
>
>
> > On Feb 15, 5:20 pm, Seanpit <seanpitnos...@naturalselection.
>
> > 0catch.com> wrote:
> > > On Feb 15, 8:14 am, richardalanforr...@googlemail.com wrote:
>
> > > > > The majority of functionally unique mutations are
> > > > > detrimental, not beneficial.
>
> > > > No, the majority of mutations are neutral. About 95%, in fact.
>
> > > Notice that I said that the majority of *functional* mutations are
> > > detrimental. Neutral mutations are not "functional".
>
> > Neutral mutations change the proteins which the gene expresses. The
> > change in the protein may not affect the functioning of the organism,
> > but it is nevertheless a functional change.
>
> A genetic mutation can occur without any change in protein sequence or
> function.
...a point you have apparently missed, as you seem to be confusing
genetic mutation with mutations affecting protein expression.
> Also, many changes in protein sequence produce no
> significant change in protein functionality.
The biological role of the new protein may be the same as it's
precursor, but there is nevertheless a change in the way it functions.
That's why neutral drift is a significant factor in evolution.
> Such changes are
> functionally neutral.
That doesn't mean that they are not changes in terms of which proteins
are involved in the biology of the organism.
> Of those changes that do affect protein
> function, the vast majority are detrimental.
No, of the changes which affect protein function, the vast majority
are neutral.
> The same thing goes for
> those changes that affect the overall organism.
No, of the changes which affect the overall organism the vast majority
are neutral. Neutral mutations can involve morphological or functional
changes, but they are called neutral because they do not affect the
reproductive fitness of the organism.
At least, that's the way geneticists use the term. What do you know
that they don't?
> The vast majority of
> such mutations are also detrimental.
No, the vast majority of mutations are neutral.
> If a change in happens to produce
> a change in protein function that does not affect the overall function
> of the organism, such a change would be beyond the powers of natural
> selection and would therefore be "neutral".
>
> Again, all non-neutral changes, regardless how you define the term,
> are largely negative.
>
> < snip rest of nonsense >
>
> Sean Pitman
Ah, running away again, Sean.
How very predictable.
So tell me, Sean. Why do you post the same unfounded assertions over
and over again? It's evident that you are not convincing anyone here,
so why persist? Why not write up your "theory" and present it to
people who are capable of understanding it?
Who *do* you think is capable of understanding your "theories"?
Of course, I have formulated the hypothesis that you do so because
your ego thrives on the fact that you can con some creationists into
thinking that you are providing scientific arguments against
evolution, and every time you post you provide additional evidence to
support that hypothesis.
You could falsify that hypothesis by writing up your "theories" into a
coherent form and submitting them to review by people who you think
capable of understanding them.
The fact that you refuse to tell us who you *do* think is capable of
understanding your "theories" merely supports my hypothesis.
Who do you think you are fooling?
By the way, every time you snip this question from my posts it adds
more evidence that my hypothesis is correct.
RF
Glenn
> On Feb 15, 5:20 pm, Seanpit <seanpitnos...@naturalselection.
>
> 0catch.com> wrote:
> > On Feb 15, 8:14 am, richardalanforr...@googlemail.com wrote:
>
> > > > The majority of functionally unique mutations are
> > > > detrimental, not beneficial.
>
> > > No, the majority of mutations are neutral. About 95%, in fact.
>
> > Notice that I said that the majority of *functional* mutations are
> > detrimental. Neutral mutations are not "functional".
>
> Neutral mutations change the proteins which the gene expresses. The
> change in the protein may not affect the functioning of the organism,
> but it is nevertheless a functional change.
>
Provide a reference that supports 95% of neutral mutations not
affecting the functioning of the organism.
richardal...@googlemail.com
_Arthur
100% of neutral mutations are not affecting the organism. That's the
very definition of Neutral Mutations.
If you read on wikipedia or any other source, it will be explained to
you why most point mutations are neutral.
Either they fall into a non-coding DNA portion (and that's 98.5% of
human DNA already), or they change the third base of a codon that
encodes to the very same protein, or the mutation change slightly the
encoding of the protein, but without affecting its folds nor its
function. Even Pitman acknowledges that you can change up to 40% of
the Cytochrome C protein without affecting its heme binding
functionality.
And then a mutation affect a visible trait, like say, the leopard
spots, without the change being either good nor bad. The leoprad cub
is born with unique spots, and that's that.
I mentionned a mutation that would give an human yellow eyes. If it
doesn't impair his or her vision, the mutation would be neutral,
unless other humans would decide to seek out or to shun that
particular individual.
Yes, most mutations are neutral, and neutral mutations are not harmful
by definition, although creationist dogma sayz otherwise.
Glenn
in the sense that they do not affect the function of the organism.
Read "A neutral mutation may or may not affect the resulting protein"
and "may not have any appreciable effect on the protein or its
function." The 95% of is represented as the percentage of neutral
mutations to *all* mutations. So Wiki claims that most mutations are
"neutral mutations", but does not claim that most mutations are
without at least some functional change, be it deleterious or
advantageous.
You failed to provide a reference supporting that most functional
changes, be they functional in the sense of allele changes affecting
proteins or having selective value, are neither detrimental or
advantageous.
_Arthur
"Uncovering the evolution of the bacterial flagellum"
http://www.newscientist.com/channel/life/mg19726431.900-uncovering-the-evolution-of-the-bacterial-flagellum.html
Your should write to the journal, explain to Dan Jones how he got it
all wrong, and that he didn't spot the Pitmann Voodoo 1000aa minimum
average likely rough best estimated Poisson structural complexity of
the flagellum "system"
Seanpit
< snip >
> > If you think otherwise, please do provide your reasoning. I've seen
> > absolutely no statistical analysis coming from you or any other
> > evolutionist for that matter when it comes to predicting the average
> > time needed to evolve novel functional systems at different levels of
> > complexity.
>
> "Evolutionists" consider that partial and new partial biological
> activities in proteins manifest from new point mutations of already
> fonctional protein.
So do I.
> The slightly better protein is selected for,
> increases in numbers thru the population, and will eventually be the
> target of other mutations, which may increase the new biological
> activity.
I agree.
> At some point, the new functionality may become more
> important than the old, so the old functionality may be lost, or
> continue in a different gene, thru gene duplication.
True.
> The sequence
> needs not to be monotonally increasing in functionality, and may even
> go thru sharply reduced functionality, you would call them "gaps".
Right.
> Such "gaps" are not expected to be a major point, most proteins are
> expected to have a gap-less path. In other words, a protein can go
> from one known biological usefulness, to a new biological usefulness,
> of "function" in Pitmanese, in a single mutation, NO GAPS.
Yep - - But the odds of this happening beyond very low levels of
functional complexity are just shy of impossible this side of
trillions of years of time. And, it just doesn't happen. There isn't
a single example. That's the whole problem with your notion.
> Human DNA carry many pseudogenes, functionless genes, which would be
> tantamount to Pitman's "gap proteins", but are not considered by
> scientist to be part of the Pitman bogus evolutionary mechanism.
Truly non-functional genetic elements would be part of the "gap
proteins". Also, random mutations and function-based selection isn't
my suggested mechanism - its yours. Beyond this, many of these so-
called pseudogenes aren't really pseudo after all. Many are actually
turning out to be significantly functional, sometimes vitally
functional.
http://www.detectingdesign.com/pseudogenes.html
You really don't seem to be up on things - mutation rates and now
pseudogenes . . .
> If most of the human DNA was made of pseudogenes, desperately flailing
> around trying to come up with "new functionalities" for no
> functionality at all, then we would have the Pitman models. But
> evolutionary scientists don't consider pseudogenes to be a driver of
> protein evolution. Functioning genes are, and their evolution to even
> better proteins or to new functionalities does not entail long
> functionless periods as the base mechanism, as in Pitman's straman
> model.
Evolutionists actually consider non-functional genetic elements to aid
in evolutionary progress along with functional elements. The problem
is that neither really helps out the very very low odds of finding
novel beneficial systems beyond very low levels of functional
complexity (i.e., beyond the 1000aa threshold) this side of trillions
upon trillions of years of time.
Sean Pitman
www.DetectingDesign.com
Seanpit
> On Feb 15, 7:48 pm, Seanpit <seanpitnos...@naturalselection.
>
>
>
>
>
> 0catch.com> wrote:
> > On Feb 15, 11:29 am, richardalanforr...@googlemail.com wrote:
>
> > > On Feb 15, 5:20 pm, Seanpit <seanpitnos...@naturalselection.
>
> > > 0catch.com> wrote:
> > > > On Feb 15, 8:14 am, richardalanforr...@googlemail.com wrote:
>
> > > > > > The majority of functionally unique mutations are
> > > > > > detrimental, not beneficial.
>
> > > > > No, the majority of mutations are neutral. About 95%, in fact.
>
> > > > Notice that I said that the majority of *functional* mutations are
> > > > detrimental. Neutral mutations are not "functional".
>
> > > Neutral mutations change the proteins which the gene expresses. The
> > > change in the protein may not affect the functioning of the organism,
> > > but it is nevertheless a functional change.
>
> > A genetic mutation can occur without any change in protein sequence or
> > function.
>
> ...a point you have apparently missed, as you seem to be confusing
> genetic mutation with mutations affecting protein expression.
Let's put it this way, of those mutations that are not neutral by
whatever definition you wish to used, the vast majority of those non-
neutral mutations are detrimental.
By your own Wiki reference, the mutations that change a protein
sequence in a functionally neutral way are usually "chemically
similar". Non-neutral mutations are generally not chemically
similar. The vast majority of non-neutral mutations are in fact
detrimental with respect to ideal protein function.
"The great majority of non-neutral mutations to duplicated genes are
expected to result in a null allele (Walsh 1995; Lynch and Walsh
1998), that is, a gene that no longer codes for a functional protein."
"Here we consider the realistic situation in which all alleles are
subject to drift, some are neutral, and of the remainder, the vast
majority are detrimental."
http://nitro.biosci.arizona.edu/courses/EEB600A-2003/handouts/ECOL600ALectureHandout3.pdf
I'm afraid you are on your own here.
> > Also, many changes in protein sequence produce no
> > significant change in protein functionality.
>
> The biological role of the new protein may be the same as it's
> precursor, but there is nevertheless a change in the way it functions.
Nope - not to any significant degree. You need to reread your own Wiki
reference:
"In genetics, a neutral mutation is a mutation that occurs in an amino
acid codon (presumably within an mRNA molecule) which results in the
use of a different, but chemically similar, amino acid. This is
similar to a silent mutation, where a codon mutation may encode the
same amino acid (see Wobble Hypothesis); for example, a change from
AUU to AUC will still encode leucine, so no discernable change occurs
(a silent mutation)."
http://en.wikipedia.org/wiki/Neutral_mutation
Notice that the Wiki article equated a neutral protein sequence change
to a "silent mutation" that encodes essentially the same amino acid
residue.
Now, there is some argument as to if there is such a thing as an
entirely neutral seqeunce change to a protein. Some argue that there
will always be at least some functional effect - however minor. But,
this is besides the point. If there is a functional effect, the vast
majority of the time, it will be functionally detrimental.
> That's why neutral drift is a significant factor in evolution.
While essentially neutral drift can and does happen, statistically, it
adds nothing to evolutionary progress over any other form of
mutation. It does not significantly improve the odds of successfully
finding novel beneficial sequences.
> > Such changes are
> > functionally neutral.
>
> That doesn't mean that they are not changes in terms of which proteins
> are involved in the biology of the organism.
Yes - that is exactly what it means. Re-read your Wiki reference.
The term "chemically similar" basically means there is no essential
functional difference. Look it up.
> > Of those changes that do affect protein
> > function, the vast majority are detrimental.
>
> No, of the changes which affect protein function, the vast majority
> are neutral.
If the protein's function has been changed to a detectable degree,
that change is not functionally "neutral" - by definition. You simply
don't understand the concept of a neutral mutation. Why am I not
suprised?
Definitions of neutral mutations:
"A mutation that has no phenotypic effect."
http://www.biochem.northwestern.edu/holmgren/Glossary/Definitions/Def-N/neutral_mutation.html
"A mutation whose fixation is independent of natural selection is
termed a neutral mutation."
http://www.pnas.org/cgi/content/full/97/13/7372
< snip rest >
Sean Pitman
www.DetectingDesign.com
Seanpit
When you suggest that most mutations are not without at least some
functional change, you are going against what the Wiki article is in
fact saying. And, I agree with the author(s) of this particular Wiki
article.
The majority of all mutations are essentially neutral. However, of
those that are not neutral, the vast majority are detrimental.
> You failed to provide a reference supporting that most functional
> changes, be they functional in the sense of allele changes affecting
> proteins or having selective value, are neither detrimental or
> advantageous.
Now that's true - by definition. If a change is not neutral, it is a
functional change - by defnition. Of those changes that are
considered non-neutral, the vast majority are in fact detrimental.
Sean Pitman
www.DetectingDesign.com
Seanpit
>
> 100% of neutral mutations are not affecting the organism. That's the
> very definition of Neutral Mutations.
Correct . . .
> If you read on wikipedia or any other source, it will be explained to
> you why most point mutations are neutral.
Yep . . .
> Either they fall into a non-coding DNA portion (and that's 98.5% of
> human DNA already), or they change the third base of a codon that
> encodes to the very same protein, or the mutation change slightly the
> encoding of the protein, but without affecting its folds nor its
> function.
Right . . .
> Even Pitman acknowledges that you can change up to 40% of
> the Cytochrome C protein without affecting its heme binding
> functionality.
Not quite. You can change up to 40% of CytoC without completely
destroying its functionality. However, a 40% change will most likely
change the degree of its functionality.
> And then a mutation affect a visible trait, like say, the leopard
> spots, without the change being either good nor bad. The leoprad cub
> is born with unique spots, and that's that.
Right . . .
> I mentionned a mutation that would give an human yellow eyes. If it
> doesn't impair his or her vision, the mutation would be neutral,
> unless other humans would decide to seek out or to shun that
> particular individual.
Or unless such a change would increase the risk of blindness or the
develpment of ocular melanoma or something like that (as is the case
with albinism).
> Yes, most mutations are neutral, and neutral mutations are not harmful
> by definition,
That's correct . . .
> although creationist dogma sayz otherwise.
That's incorrect. I'm a creationists and I have no problem with most
mutations being essentially neutral. They are. The issue here is
over Richard arguing that of those mutations that are not neutral, the
majority of them are detrimental. Richard somehow thinks to argue
against this concept by suggesting that most non-neutral mutations are
actually neutral - which contradicts the very definition of a neutral
mutation.
Sean Pitman
www.DetectingDesign.com
Seanpit
I made the statement that the majority of functionally unique
mutations (i.e., non-neutral mutations) are detrimental. This is a
fact. Richard doesn't seem to understand this concept or the
Rodjk #613
Of course he knows it, he is just too dishonest to admit it.
Rodjk #613
Seanpit
> Sean, theres a brand new article on the New Scientist,
>
> Your should write to the journal, explain to Dan Jones how he got it
> all wrong, and that he didn't spot the Pitmann Voodoo 1000aa minimum
> average likely rough best estimated Poisson structural complexity of
> the flagellum "system"
I've covered a far better essay on the evolution of the flagellum by
Matzke on my website.
http://www.detectingdesign.com/flagellum.html
Please do list off the passage in this New Scientist article where the
author describes any steppingstones in the proposed evolutionary
pathway of the flagellum that require no more than a few dozen
residues additions or changes to get from one to the next. If you can
find any evidence of such small gaps between the proposed
steppingstones in this particular evolutionary pathway, I'd be very
interested.
You do understand that this form of evolution is far different than
your reference to the evolution of blue eyes from brown? Do you
understand the difference? Flagellar evolution is in a completely
different league in comparison.
Sean Pitman
www.DetectingDesign.com
Seanpit
> On Feb 14, 12:04 am, Seanpit <seanpitnos...@naturalselection.0catch.com> wrote:
>
> )
> [SP]
> > You also know that I wasn't talking about "concentration" of
> carnivore
>
> > remains in the passages you reference from my website. This is a
> > deliberate mischaracterization and strawman building on your part.
> > What I was talking about are layers in which dinosaurs are found
> > without much to each - like the Morrison formation.
>
> What on earth do you mean "without much to each"?
An obvious typo in context. Should read, "without much to eat".
> That doesn't even
> make sense as English! Do you mean that small numbers of individuals
> of each species are found in each location?
If you have to reach for spelling mistakes and typos, what's the
point? This is your first big challenging question? How lame can you
get?
< snip rest of nonsense >
Sean Pitman
www.DetectingDesign.com
Glenn
That is not going against the Wiki article. It does not claimor
indicate in any way that most mutations are without any functional
change. But then I don't think much of the way it is written. The
words "may not have", "appreciable" and functioning "corrrectly" are
weasely.
>
> The majority of all mutations are essentially neutral. However, of
> those that are not neutral, the vast majority are detrimental.
>
> > You failed to provide a reference supporting that most functional
> > changes, be they functional in the sense of allele changes affecting
> > proteins or having selective value, are neither detrimental or
> > advantageous.
>
> Now that's true - by definition. If a change is not neutral, it is a
> functional change - by defnition. Of those changes that are
> considered non-neutral, the vast majority are in fact detrimental.
>
And according to Wiki, a neutral mutation *may* be one that affects a
protein and *may* have an "appreciable", or at the least some effect
on a protein and it's function. I suspect that this is all phrased so
as to accomodate neutral evolution as a significant evolutionary
mechanism, whereby slightly advantageous and disadvantageous changes
to an organism as a result of slight changes to protein structure and
function are allowed to pass through the filter of natural selection
until cumulative changes result in a phenotypic change suddenly under
selective pressure. It seems silly to assume that evolutionists are
using "neutral" to refer to the majority of changes to genes as "no
change at all".
>