|
Register | Sign In |
|
QuickSearch
EvC Forum active members: 64 (9164 total) |
| |
ChatGPT | |
Total: 916,838 Year: 4,095/9,624 Month: 966/974 Week: 293/286 Day: 14/40 Hour: 3/2 |
Thread ▼ Details |
|
Thread Info
|
|
|
Author | Topic: scientific end of evolution theory (2) | |||||||||||||||||||||||||||||||||
peter borger Member (Idle past 7693 days) Posts: 965 From: australia Joined: |
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 BLOWIt 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 wishesPeter ASSUREDLY, THE THEORY HAS FALLEN!! ------------------ [This message has been edited by peter borger, 07-08-2002]
|
|||||||||||||||||||||||||||||||||
edge Member (Idle past 1733 days) Posts: 4696 From: Colorado, USA Joined: |
quote: LOL! Funny how no one has noticed but you Pete.
|
|||||||||||||||||||||||||||||||||
TrueCreation Inactive Member |
You summarized some of your thoughts over in this thread:
http://www.evcforum.net/cgi-bin/dm.cgi?action=msg&f=5&t=6&m=163#163 I'll just repost my comments:
quote:
|
|||||||||||||||||||||||||||||||||
peter borger Member (Idle past 7693 days) Posts: 965 From: australia Joined: |
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 wishespeter
|
|||||||||||||||||||||||||||||||||
peter borger Member (Idle past 7693 days) Posts: 965 From: australia Joined: |
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 wishesPeter [This message has been edited by peter borger, 07-09-2002]
|
|||||||||||||||||||||||||||||||||
Peter Member (Idle past 1506 days) Posts: 2161 From: Cambridgeshire, UK. Joined: |
quote: Not in complete agreement with the above, since random mutationand 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. BUT, for now I would agree that falsifying either or both of thesewould cause a huge shake-up to the evolutionary camp (to say the least quote: Natural selection doesn't explain EVERY trait in an organism, almostby definition. The interpretation of the above example suggests that ALL traitsshould be generated via natural selection, but that is not the case. Traits which DO provide a survival advantage are selected for,but there are other genes on the same chromosome, and other chromosomes within the gamete which have to be carried forward because they are all part and parcel of the same organism/gamete. More importantly, natural selection cannot work at all withoutthis type of redundancy. For natural selection to work at all there needs to be variability within the population that, in the current situation/environment, provides no survival advantage but that might should conditions change. Many of the stated 'things the human mind are good at' are a by-product of higher 'intelligence', and I'm reasonably surethat that has given humans the survival edge that is denied them in purely physical prowess. quote: If pretty much all of the salamander can regenerate, then thatsurely suggests that regeneration is a general characteristic of salamander cells. The last point would tend to suggest that some types of cell, even in man, can regenerate too. The disappearance of 'advantageous' traits is NOT contrary tonatural selection. If by shedding that trait a trait of more immediate benefit is preserved, then so be it. Genes are not passed on one at a time ... they are linked togetherand thus the baby can get thrown out with the bath-water in some cases. quote: I don't know much about this plant, but plants in general survivebetter if they are not competing for resources with other plants don't they ? Wouldn't that suggest that there would be a survival advantage toa seed that fell further from the parent ? Is that story-telling ? :0)
quote: Natural selection, by definition, requires such redundancy. There must be variability within the population, which has NOnet survival impact in the current environment, but if the environment changes might. quote: The redundancy and 'knock-out' effects add support for ToE,and detract from a couple of the major arguments against it put forward by creationists. If you can modify the genes, without any noticeable phenotypedifferences then we no longer require transitional fossils, because you can have a genetic modification that isn't immediately expressed. It is even concievable that we might see a sudden and abrupt change in phenotype because of this phenomena. Equally it knocks-out the argument that mutations would bedetrimental and lethal. If we can add a stop-codon that has little or no discernable effect on the organism then we can have mutations. Perhaps these studies should be extended to generation by generationadd variations to see if a new species can be produced ? That would put more of a dent in evolution (if it couldn't) thananything you have described here. quote: The examples you have cited are examples of traits for which thereis no apparent selective pressure. That's OK as far as ToE is concerned. Not ALL traits in organismsare there because of selective pressure, but maybe they are on the same chromosome as one that was. The genetic redundancy you state is required by natural selection.
|
|||||||||||||||||||||||||||||||||
peter borger Member (Idle past 7693 days) Posts: 965 From: australia Joined: |
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]
|
|||||||||||||||||||||||||||||||||
peter borger Member (Idle past 7693 days) Posts: 965 From: australia Joined: |
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
|
|||||||||||||||||||||||||||||||||
Peter Member (Idle past 1506 days) Posts: 2161 From: Cambridgeshire, UK. Joined: |
quote: Could you perhaps at least respond to the suggestion (and I'm not theonly one making it) that the genetic redundancies you are citing are actually both required and predicted by current evolutionary thinking ? I've put forward my reasons for this in previous posts.
quote: Not received anything.
quote: There are several
|
|||||||||||||||||||||||||||||||||
peter borger Member (Idle past 7693 days) Posts: 965 From: australia Joined: |
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]
|
|||||||||||||||||||||||||||||||||
Peter Member (Idle past 1506 days) Posts: 2161 From: Cambridgeshire, UK. Joined: |
I'm not sure I'd heard of much research into genetic
redundancy, but natural selection has always assumed that some parts of the genome would produce effects that are apparently not necessary for the organism's survival. If that were not the case, how could natural selection work at all ? Your suggestion that ALL genetic traits have to have emerged bynatural selection, is a little strange. Why is that the case ? Natural selection says that selective pressure is placed onthose traits which provide a net survival advantage. This implies that no survival advantage/disadvantage means no selection either way, which means distribution is just about genetic characteristics of the allele/gene, and on which chromosome it resides. You seem to have provided a lot of raw data on GR, so I acceptthat it exists. Could you elaborate your case for why this refutes natural selection. From your posts so far that doesn't seem very clear. And you are still not repsonding to suggestions that redundancyis necessary for and predicted by natural selection.
|
|||||||||||||||||||||||||||||||||
peter borger Member (Idle past 7693 days) Posts: 965 From: australia Joined: |
Dear Peter
I could agree to this if1) 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 wishesPeter [This message has been edited by peter borger, 07-12-2002]
|
|||||||||||||||||||||||||||||||||
Peter Member (Idle past 1506 days) Posts: 2161 From: Cambridgeshire, UK. Joined: |
quote: Why should redundant genes change at a rate any different fromany other gene ? I don't see how the relationship (or lack of it) between GR andGD has any bearing on the issue at hand. The way I see it is this, for natural selection to occur in a waythat 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. We may even say, that the existence of genes which have noeffect 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. Loose the enzyme and you loose the effect, but the section of genome is still there. This sort if change can cause the loss of teeth in birds, or the loss of appendages in crustaceans ... i.e structural modification. How ... in DETAIL ... is genetic redundancy incompatiblewith NDT ?
|
|||||||||||||||||||||||||||||||||
nator Member (Idle past 2197 days) Posts: 12961 From: Ann Arbor Joined: |
[QUOTE]
ASSUREDLY, THE THEORY HAS FALLEN!!
[/B][/QUOTE] Amazing, truly! When can we expect to see your analysis published in "Science" and "Nature"? When will you know when you have won the Pulitzer? What will you do with the money and fame, I wonder? ------------------"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"
|
|||||||||||||||||||||||||||||||||
peter borger Member (Idle past 7693 days) Posts: 965 From: australia Joined: |
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 andGD 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
|
|
|
Do Nothing Button
Copyright 2001-2023 by EvC Forum, All Rights Reserved
Version 4.2
Innovative software from Qwixotic © 2024