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Author Topic:   scientific end of evolution theory (2)
Peter
Member (Idle past 1478 days)
Posts: 2161
From: Cambridgeshire, UK.
Joined: 02-05-2002


Message 17 of 214 (13619)
07-16-2002 4:23 AM
Reply to: Message 16 by peter borger
07-15-2002 9:40 PM


quote:
Originally posted by peter borger:
Dear Peter,
You wonder:
1) "Why should redundant genes change at a rate any different from
any other gene ?"
I invite you to read a book on molecular evolution and study the neutral theory (Kimura). A redundant gene is a gene that can be knocked out without any effect on the organism. In contrast to essential genes, redundant genes are not under selective constraint and thus a lot of variation is expected. In particualr a lot of variation is expected at the socalled "silent" positions and third codon "wobble" positions. If you do not find variation than you have a problem, because the prediction you made by molecular evolutionary theory was wrong. This is called a falsification. If you find your theory falsified than you have to rethink your theory.

Kimura: "Of course, Darwinian change is necessary to explain change at the phenotypic level -fish becoming man- but in terms of molecules, the vast majority of them are not like that."
http://www.tulane.edu/~eeob/Courses/Heins/Evolution/lecture14.html#INTRODUCTION
The above link is about Nuetralist Theory. Basically it does not
refute natural selection as the mechanism behind adaptation,
it simply says that natural selection is not the whole story.
I.e. it says that not all genes are fixed in populations by natural
selection ... which is more or less what natural selection already
implies since it focusses on the passing on of those traits
which DO have a survival impact.
http://www.xrefer.com/entry/462336
has the following (my emphasis in bold)::
"Its [neutral theory's] proponents,while recognizing the importance of selection in determining functionally significant traits,hold that the great majority of the differences in macromolecular structures observed between individuals in a population are of no adaptive significance and have no impact on the reproductive success of the individual in which they arise. Hence, frequencies of the corresponding mutant alleles are governed by purely random events. This contrasts with the orthodox neo-Darwinian view that nearly all evolutionary changes have adaptive value for the organism and arise through natural selection"
I think a perceptual problem has arisen in re-defining Darwin's
changes in traits over time to changes in allele frequency over
time.
The link between allele frequency and traits seems to be the stumbling
block ... it's kind of a 'systems' problem. Applying functionalist
reductionism to the problem doesn't appear approriate because of
emergent properties.
Non-the-less, not even Motoo Kimura was suggesting that natural
selection didn't happen ... only that it wasn't the whole story.
Hmm ... perhaps Syamsu's 'General Theory of Reproduction' would
have some benefits after all
quote:
Originally posted by peter borger:
You say:
1)"I don't see how the relationship (or lack of it) between GR and
GD has any bearing on the issue at hand."
Evolution theory says that all genes have been derived from gene duplications. (the hypothesis that they are derived from chromosome duplication has been falsified over and over by Hughes et al). Thus, if redundant genes are derived from duplications, one expects to find a correlation between duplication and redundancy.) This prediction has clearly been falsified in Saccharomyces (Winzeler et al; Science 1999, volume 285, p901). There was no correlation whatsoever. So we do not know the origin of genetic redundancies.

Doesn't that just mean that we do not yet know the complete
story about how genes are formed (which I thought was common
knowledge) ?
Not knowing something bears little on any topic, surely ?
quote:
Originally posted by peter borger:
You say:
3) "The way I see it is this, for natural selection to occur in a way
that drives evolution, there must, at any one snap-shot of a
species genome, be elements of the genome which apparently
serve no survival purpose. These can be passed to a subsequent
generation (regardless of fitness) because they are attached
to genomes which have, elsewhere, aspects which DO provide
a survival advantage. If the organism changes environment (or
its environment changes) those 'redundancies' may contribute
to survival ... in which case they become non-redundant."
How do you think genetic redundancies, if duplicated genes, can stably reside in the genome, while there is no selective constraint on these genes? They should change rapidly even if they are linked to possible survival traits. It is a major problem, and nobody knows the answer.
In addition, the change of environment and an additional survival improvement due to these genetic redundancies implies that redundant genes should be change more rapidly (because according to your theory this is the reservoir the organisms has to drain for adaptation). And a correlation between genetic redundancies and duplications is not what we see (see reponse 2).

If they are carried on the same chromosome as a survival trait,
they would be subject to selective pressure by default. You don't
inherit one gene off of a chromosome, you inherit the entire
chromosome.
Likewise, survival doesn't depend on one gene, it depends on the
sum of all the genes and how that relates to the phenotype. Natural
selection operates on the expression of genes (i.e. traits).
And isn't this issue what Kimura et al talked about anyhow ?
quote:
Originally posted by peter borger:
You say:
4) "We may even say, that the existence of genes which have no
effect even when removed is consistent with a macro-evolutionary
scenario. Genes do no operate in isolation (at all times) and
often require another enzyme to activate them."
Here you introduce (irreducible) complexity and I am not going to respond to that here. That is not the issue here. It is an unsolved problem, that I will address someday.
The existence of genes in general should also be explained. You just ignore that fact. However, than we talk about the origin of life. It is another unsolved mystery.

I think it is directly relevent. You are interpreting genetic
redundancy as a refutation of ToE, I am supplying an alternative
interpretation that is, if acceptable, in keeping with ToE.
quote:
Originally posted by peter borger:
You say:
5) "This sort if change can cause the loss of teeth in
birds, or the loss of appendages in crustaceans ... i.e structural
modification."
I am not interested in the loss of characteristics, they are easy to comprehend. I am interested in the gain of characteristics. Another unsolved mystery.

Hmm ... tricky one that. Is it a LOSS of teeth, or the GAIN of a
beak ?
[This message has been edited by Peter, 07-16-2002]

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 Message 16 by peter borger, posted 07-15-2002 9:40 PM peter borger has not replied

singularity
Inactive Member


Message 18 of 214 (14101)
07-25-2002 12:58 AM
Reply to: Message 1 by peter borger
07-08-2002 10:19 PM


The issue of genetic redundancies seems like the most laughable example of an observation which supposedly undermines the theory of evolution.
To turn the question around- why would god create organisms with masses of "redundant" genes in them? If the redundancy is completely purposeless then why would god include it at all?
Doesn't it seem intuitively obvious that the "redundancy" is in fact a necessity for evolution, only that we haven't figured out exactly what it does yet?
"Created" organisms should be complete and perfect. Evolved organisms would be still evolving and would display evidence of their origins. I think genetic redundancy is evidence of this process.
Remember that the earlier details of evolutionary theory were based on studying microorganisms which with their higher rate of turn over of generations tend toward much smaller and compact genomes. You would be hard pressed to find genetic redundancy in a virus for example (often genes overlap for even higher efficiency). Multicellular organisms have more complex and therefore apparently redundant genomes in order to facillitate their evolution by nonrandom processes (namely gene splicing). Random mutation is not a pillar of evolutionary theory, only one of the mechanisms by which diversity arises. Gene transfer between organisms is already emerging as another important process.
On the issue of human appreciation for specific complex stimuli (music, art etc) there are interesting theories that suggest the evolution of the human brain was fuelled by sexual selection, in a similar process to the evolution of the "functionless" peacock's tail. Complex display behaviours like singing and dancing were used in order to identify the fittest mates in homonid societies (as they still are to some degree). This accounts for the rapid emergence of human intelligence and the reason why human intelligence seems to be in excess of what is necessary for survival alone. For example I don't doubt that Che Guevara would have had less chance of bedding the lovely lady in the story after embarrasing himself as described
Regeneration of organs may have been selected against for several reasons, the most likely being that is may be linked to cancer and immune disfunction. This fits with the characteristic being lost in organisms with longer life spans. Frogs and lizards rarely live long enough to get bowel cancer or arthitis. Interestingly a strain of knock out mice have been developed which have regained most of the regeneration abilities of amphibians (I think I found the article in New Scientist). The gene silenced was related to immune function. This should highlight the oversimplification of the assumption that fitness is a one dimensional property which seems to underpin your post.
The liana story is a bit presumptious. Has anyone actually studied what the liana needs in order to survive and compete within its environment? My guess would be that the tropical rainforest is an extremely competitive environment for seedlings. They usually only succeed in growing when a mature tree falls and opens a hole in the canopy. The liana may need to disperse its seeds extremely widely in order to optimise the chances that any one seed will be close enough to an opening in the canopy. Given that seed dispersal is so critical to a species survival and therefore subject to the most selective pressure I think this is a poor example of "redundancy". A plant with the face of christ imprinted on its leaves would be a more convincing example of the "work of god".
I would be interested to hear what the creationist explanation for all the "redundancy" in the natural world is. Why did god go to so much bother to create things which you claim have absolutely no function? Was he/she/it just showing off? Did he/she/it loose track of how many copies of transketolase it put in marine polychaete worms?
Shane

This message is a reply to:
 Message 1 by peter borger, posted 07-08-2002 10:19 PM peter borger has replied

Replies to this message:
 Message 19 by peter borger, posted 07-25-2002 1:22 AM singularity has not replied
 Message 21 by peter borger, posted 07-26-2002 1:45 AM singularity has not replied

peter borger
Member (Idle past 7665 days)
Posts: 965
From: australia
Joined: 07-05-2002


Message 19 of 214 (14103)
07-25-2002 1:22 AM
Reply to: Message 18 by singularity
07-25-2002 12:58 AM


dear Singularity,
You wonder:
"To turn the question around- why would god create organisms with masses of "redundant" genes in them? If the redundancy is completely purposeless then why would god include it at all?"
Ever heard of a multipurpose genome? Ever heard of the adaptation hypothesis?
You say:
"Doesn't it seem intuitively obvious that the "redundancy" is in fact a necessity for evolution, only that we haven't figured out exactly what it does yet? "
19th century logic. I recommend you to read the complete thread and the references.
You say:
"I think genetic redundancy is evidence of this process."
Read before you speak. I recommend you to read my references.
You say:
"Multicellular organisms have more complex and therefore apparently redundant genomes in order to facillitate their evolution by nonrandom processes (namely gene splicing)."
Gene spicing is not confined to multicellular organisms (you probably meant eukaryota? But it is also not restricted to eukaryota)
Furthermore:
"Random mutation is not a pillar of evolutionary theory, only one of the mechanisms by which diversity arises."
It is the first pillar of NDT.
(You are free to ignore that.)
And:
"Complex display behaviours like singing and dancing were used in order to identify the fittest mates in homonid societies (as they still are to some degree)."
Evo BLAH-BLAH. Never seen an explanation beyond storytelling. (I recommend you to read the article in Science 2001 firts issue january).
[I mean the first issue of 2002, pb]
"been selected against for several reasons, the most likely being that is may be linked to cancer and immune disfunction."
Storytelling. I am not interested in the loss of a trait. Selection against? Please explain how the trait arose first! (A assume you have your information here: Alvarado, A.S. Regeneration of the metazoans: why does it happen? Bioessays 2000, Volume 22: p578-590). It is a lot of storytelling without any scientific backup.
And:
"The liana story is a bit presumptious."
Ever thought about the genetics involved in autostability? Go to a botanical museum and have a carefull look at the seed, and ponder the genetics involved. I did.
best wishes
Peter
[This message has been edited by peter borger, 07-25-2002]

This message is a reply to:
 Message 18 by singularity, posted 07-25-2002 12:58 AM singularity has not replied

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John
Inactive Member


Message 20 of 214 (14131)
07-25-2002 9:09 AM
Reply to: Message 19 by peter borger
07-25-2002 1:22 AM


[QUOTE]Originally posted by peter borger:
[b]Ever heard of a multipurpose genome? Ever heard of the adaptation hypothesis?[/QUOTE]
[/b]
But why, if everything was created and presumably created to fit its niche, why would the ability to adapt be a feature? No significant environmental changes have occured in the last 6000 years, as an omniscient God would know. Why would animals need to adapt?
quote:
"Complex display behaviours like singing and dancing were used in order to identify the fittest mates in homonid societies (as they still are to some degree)."
Evo BLAH-BLAH. Never seen an explanation beyond storytelling.

Just look at how these behaviors are used today...
------------------
www.hells-handmaiden.com

This message is a reply to:
 Message 19 by peter borger, posted 07-25-2002 1:22 AM peter borger has not replied

peter borger
Member (Idle past 7665 days)
Posts: 965
From: australia
Joined: 07-05-2002


Message 21 of 214 (14183)
07-26-2002 1:45 AM
Reply to: Message 18 by singularity
07-25-2002 12:58 AM


dear Shane,
You laugh that:
"genetic redundancies seems like the most laughable example"
Apparently you've never heard of genetic redundancies and the problems they cause evolution-theorists. I recommend you to read relevant literature on the topic. That would improve our discussion.
Best Wishes.
Peter

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Replies to this message:
 Message 22 by nator, posted 07-26-2002 8:45 AM peter borger has replied

nator
Member (Idle past 2169 days)
Posts: 12961
From: Ann Arbor
Joined: 12-09-2001


Message 22 of 214 (14196)
07-26-2002 8:45 AM
Reply to: Message 21 by peter borger
07-26-2002 1:45 AM


quote:
Originally posted by peter borger:
dear Shane,
You laugh that:
"genetic redundancies seems like the most laughable example"
Apparently you've never heard of genetic redundancies and the problems they cause evolution-theorists. I recommend you to read relevant literature on the topic. That would improve our discussion.
Best Wishes.
Peter

You know, maybe you would like to provide some references to the literature which supports your position.
Genetic redundancies are PREDICTED by evolutionary theory. They are not a problem for it.
Remember that web search I did? I found over 9,000 hits when I searched Google for "genetic redundancy evolution".
How is it that I do a search on this phrase and come up with lots and lots of hits which consist of scientific articles which talk about genetic redundancy in an evolutionary context in a way which strongly suggests that it is expected and not a surprise nor a problem?
Here are some of the examples:
On the Evolution of Redundancy in Genetic Codes
www-evo.stanford.edu/~ardell/ArdellSella01.pdf
Wagner, A. (1996) Genetic redundancy and its evolution in networks of transcriptional regulators. Biological Cybernetics 74, 559-569.
http://samba.unm.edu/~wagnera/Publications.html
Brookfield, J.F.Y. (1997) Genetic redundancy. Advances in Genetics 36: 137-155.
http://www.nottingham.ac.uk/genetics/publications/1997publications.html
Nowak, M. A., M. C. Boerlijst, J. Cooke, j. Maynard Smith. 1997. evolution of genetic redundancy. Nature 388:167-171.
http://cwx.prenhall.com/bookbind/pubbooks/freemanea2/chapter2/custom3/deluxe-content.html
(Emphasis added below)
Molecular Coevolution amongst Genes Controlling Morphology in Species of Drosophila and Musca
Project supervisor
rofessor G.A. Dover
There are several thousand species of Drosophila which differ in the genetic operations leading to species-specific, and presumably adaptive, morphologies. Development in D.melanogaster is controlled by a defined number of genes that interact one with another in precisely controlled hierarchies. Interestingly, there is genetic redundancy at both the DNA level and in terms of the developmental pathways. As with other multiple-copy systems, the internal tolerance provided by such redundancy allows for a molecular co-evolution between pairs of interacting genes, envisaged as the product of turnover amongst repeats and selection in the establishment of species-specific ontogenies.
http://www.le.ac.uk/ge/staff/gad_2.html
These are only a few examples.
Tell me again how genetic redundancy is a problem, or at all unexpected, or NOT actually predicted and required, for/in Evolutionary Theory?
------------------
"We will still have perfect freedom to hold contrary views of our own, but to simply
close our minds to the knowledge painstakingly accumulated by hundreds of thousands
of scientists over long centuries is to deliberately decide to be ignorant and narrow-
minded."
-Steve Allen, from "Dumbth"

This message is a reply to:
 Message 21 by peter borger, posted 07-26-2002 1:45 AM peter borger has replied

Replies to this message:
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 Message 24 by peter borger, posted 07-29-2002 12:24 AM nator has not replied

peter borger
Member (Idle past 7665 days)
Posts: 965
From: australia
Joined: 07-05-2002


Message 23 of 214 (14350)
07-28-2002 11:31 PM
Reply to: Message 22 by nator
07-26-2002 8:45 AM


Dear Schrafinator,
Thanks for your references. However, I already had them and I have carefully studied them. If you read them you will notice that genetic redundancies are a huge problem for these theoretical biologists. In fact, I have sent a mail to one of the authors you refer to (concerning the actinin redundancy), but never got a reply, demonstrating the problem evolution has to deal with. Thanks anyway.
Best wishes
Peter

This message is a reply to:
 Message 22 by nator, posted 07-26-2002 8:45 AM nator has not replied

peter borger
Member (Idle past 7665 days)
Posts: 965
From: australia
Joined: 07-05-2002


Message 24 of 214 (14358)
07-29-2002 12:24 AM
Reply to: Message 22 by nator
07-26-2002 8:45 AM


dear S,
You write:
"Tell me again how genetic redundancy is a problem, or at all unexpected, or NOT actually predicted and required, for/in Evolutionary Theory?"
I have the feeling that we are running around in circles. I already mentioned on this site that:
1) there is no correlation between gene duplication and genetic redundancies. Actually, the evolutionary prediction was that there should be a correleation between duplication and redundancy (the Backup hypothesis). It could not hold after checking the complete genome of Saccharomyces (the reference is: Winzeler et al. Science 285, p901-906). Also read Tautz. A genetic uncertainty problem (Trend in Genetics 2000, vol.16, No. 11, p475-477) and all references therein.
2) redundant genes are supposed to change with a faster rate than essential genes (neutral theory prediction), since they are not under selective constraint. It is not true. Redundant genes do not change faster or slower in comparison with essential genes. Thus, we have another falsification.
The exact problem is:
1) where do redundancies have their origin, and
2) how do they reside stable in the genome?
Nobody knows an answer to this, and as soon as one starts to calculate on it (as I did) one has to introduce neutral selection!
Thus, there is a major problem that cannot be solved by the current concept of evolution theory. In my opinion, the current concept of evolution theory has fallen and should be replaced by something else.
Maybe SLPx(?), who supposed to be have a PhD in evolution theory has got a naturalistic solution, because I do not have it.
Best Wishes
Peter

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Replies to this message:
 Message 25 by mark24, posted 07-29-2002 8:01 AM peter borger has replied
 Message 30 by Peter, posted 07-30-2002 3:46 AM peter borger has replied

mark24
Member (Idle past 5195 days)
Posts: 3857
From: UK
Joined: 12-01-2001


Message 25 of 214 (14381)
07-29-2002 8:01 AM
Reply to: Message 24 by peter borger
07-29-2002 12:24 AM


quote:
Originally posted by peter borger:
2) redundant genes are supposed to change with a faster rate than essential genes (neutral theory prediction), since they are not under selective constraint. It is not true. Redundant genes do not change faster or slower in comparison with essential genes. Thus, we have another falsification.
2) how do they reside stable in the genome?

Sorry Peter B, you can’t make any judgement on neutral/non-neutral rate until you can scientifically prove there is absolutely no function in the genes that you purport should display neutral rate mutation.
This is your own standard, remember?
No judgement allowed = no falsification.
These genes do not reside stable in the genome, except perhaps at the 100% fixation level. Genetic drift acts upon their frequencies.
Mark
------------------
Occam's razor is not for shaving with.

This message is a reply to:
 Message 24 by peter borger, posted 07-29-2002 12:24 AM peter borger has replied

Replies to this message:
 Message 26 by peter borger, posted 07-29-2002 8:40 PM mark24 has replied
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peter borger
Member (Idle past 7665 days)
Posts: 965
From: australia
Joined: 07-05-2002


Message 26 of 214 (14416)
07-29-2002 8:40 PM
Reply to: Message 25 by mark24
07-29-2002 8:01 AM


Dear mark,
Firstly, I recommend you to read a book on neutral evolution.
Secondly, problem is that evolutionists NEVER make any predictions. So I have taken the opportunity to do it for them by applying the rules that are operable at the molecular level. None of the predictions can hold, demonstrating the weakness of the theory. (I already did an evolutionary prediction that can readily be checked in the genome)
Thirdly, you are entitled to have your opinions/beliefs. I do not mind. The only thing I show is that evolution does not work at the molecular level, and this should be conclusive to any scientist (why do you think molecular biologist increasingly object to evolution theory? Most molecular biologist I know are agnostics: they simply don't know).
Best wishes
Peter

This message is a reply to:
 Message 25 by mark24, posted 07-29-2002 8:01 AM mark24 has replied

Replies to this message:
 Message 31 by mark24, posted 07-30-2002 5:02 AM peter borger has replied

John
Inactive Member


Message 27 of 214 (14439)
07-29-2002 10:33 PM
Reply to: Message 1 by peter borger
07-08-2002 10:19 PM


quote:
Originally posted by peter borger:
From information theory it has already become clear that randomness can not account for information gain. An extensive discussion on this topic has come to a grinding halt because of definitions (nothing new, if you can't win a discussion blame definitions).
I thought that was the tactic you employed.
[quote][b]Che Quevera demonstrates the most straightforward example of a redundant trait of the human brain: the ability of hearing music. The absence of this trait does not affect the fitness/survival, as clearly demonstrated by individuals suffering from amusia.[/quote]
[/b]
It proves that an individual can survive with tone deafness in modern society. What is does not prove is that this trait wasn't useful at some earlier stage.
quote:
nobody has been able to suggest any plausible survival payoffs for most of the things that human minds are uniquely good at, such as humour, story-telling, gossip, art, music, self-consciousness, ornate language, imaginative ideologies, religion and morality [and arrhythmics].
You've got to be kidding. All of this stuff has survival value for an animal that depends on society to survive. Read up on cultural ecology, Marvin Harris in particular.
quote:
Of course, evolutionists will strongly object against this example of redundancy with a lot of "story telling"
Hopefully story-telling of better quality than your own.
quote:
The regeneration of a new lens is a feature which can not be explained by natural selection, simply because there has never been evolutionary pressure to evolve this capacity.
Could be a side effect of the ability to regenerate a tail.
quote:
Proponents of the theory of evolution must admit that the phenomenon of regeneration cannot be explained by natural selection and turn evolution upside down.
Why? You said yourself that regeneration is a superb survival trick.
[quote][b]They pose the idea that regeneration is a remnant of a common primitive characteristic exhibited by all primordial life forms and it has disappeared in the major part of organisms today due to selection against[/quote]
[/b]
quote:
It is, even for evolutionists, hard to conceive why an apparent advantageous characteristic was selected against.
Unless the author's contention that regeneration is a common primative characteristic can be upheld, this argument is worthless. I, for one, doubt the premise.
quote:
Notably, the disappearance of advantageous characteristics violates the basic principle of the theory of evolution as formulated by Darwin.
Not if is a trade-off for another trait that is more advantageous, or if said trait were not advantageous for a long period of time-- as is the case with eyes in deep cave dwellers.
quote:
Other intriguing questions involving the phenomenon of regeneration are why does the human liver regenerate and why do bones?
Why does bone heal? Your objection is WHY DO BONES HEAL?
quote:
To disperse and enlarge the liana’s (it's a liana!) habitat the seeds do not need to evolve this trait, and therefore it is a redundant trait.
How do you know? You have to support this claim for your objection to stand.
------------------
http://www.hells-handmaiden.com

This message is a reply to:
 Message 1 by peter borger, posted 07-08-2002 10:19 PM peter borger has replied

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 Message 28 by peter borger, posted 07-30-2002 1:32 AM John has replied

peter borger
Member (Idle past 7665 days)
Posts: 965
From: australia
Joined: 07-05-2002


Message 28 of 214 (14463)
07-30-2002 1:32 AM
Reply to: Message 27 by John
07-29-2002 10:33 PM


dear John,
In response to all your critique, I would like to stress that I used the examples of macroredundancy to introduce genetic redundancy. In fact, genetic redundancy is problem that brings evolution theory to its knees. since, none of the evolutionists seem to understand/acknowledge the implications of my postings for evolution theory, let me try and explain that redundant genes are the final blow to ET.
Read my example of actinins again:
"Also humans demonstrate genetic redundancy. Although it is non-ethical to generate human knockouts, sometimes a gene is inactivated by a mutation that generates a stopcodon in that gene. For instance, the alpha-actinin3 gene.
The a-actinins comprise a group of actin-binding proteins encoded by a multigene family. In skeletal muscle, they are a major structural component of the Z-lines that anchor the actin-containing thin filaments and maintain the spatial relationship between myofilaments. In humans, two genes (ACTN2 and ACTN3) encode the closely related a-actinin-2 and a-actinin-3 skeletal muscle isoforms. ACTN2 is expressed in all skeletal muscle fibres, whereas expression of ACTN3 is limited to a subset of type 2 (fast) fibres. A careful screening of muscle biopsies with dystrophic (118 specimens), myopathic (74), neurogenic (20) and normal (55) features demonstrated that all specimens contained normal a-actinin-2 expression. Deficiency of a-actinin-3 was identified in 51 of the 267 cases (19%), and was due to a common non-sense mutation that introduced a premature stop codon. So, the proper a-actinin-3 protein cannot be synthesised. Surprisingly, the deficiency was not associated with any particular histopathological or clinical phenotype [North, K.N. et al. A common non-sense mutation results in a-actinin 3 deficiency in the general population: Evidence for genetic redundancy in humans. Nature Genetics 1999, Volume 21: p353-354.]. Thus, deficiency of the a-actinin-3 does not result in any form of disease, probably due to compensation by the closely related family member a-actinin-2. The non-phenotype of a-actinin-3 deficiency is clear-cut evidence for genetic redundancy in humans.
The a-actinin-3 gene demonstrates a very high degree of homology within vertebrates and excludes the possibility of recent gene duplication in humans as an evolutionary explanation. The inactivation of the ACTN-3 gene demonstrates the fate of redundant genes. As time passes by they get inactivated by random mutaion and linger on in the genome as pseudogenes (and provides a nice explanation for "classical pseudogenes" by the way). Obviously, natural selection does not seem to act on the ACTN-3 gene."
What exactly is the problem with the redundant actinins? Let's have a careful look.
According to NDT, duplication gave rise to two alpha-actinin.
A close look at these redundant genes reveals that the differences are the result of point-mutations. Neutral evolution rate is about 10(exp)-9/nucleotide/year, and recent genome wide studies present evidence that purifying selection worked upon duplicated genes (A. Wagner, mini-review in Genome Biology 2002). The ACTN2 and ACTN3 genes are approximately 3000 bp, and share 85% sequence homology. Moreover, the ACTN3 gene is highly conserved within mammals.
1) These data say that approximately 450 bp changes occurred on neutral positions, i.e. positions not under selective constraint.
2) These data mean that it would take about 10(exp)6 years for 3 random mutations to occur in the duplicated gene. Thus 150 million years for 450 neutral mutations.
3) These data imply that after each point-mutation there was (neutral) purifying selection. So, here we have to introduce neutral purifying selection again. What exactly is selection on neutral genes? Not a single evolution biologist was able to tell me, thus far.
As you see, it is highly doubtful that the mechanism that keeps genes (unchanged) in the genome is by natural selection. [In fact this example is a falsification of natural selection. Thus, I demonstrated that both random mutation (see previous posting) and natural selection (this is not the only example) can be falsified at the molecular level. Conclusion: NDT RIP].
best wishes
Peter

This message is a reply to:
 Message 27 by John, posted 07-29-2002 10:33 PM John has replied

Replies to this message:
 Message 33 by John, posted 07-30-2002 11:28 AM peter borger has replied

monkenstick
Inactive Member


Message 29 of 214 (14471)
07-30-2002 3:36 AM


This is quite funny
You seem to think that your interpretation of an article published in a major science journal constitutes the downfall of NDT. May I ask why it is you think that no other scientist who has read these articles thinks they falsify NDT?
It reminds me of someone who thinks they've invented a perpetual motion device

Peter
Member (Idle past 1478 days)
Posts: 2161
From: Cambridgeshire, UK.
Joined: 02-05-2002


Message 30 of 214 (14472)
07-30-2002 3:46 AM
Reply to: Message 24 by peter borger
07-29-2002 12:24 AM


Why should these 'redundancies' (and you have yourself
stated that they are more likely to be 'of unknown function'
in any case) have a different mutation rate than any other
section of DNA ? (I've asked this before and you haven't given
an answer).
DNA is subject to copy errors, and any part can be mis-copied.
Trying to claim that gene selection happens at the individual
gene is a little ridiculous isn't it?
Aren't large numbers of genes present on each chromosome?
Wouldn't that mean (and I'm not talking about duplication) that
a gene that exists on the same chromosome as a gene that produces
a phenotypic effect of use would be preserved with the trait
in question?
If we didn't have sections of genetic make-up (with currently
unknown function and apparently no survival benefit to the
organism) we couldn't have natural selection at all, could we?
(This has been asked before and you have not answered).
You have in no way refuted random mutation. You have said that
some DNA sites have a higher tendancy to be copied wrong. That
does not make the mutation non-random. Giraffes don't generate
mutations to neck lenght control mechanisms becuase they need
longer necks.
Peppered moths (and they MUST rest somewhere during in the day
even if it is not near a biologist's trap ... most moths I have
seen during the day are sitting high on the wall of my house, or
on a high window) show a natural variation, and the distribution
of that variation can be affected by environmental conditions.
That IS natural selection isn't it?
That we haven't found the exact molecular level explanation does
not refute the theory ... it just means there are pieces of the
puzzle missing ... we already know that.
Redundancy doesn't refute ToE, it is an expected feature.
Mutation enables evolution, and mutation happens. you have not shown
that there are any non-random mutations in the sense that 'random
mutation' is used in ToE, only that some sites are more prone to
copy errors. This is good for ToE, it means that there is an
observed mechanism that can explain away the 'you can't get enough
mutations for that' arguments.
Read some 'Information Science' literature (or cite that
which you have read) before agruing from Information Theory.

This message is a reply to:
 Message 24 by peter borger, posted 07-29-2002 12:24 AM peter borger has replied

Replies to this message:
 Message 39 by peter borger, posted 07-30-2002 10:43 PM Peter has replied

mark24
Member (Idle past 5195 days)
Posts: 3857
From: UK
Joined: 12-01-2001


Message 31 of 214 (14486)
07-30-2002 5:02 AM
Reply to: Message 26 by peter borger
07-29-2002 8:40 PM


quote:
Originally posted by peter borger:
Dear mark,
Firstly, I recommend you to read a book on neutral evolution.

What has this got to do with your hypocrisy? I’m well aware of neutral theory.
quote:
Originally posted by peter borger:

Secondly, problem is that evolutionists NEVER make any predictions. So I have taken the opportunity to do it for them by applying the rules that are operable at the molecular level. None of the predictions can hold, demonstrating the weakness of the theory. (I already did an evolutionary prediction that can readily be checked in the genome)
Thirdly, you are entitled to have your opinions/beliefs. I do not mind. The only thing I show is that evolution does not work at the molecular level, and this should be conclusive to any scientist (why do you think molecular biologist increasingly object to evolution theory? Most molecular biologist I know are agnostics: they simply don't know).
Best wishes
Peter

You have not shown evolution cannot work at the molecular level without being a hypocrite. Why? Because for your argument to be true, you need to demonstrate that the sequences you purport to be functionless, are. This is exactly the criteria you say evolutionists need to meet before they can derive phylogenies from transposons.
In fact all you’ve done is to hit upon the pseudogene in question having some function.
This is the third or fourth time I’ve posted this, why aren’t you addressing the main point?
YOU CAN’T HAVE IT BOTH WAYS!!!!!!!!!!
Mark
------------------
Occam's razor is not for shaving with.

This message is a reply to:
 Message 26 by peter borger, posted 07-29-2002 8:40 PM peter borger has replied

Replies to this message:
 Message 32 by mark24, posted 07-30-2002 5:34 AM mark24 has not replied
 Message 38 by peter borger, posted 07-30-2002 9:57 PM mark24 has replied

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