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Author Topic:   scientific end of evolution theory (2)
peter borger
Member (Idle past 5806 days)
Posts: 965
From: australia
Joined: 07-05-2002


Message 1 of 214 (13114)
07-08-2002 10:19 PM


Dear All,

Evolution theory relies on two pillars (random mutation and natural selection). If these pillars cannot hold than the theory of evolution has no foundation, and all explanations that rely on it are invalid.

Evidence is accumulating that shows the NDT to be wrong, since both randomness and natural selection seem not to be valid.

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). It is, however, brilliantly clear that all observed mutations do not gain information, and that should be very conclusive, and end the discussion.

However, that will not be the topic of today. Let's focus on the end of natural selection.
Let me start explaining argument 4, (genetic) redundancies, and why it inevitably leads to the fall of NDT. I will do this by a couple of examples that are easy to comprehend. Next, I will give examples of genetic redundancies.

Example 1)
“Che Guevara was widely recognised as a man of many talents. Yet one talent the 1960s revolutionary lacked was the ability to hear music, a shortcoming he was acutely aware of. According to one account, Guevara was at a party one evening when he spotted a nurse he wanted to dance with. He asked a friend to give him a nudge when the orchestra struck up a tango. But the friend got the signal mixed up, sending Guevara out on the dance floor to dip and swirl his partner absurdly to the tune of a soft Brazilian samba. Guevara suffered from congenital amusia, a nearly total tone deafness that turns music into mere noise. Although 5% or more of some populations suffer from this syndrome, it has not been widely studied” (Balter, M. What makes the mind dance and count. Science 2001, volume 292: p1636-1637.).

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. The brain has several additional intrinsic -apparently redundant - capacities that have puzzled scientists and philosophers for ages. And still, “…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]. How could evolution favour such apparently useless embellishments? The fact that there are no good theories of these adaptations is one of science’s secrets.” [(Miller, G. The Mating Mind, William Heineman: London, 2000: p18]

Of course, evolutionists will strongly object against this example of redundancy with a lot of "story telling" and therefore I will proceed to the next:

Example 2:
Several amphibians and lizards display the remarkable feature of regeneration. When physically threatened, for instance when caught by a predator, the tail of the animal instantly becomes detached from the body and starts living a life of its own. For the predator it is as if the pray has split in two, and it must be completely astounded by the sudden apparition of another pray. Usually the predator is left behind with the smaller part of the meal: the wiggling tail.
If the lizard managed to flee its tail will regenerate and within a couple of months it has grown a complete new one. Evidently, it is a superb survival trick, since it provides the animal an opportunity to escape.
The phenomenon of regeneration has attracted a great deal of scientific attention, and biologists are still trying to elucidate the underlying mechanism. In previous centuries dissection of living amphibians was the way to go to get insight into regeneration. In 1768 Lazzaro Spallanzani published that tadpoles were capable of regenerating their tales, and that salamanders could regenerate most of their body parts, including tail, jaws and eyes (Alvarado, A.S. Regeneration of the metazoans: why does it happen? Bioessays 2000, Volume 22: p578-590).
In one of his renowned experiments the lens from the eye of the salamander was carefully removed. Surprisingly, the animal’s lens completely regenerated. Within a few weeks a perfectly shaped new lens had developed in place of the removed lens. 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. An example of a hidden redundant trait is uncovered.
Proponents of the theory of evolution must admit that the phenomenon of regeneration cannot be explained by natural selection and turn evolution upside down. 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 (Wauau, that sounds very scientific, isn't it) (Alvarado, A.S. Regeneration of the metazoans: why does it happen? Bioessays 2000, Volume 22: p578-590).
It is, even for evolutionists, hard to conceive why an apparent advantageous characteristic was selected against. Notably, the disappearance of advantageous characteristics violates the basic principle of the theory of evolution as formulated by Darwin.
Other intriguing questions involving the phenomenon of regeneration are “why does the human liver regenerate and why do bones?”

Example 3)
To disperse, seeds need to be transported away from the parent tree or plant, and this is accomplished in a variety of ways. The most perfect seed is undoubtedly that of the tropical liana (Zanonia macrocarpa). It grows high up in the canopy of the rainforest of south-eastern Asia. The liana seed develops two very elastic, curved wings. The seed is a perfect flying wing, as it exhibits auto-stability. Auto-stability means that the seed’s centre of gravity and centre of lift, two imaginary points where the force of gravity and the force of lift act on the seed, are independent of the seed’s position in space. Hence, it does not have the propensity to spin around its axes. When the seeds release the glider carries them away for miles: autostable.
What make the Zanonia’s seeds so remarkable is that natural selection should account for the evolution of auto-stability. What on earth could have been the driving force on the tropical liana to evolve seeds with perfect auto-stability? Randomness and selection? 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.

To my knowledge, NDT does not include the evolution of redundant traits. Maybe they call them exaptation, or so, but giving them a name doesn't make it a scientific explanation.

The big surprise of contemoprary molecular biology was the dicovery of redundant genes. Let me introduce how they were discovered.

KNOCKOUTS:
The discovery of the primary biochemical rules of life in the second half of the 20th century have tremendously contributed to the comprehension of life on earth. From the knowledge of molecular biology sophisticated techniques emerged to perform studies on gene and protein function. One promising tool for such studies was a set of methods that had been devised to interfere with gene activity. Bio-scientists would now be able to study the function of proteins in detail by the disruption of the corresponding genes.

Disruption of a gene in animals, mostly mice, is usually performed by making use of the natural genetic mechanism of homologous recombination of DNA. Scientists artificially introduce DNA that specifies a selection marker into the reproductive cells (egg cells) of the mouse. During homologous recombination, the gene of interest is exchanged by the artificial DNA fragment and replaces the gene of interest. Hence, this gene is inactivated and can no longer produce a functional protein. Instead, the selection marker is expressed and mice expressing it can be sorted out. Organisms of which both genes of the diploid genome have been inactivated - in which the protein has been knocked out - can be selected and are called knock-out organisms. They are generally referred to as knockouts.

SURVIVING A KNOCKOUT BLOW
It was expected that knocking out genes in an organism would results in an altered fitness of that organism and enable scientists to deduce the function of the gene-product by the phenotype of the knock-outs. In other words, from the characteristics of the knockouts the function of the protein should become evident. To this end knockouts have been generated in a multitude of organisms, including yeast, plants and animals. Today, the functions of several hundreds of gene products have been elucidated in knockouts and these organisms have immensely increased our knowledge.
An unexpected phenomenon was also revealed in knockouts. It was expected that all genes have functions, and that knocking them out would inevitably lead to detectable phenotypes. The discovery of redundancy on the molecular level proved this vision to be wrong. It was found that a lot of genes can be knocked out without any - or only minor - detectable effects on the phenotype of the organism! Now, this phenomenon is commonly known as genetic redundancy. Genetic redundancy is defined as the situation in which the disruption of a gene is selectively neutral. Inactivation of the gene does not affect the fitness of the organism.
Despite knockouts lack genetic information (have a different genotype) the physical appearance (phenotype) of the organism has not changed at all. The knockouts are indistinguishable from their sisters and brothers who do not have the knockout genotype. From these knockout studies an obvious paradox emerges:

“HOW CAN THERE BE GENES WHITHOUT NATURAL SELECTION?“

Genetic redundancies have been observed in all species studied. A dramatic example was found in Arabidopsis (=small flowering plant of the mustard family). In a recent study two molecular plant biologists reported that fewer than 2% of approximately 200 Arabidopsis knockouts displayed significant morphological alterations. It appeared that many Arabidopsis knockouts do not affect plant morphology even in the presence of severe physiological defects (Bouche, N. and Bouchez, D. Arabidopsis gene knockout: phenotypes wanted. Current Opinions in Plant Biology 2001, Volume 4: p111-117.).

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.

Redundancies are a general phenomenon in any biological system and doubt the significance of natural selecetion in the generation and maintenance of genetic information.

From evolutionists I expect that they understand the concepts and molecular backgrounds (and implication for their theory) of all above, otherwise it does not make sense to discuss on this topic.
NB: Let's keep it scientifically. We need only one observation that cannot be explained by natural selection and the theory has to be revised. I already demonstrated several of them and I will give even stronger examples if you like.

Thus, there is the challenge.

Best wishes
Peter

ASSUREDLY, THE THEORY HAS FALLEN!!

------------------

[This message has been edited by peter borger, 07-08-2002]


Replies to this message:
 Message 2 by edge, posted 07-08-2002 11:11 PM peter borger has not yet responded
 Message 4 by TrueCreation, posted 07-09-2002 1:06 AM peter borger has responded
 Message 7 by Peter, posted 07-09-2002 4:04 AM peter borger has responded
 Message 15 by nator, posted 07-15-2002 12:31 PM peter borger has not yet responded
 Message 18 by singularity, posted 07-25-2002 12:58 AM peter borger has responded
 Message 27 by John, posted 07-29-2002 10:33 PM peter borger has responded

  
peter borger
Member (Idle past 5806 days)
Posts: 965
From: australia
Joined: 07-05-2002


Message 5 of 214 (13132)
07-09-2002 1:26 AM
Reply to: Message 4 by TrueCreation
07-09-2002 1:06 AM


What according to you are the pillars of NDT?
What do they imply for the maintenance of genetic information?

Funny that you mentioned the so called phylogenetic backup. It is only superficial evidence for evolution. I could give you several examples of genes that violate the species trees. A complete subdiscipline of phylogeny is concerned with reconsiliation of these trees through hypothetical additions and/or deletions of putative duplicated genes.
From the "discipline of reconciliation" a number of prediction have been done regarding putative gene duplication. Recently, the sequencing of the human genome has been completed. It will shed light on the validity of their method. I checked their claims on IL-1beta, because I am becoming rather suspicious about evolutionists' claim that their theory can account for origin of genes by duplication and selection.

To explain the incongruence between the gene tree and species tree, four duplications of an ancestor IL-1 gene is required. (see R. Page text book on Molecular Evolution), the third giving rise to the incongruence. However, there is no duplication in the human genome that could explain the deviation from the species dendrogram.

I would like you to have a look at chromosome 2. Eight members of the IL-1 related genes are present in man’s chromosome 2, to be precise in location 2q11-2q14. Sequence comparison of the IL-1 related genes does not present evidence that a recent duplication of IL-1 beta took place in this region. On the contrary, the dendrogram of the IL-1 genes clearly demonstrates that the common ancestor copy of the IL-1 beta gene duplicated 3 times maximally, and gave rise to IL-1alpha (Smith, D.E. et al. Four new members expand the interleukin-1 superfamily Journal Biological Chemistry 2000, vol275, pp1169-1175).

This is a clear-cut falsification of common descent and demonstrates that the mathematical solution of incongruencies are nothing but a tool to keep the hypothesis of common descent from falling. Of course this is not the only deviation of gene trees from species trees. Any textbook on molecular evolution will demonstrate a couple of them, and how to solve them (although not all of them can be solved). A close look, as I showed you above, will reveal that their method is invalid.

best wishes
peter


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peter borger
Member (Idle past 5806 days)
Posts: 965
From: australia
Joined: 07-05-2002


Message 6 of 214 (13137)
07-09-2002 2:59 AM
Reply to: Message 4 by TrueCreation
07-09-2002 1:06 AM


I could agree with you if there were an association between duplications and redundancies, but there isn't (In: Krakauer D.C. and M.A. Novak. Evolutionary preservation of redundant duplicated genes. Cell & Developmental Biology 1999, Volume 10: p555-559.)

If you do not read the references I mention in my postings, than please do not respond.

By the way, it is a common human habit to copy the opinion of others, in this the evolutionist's "meme". As an agnostic scientist I rather prefer to objectively look for myself. I did this thouroughly and now I will simply confront this site with all the falsification of evolution theory. (See my previous letter to you on IL-1-beta incongruency, it is just another falsification. Or do you wish to discuss the second copy of cytochrome c in rat's testis?).
After that I will never discuss the hypothesis of evolution again.

Assuredly, the theory has fallen

Best wishes
Peter

[This message has been edited by peter borger, 07-09-2002]


This message is a reply to:
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peter borger
Member (Idle past 5806 days)
Posts: 965
From: australia
Joined: 07-05-2002


Message 8 of 214 (13297)
07-10-2002 9:54 PM
Reply to: Message 7 by Peter
07-09-2002 4:04 AM


Dear Peter,
Your arguing doesn't make sense considering the underlying molecular mechanisms. It is story telling. These are 19th century arguments.
I was expecting this and therefore I introduced genetic redundancies.
There is no correlation between duplication and redundancies, and redundant genes do not evolve faster than essential genes (this is already and argument that brings down NDT). I will provide more shattering evidence that the NDT has fallen with examples from scientific journals, and thus evolution theory lacks a foundation. That is, if you accept my invitation.
I've sent you a mail yesterday where I outlined the rules/definitions. Have a look at it and tell me you agree. You are free to adjust them to what you think is appropriate. Next, I will finish off with NDT.
Question: Who is the utmost defender of evolution theory at this site. I like him/her to respond too.
Best wishes,
Peter

[This message has been edited by peter borger, 07-10-2002]


This message is a reply to:
 Message 7 by Peter, posted 07-09-2002 4:04 AM Peter has responded

Replies to this message:
 Message 10 by Peter, posted 07-11-2002 3:02 AM peter borger has responded

  
peter borger
Member (Idle past 5806 days)
Posts: 965
From: australia
Joined: 07-05-2002


Message 9 of 214 (13300)
07-10-2002 10:15 PM
Reply to: Message 7 by Peter
07-09-2002 4:04 AM


You state:
"Not in complete agreement with the above, since random mutation
and natural selection are the supposed mechanisms of evolution
you could perhaps argue that even if they were not quite right,
that evolution itself could still happen by some other mechanism"

I agree to this and I will demonstrate later that after NDT has fallen there is an alternative.
Peter


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 Message 7 by Peter, posted 07-09-2002 4:04 AM Peter has not yet responded

  
peter borger
Member (Idle past 5806 days)
Posts: 965
From: australia
Joined: 07-05-2002


Message 11 of 214 (13341)
07-11-2002 4:49 AM
Reply to: Message 10 by Peter
07-11-2002 3:02 AM


Till now I haven't received a single response that actually gave me the idea that the concept "genetic redundancy" (GR) was ever heard of, although I included all nessecery articles on the topic in my second posting (scientific end of evolution theory 2). This makes it a bit hard for me to actually start the discussion. I once more recommend you to read the references. Also read this one: (surviving a knockout blow, Nature, january 2002). Than you will understand the concept and why it is the final devastating blow to evolution theory. I can already reveal to you that there is no correlation between genetic redundacy and gene duplication so the backup hypothesis posed in the 1990th could not hold (as evident from the genomes of Saccharomyces and Arabidopsis). That may ring a bell. Still, GR have severe implications for your theory. To every evolutionist who reads this message: Prepare properly, otherwise I will obliterate the NDT.

Best wishes,
peter

[This message has been edited by peter borger, 07-11-2002]


This message is a reply to:
 Message 10 by Peter, posted 07-11-2002 3:02 AM Peter has responded

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peter borger
Member (Idle past 5806 days)
Posts: 965
From: australia
Joined: 07-05-2002


Message 13 of 214 (13434)
07-12-2002 6:35 PM
Reply to: Message 12 by Peter
07-12-2002 3:52 AM


Dear Peter

I could agree to this if
1) GR correlelated with gene duplications (as I wrote before) and
2) redundant genes change more rapidly than essential genes
They do not.
It is falsification of molecular evolution.

State of the art is that NDT has fallen (See also my falsification of random mutation).
It means that your theory lacks any scientific foundation. That is pretty bad for a theory.
In the meantime I did not get any response to my falsification, but I am used to that already.
Why do you think that I dare challenging everybody in overthroving NDT? Because it has fallen! It should be replaced by something else, that more accurately describes what we see. I am working on such new theory.
See also my reply to Mark and Quetzal in the matter of pseudogenes, retroviruses, transposons. I simply proved that they cannot be taken as an argument to sustain common descent.

The debate about random evolution versus design can be concluded. There is design. Also objectively read Spetner, and objectively read Dr E. MAx's rebuttal to Spetner's claim that mutations cannot increase information (i.e. specificity) on the true-origin website (not on the TALk-Origin website, since Dr Max changed things in Spetner's version (pretty bad, isn't it). Maybe that will open up your eyes.

I will soon send in an extensively discussed example of genetic redundancy that will overthrow selection. I already posted it to Syamsu in a brief version.

Best wishes
Peter

[This message has been edited by peter borger, 07-12-2002]


This message is a reply to:
 Message 12 by Peter, posted 07-12-2002 3:52 AM Peter has responded

Replies to this message:
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peter borger
Member (Idle past 5806 days)
Posts: 965
From: australia
Joined: 07-05-2002


Message 16 of 214 (13600)
07-15-2002 9:40 PM
Reply to: Message 14 by Peter
07-15-2002 3:40 AM


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.

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.

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).

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.

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.

I hope to have informed you properly.
Best wishes,
Peter


This message is a reply to:
 Message 14 by Peter, posted 07-15-2002 3:40 AM Peter has responded

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peter borger
Member (Idle past 5806 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]


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peter borger
Member (Idle past 5806 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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peter borger
Member (Idle past 5806 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
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peter borger
Member (Idle past 5806 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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 Message 22 by nator, posted 07-26-2002 8:45 AM nator has not yet responded

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

  
peter borger
Member (Idle past 5806 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 responded

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

  
peter borger
Member (Idle past 5806 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 responded

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

  
peter borger
Member (Idle past 5806 days)
Posts: 965
From: australia
Joined: 07-05-2002


Message 36 of 214 (14530)
07-30-2002 9:20 PM
Reply to: Message 33 by John
07-30-2002 11:28 AM


Dear John,
No, but they are highly conserved in mammals,
Peter

[This message has been edited by peter borger, 07-30-2002]


This message is a reply to:
 Message 33 by John, posted 07-30-2002 11:28 AM John has responded

Replies to this message:
 Message 45 by John, posted 08-02-2002 1:22 AM peter borger has not yet responded

  
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