Evolution Requires Reduction in Genetic Diversity

I'm feeling a bit better today, the allergies seem to have let up. Yes, the vertical scale is age -- relative age from layering and the law of superposition. The words are the geological names of the layer formations, and yes the fossils are of course embedded in those layersThe horizontal scale is size (and traits related to size, like weight). Thus we have a genetic trait that is expressed in the phenotypes within the population -- the line shows the variation within each population and the thicker sections are to denote the majority of the distribution (which is not always the center of the whole distribution).Let me see if I can reproduce it within the limits of text the graphic data from Message 413Please recognize that this is an approximation of the graph, but that the relative lengths and positions are as accurate as I can make them. I hope this is easier on your eyes.Now I'll repeat what I said in Message 413 about the graph: Note that I have inserted the numbers for the lines: "1" for the line described in (a), "2" for the line described in (c) and "3" for the line described in the 2nd paragraph after (d), so you can see where they fit on the data.Of additional interest is that the red line with an * and no thick section is about where the division of the parent population into two sub-groups begins, with large variants to the right and small variants to the left, which then becomes a gap in the data that shows absence of interbreeding between these daughter populations.If we only looked at the data from the red line up, then your argument that the traits are split between the populations with each daughter population losing traits the other population has could be applied.However when we look at the longer history we see that traits that should have been lost from P.rastoni in the P.jarrovii population reappear.Either traits are not lost but go from hidden to expressed and from expressed to hidden ... or new traits evolve.I await your explanation.Enjoyps -- that text diagram will not copy well for reasons beyond my control

I'm concentrating on population genetics, how sexually reproducing creatures develop new phenotypes by losing genetic diversity through new combinations that occur because of selection and isolation. Although I think I have a fair grasp of how genetics works at the genome level, and that much understanding IS necessary to the argument, if someone starts putting up charts from the genetics laboratory it's just a snow job designed to avoid addressing MY points. Bacteria are not anywhere near the level of this discussion I'm focused on, I don't trust anything said about how their genetics is a model for genetics in general, and since it always comes up when nobody has any evidence on the level I'm talking on I regard it as a cheat. The kind of evidence that matters in this discussion is on the level of claims to known mutations in whatever species we are talking about, their KNOWN functions, what they are KNOWN to code for and the KNOWN results of such mutations in KNOWN cases, plus proof of changes in genetic diversity from subpopulation to subpopulation of an actual living species and so on. Here I get a lot of assertions of increased genetic diversity without a shred of evidence, and Denisova in particular asserts it more on the basis of the ToE's assuming it than any actual known facts. E. coli may demonstrate some interesting genetic information, but only about E. coli and not about my argument. That's really quite a handicap you are imposing on me here. To my mind I just stated the scientific outline of my argument about what junk DNA is. I believe it clearly fits with the known facts of the percentage of DNA in the genome and offers an alternative explanation that nobody would guess at if I didn't spell it out from time to time when relevant issues come up. Granted, it's a statement of my theory rather than any kind of proof, but you know what, various hypotheses are really all anybody has for junk DNA, so what's wrong with stating mine? I think it helps put my overall argument into perspective.. Edited by Faith, : No reason given.

Drat, RAZD, I know you went to a lot of trouble reconstructing that chart for me and I thank you for that, but I still look at it and your descriptions and feel I don't have any idea what point you are trying to make. Not even enough to venture a good guess. I wish I did because I have no doubt it is not the challenge to my argument you think it is, just as the greenish warblers aren't. I don't know how to deal with this problem, I'd like to be able to understand it so I could answer it but it just makes my head spin reading through it. I've looked at some websites that discuss Pelycodus too. Sorry, I just don't have a way of addressing this. Edited by Faith, : No reason given.

I would say this is ultimately what genetic diversity is, however, for all practical purposes it is impossible (at this time) to quantify this extent of genetic diversity. I raised concern about this in my Message 459 item #5. There is no paper that will describe all 1.5M unique alleles within a population. Showing a "new" allele in a population does not necessarily show that the overall number of alleles has increased.More important to diversity is what proportion of the loci are polymorphic and what fraction of the individuals are heterozygotic at a given loci. Not only are these the measures that are important to conservation, they are more readily measured. If Faith's hypothesis is correct, I don't think there should be any loci that increase in diversity (she would need to confirm that) so studies that describe even a few loci should be sufficient to show diversity can increase.Another point about diversity is that it exists in regions that are not considered alleles. Considering, for example, that less than 2% of the human genome is coding sequences and would not be alleles in the classic sense, it would seem unreasonable to exclude 98% of the genetic diversity in discussions of genetic diversity. Species can be defined reasonably well (despite the problems with defining species), but I don't think that genetic diversity can be as easily defined in the same way. In fact, IMO that is the basic principal at issue in this discussion.HBDEdited by herebedragons, : grammar

So let's try to break it down verbally.The bottom horizontal line represents a population (Pelycodus ralstoni) with variations in the size of individuals in the population, and the predominant size is represented by the thicker section of the line.Other lines represent populations of the same species at later times, as they are embedded in layers above the bottom layer, the higher they are the younger they are.The ages are relativistic based on the geological layers and the law of superposition.Each of the fossil lines overlap the lines of the layer below and the layer above and thus they show continuity of the species from one line to the next.The variable in question is size. What we see is that size in each population differs in distribution from one layer to the next, and this would be due to the alleles that govern body size.There is an overall general trend from the original smaller fossils to larger fossils as you rise from the bottom layer to Pelycodus trigonodus, about half-way up the chart, and at this point all the fossils at this level are larger than all the fossils of the bottom original population layer. This is shown by the vertical line marked by the 1's in the diagram.This trend continues through Pelycodus jarrovii, about 3/4ths up the chart and up to the red line. At this point the population divides, with one population continuing the trend to larger fossils up to the top of the chart with N.venticolis.The vertical line marked with the 2's shows that these top larger fossils are all larger than the Pelycodus trigonodus population, which are all larger than the original population at the bottom. None of the Pelycodus trigonodus population are the same size as either the top or the bottom, so the size of the fossils in N.venticolis are twice removed from the size of the original population.But the population at the red line splits and forms two populations with different sizes:

• the ones to the right keep the larger fossils size and the trend to larger fossils in higher\newer layers
• the other population takes the small size from the red line and reverses the trend, and instead trends to smaller fossil sizes in the higher\newer layers.

Line 3 is a vertical line from the left end of Pelycodus jarrovii, and following it down we see that all the original base population were smaller than the smallest fossil at the Pelycodus jarrovii level -- so all of those alleles should be lost to the species at this point according to your hypothesis.But as we follow the line up we see the second population trending smaller crosses this line and continues to get smaller up to N.nunienus, when all of the fossils are to the left of line 3 ... when alleles for these sizes should not be available anymore, having been lost. In fact ~half of N.nunienus are the same size as Pelycodus ralstoni.Here it is again: In evolutionary terms it makes sense for the two lineages to diverge in size as that means they forage for food in different locations rather than compete for the same resources.Because evolution theory does not depend on a finite supply of alleles there is no conflict with variation back and forth in size from small to large and then to small again.Because your hypothesis does depend on a finite supply of alleles there is a conflict when one set (ie - for small size) is lost. You can invent new alleles for the larger fossils from your hidden allele magic black box, but not for a return to small size alleles, because you have been adamant that they are lost as the population diverges from the parent population.Enjoy

I'm going farther back in the thread to catch up than I'd intended. Overwhelming amount of stuff to try to deal with. Perhaps my last post to Admin will help clarify I already answered that the addition of VIABLE alleles to a gene must involve some form of mutation, a healthy form as opposed to the vastly predominant useless and deleterious forms, but I'd restrict the process to those healthy functions since deleterious and neutral alleles are disease processes.Also, I don't see how the dead genes in junk DNA could be a source of alleles for OTHER genes still living, but if alleles can switch from gene locus to gene locus, that easily solves my problem: all the alleles formerly of the genes that are now junk DNA would just have been transferred to the still-living genes, but I've never heard of this being observed to occur.But the main thing I want to know is what the great numbers of alternate alleles actually do, such as the 59 for one gene I think you mentioned. How many of them code for an identifiable unique trait, how many are just redundant, coding for the same trait as the allele they replaced despite some differences in the DNA sequence, which I guess is what is meant by a "neutral" mutation? and how many disabled an allele, replacing it with nothing that codes for anything at all so effectively killing it?, and so on and so forth. Perhaps none of them really contributed anything useful to the trait the gene codes for. Do you happen to know? Of course. Your point is? Many suggestive facts that aren't evidence, such as the vulnerability to extinction of so many species in the wild. The thing is science isn't looking for what I'm looking for or they might have found it by now. But as long as they accept the assumptions of the ToE the evidence awaits some creationist scientific work that would need more consensus from the creationist community to get funded etc. Uh huh, and I've dealt with this fact many many times in discussions about all this. Genes of course. The loss of alleles is the loss of genetic diversity but a gene still functions with two of the same allele, which is homozygosity or the condition of fixed loci which usually exists for all the main traits in a breed, which is the definition of its being"truebred." I'm not superclear about what happens if that last allele becomes unfunctional but I think it works something like this: if even one copy of that allele dies, say by a mutation that destroys its normal coding, so that it can't form a functioning pair at all, then there is no more trait at all, no more living gene at all, so if that genome is nevertheless passed on, the offspring will inherit a dead gene, another corpse in the junk DNA cemetery. Over generations the gene should just keep getting deader as it were as that dead allele gets passed on, even if there remain individuals that continue to possess the functioning homozygous pair. Yes, I think it shows a previously enormously fertile and healthy genome that it could function at all as it is now. I did suggest that many immunities and abilities to absorb nutrients and health-protecting functions of organs were lost, all things that would ward off disease and promote great longevity, as well as perhaps simply many interesting variations on all the recognizable traits such as skin color etc. The fossil record shows an enormous variety of races of creatures that no longer exist as well as varieties of some that do have living counterparts, which variety suggests a lot more trait variability before the Great Bottleneck wiped it all out. Addressed above. Again I'd ask, can you account for the functions of those 59 alleles?

I think Percy's definition is good. But we don't need to account for ALL the genes and their alleles. What I've suggested is focusing on the genes for the particular traits that are most characteristic of the subpopulations, such as the genes for the plumage that varies from subpopulation to subpopulation in the greenish warblers ring species. If this is possilble. Avoiding hybrid zones and focusing on the populations that originally migrated from an identifiable "mother" population. If these can be clearly identified, and if the genes for the characteristic traits can be identified.It's where the populations differ most phenotypically that the loss of alleles should show up clearest. I'd expect maybe a half dozen traits per subpopulation to be evidence of loss of diversity as the subpopulations formed from each other around the ring. There could be multiple genes for each trait to look at too. Also, in many cases even the original population may have lost enough diversity to make this particularly difficult. I can't be sure it's even possible but this is what I'd expect to focus on. If a population is homozygous at a number of loci where in the previous populations there was heterozygosity this would be clear evidence of loss of genetic diversity. A mere loss of alleles at a locus that remains heterozygous would entail a count for many individuals which might be too much to ask. I'm not sure how this works with polymorphism but whatever is readily measured AND important is certainly where the focus should be. That's what I expect too. However, mutations DO occur. My expectation would be that none of them makes an actual functioning allele, that is, an allele for a new unique trait, and besides it probably wouldn't affect the phenotype right away anyway, it would have to be passed on and pair up with itself to find out what it does and that's too boggling to consider. Mutations that are merely a slightly different sequence that doesn't change the coding shouldn't be counted as increasing genetic diversity. I focus on alleles because they're easy to grasp. If it's possible to measure changes in diversity in other regions you'd have to explain the processes and make a case for it.Edited by Faith, : No reason given.

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That's really quite a handicap you are imposing on me here. To my mind I just stated the scientific outline of my argument about what junk DNA is. I believe it clearly fits with the known facts of the percentage of DNA in the genome and offers an alternative explanation that nobody would guess at if I didn't spell it out from time to time when relevant issues come up. Granted, it's a statement of my theory rather than any kind of proof, but you know what, various hypotheses are really all anybody has for junk DNA, so what's wrong with stating mine? I think it helps put my overall argument into perspective.

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I don't think that requiring you to be scientific could be a restriction on any view that you call scientific.But no, your idea that: is pretty silly really. How do genes "die" ? They certainly can't be "killed" just by a bottleneck. How does this hypothesis explain the quantity of junk DNA ? What evidence is there that all junk DNA is "dead" genes ?Really it looks like nonsense made up by somebody with no real understanding at all.

Bacteria also have populations.
Bacteria also experience selection and isolation. YOUR points were:

• there is no genetic innovation, that is genetic mutations plus (natural) selection cannot lead to a gain in genetic diversity
• genomes are deteriorating, leading to ever more junk DNA.
• phenotype diversity is only due to Mendelian genetics of existing genetic diversity
• because there is no genetic innovation, every instance of breed or subspecies diversification inevitably leads to a loss in genetic diversity.

Every of these points may be addressed directly on there own.
No. 1 is perfectly well addressed by the E. coli example.
And you STILL did not provide ANY reason why basic genetic processes, occurring in E. coli genomes, won't all of a sudden work in the genomes of sexually reproducing eukaryotes.So you are basically arguing that mutations won't happen in sexually reproducing eukaryotes, neither natural selection while the only thing that seems to work in those is Mendelian mechanisms.And YOU say you have a fair grasp of how genetics works at the genome level?EVEN IF you were concentrating on sexually reproducing species, EVEN THEN mechanisms in prokaryote genomes in terms of mutations and natural selection are PERFECTLY WELL suited to draw conclusions about the former. YES THEY ARE. They directly falsify your proposition that genetic mutations plus natural selection cannot bring genetic innovation, the VERY HEART of your arguments. First of all you I AM talking on your level.
Because the very core of your claims is based on the proposition that there is no genetic innovation possible, let alone by mutations in conjunction with natural selection.Which is DIRECTLY addressed by the E. coli experiment.BTW, calling someone is cheating is VERY RUDE. OF COURSE you want to focus on KNOWN genes.
That will shy you away from having the perilous requirement to back up you claims on genetic deterioration and to provide evidence that in reality there is no genetic innovation occurring through mutation in conjunction with selection.How convenient. I call it immunisation of your own ideas against contra-arguments. Talking about cheating. I BEG YOUR PARDON??????????????
GOOD HEAVENS.FIRST you suspend my arguments for no valid reason AND THEN you say I didn't provide any. LET ALONE the OTHER evidence I provided.As a matter of fact, of the both of us, I am the only one who is providing evidence for his position IN THE FIRST PLACE.Despite MANY calls by me or the others here, you pertinently refuse to back up ANY of your basic claims by ANY empirical evidence.

SURE IT DID. That comes when you focus on detail by detail and refuse to address the WHOLE picture and import of a post. Irrelevant red herring.
The POINT MADE here is that there apparently was a gain in the number of alleles from the alleged times of Adam and Eve (max. 4 genes per gene) to the observed number of alleles in MANY genes.How convenient to focus on the gene I used as an EXAMPLE and to dive into irrelevant details. If you feel that ALL those alleles in ALL THOSE genes which have more than 4 of them, are redundant, obsolete or non-functional, GO AHEAD and prove your case.An ASTONISHING question,"How many of them code for an identifiable unique trait, how many are just redundant", for someone who claims to have understanding of genetics. So you are implying that in all genes with more than 4 alleles, those alleles are redundant or whatever you call them to be?Sure.

The Lenski E. coli example addresses your main point (that evolution is driven by reductions in genetic diversity) more directly than any other. The E. coli example satisfies these criteria by providing "KNOWN" facts better than any other raised in this thread. Regarding E. coli, your statement that it is "without a shred of evidence" is hard to credit. Again, that example has more "actual known facts" than any other mentioned here. It is Denisova's responsibility to bring those facts out, and if he hasn't or if the facts don't support his premise then you should challenge him about it. You seem to be committing a significant fallacy. How is the example of E. coli gaining genetic diversity not relevant to your claim that genetic diversity can only decrease? More generally, how is it that the E. coli example is irrelevant because it is only about E. coli, but your sheep example *is* relevant even though it is only about sheep?I'm ruling that the Lenski E. coli experiments are directly related to the topic and cannot be dismissed. Not at all - I'm just stating a fundamental requirement of science: evidence. What you've provided so far is a hypothesis. It's based upon the Bible, but for EvC Forum that's fine. What you must do next is provide evidence for your hypothesis. Let me be specific: Your hypothesis contains an apparent contradiction, since first you state that genes dying are a long term result of the Fall, but then you state it was a result of the Flood. But my main concern is that you understand that your main responsibility is providing evidence for your hypothesis. For example, people will reasonably expect that evidence will be forthcoming for genes dying around 6500 years ago (the Fall) and 4700 years ago (the Flood). And they'll expect that evidence will be forthcoming for how a mass die-off by drowning can affect genomes. All I meant in my message is that you must understand that issuing hypotheses is accompanied by an obligation to support those hypotheses with facts. A statement that they're consistent with what is already known is not evidence, plus in this case that must remain an open question (at a minimum) since the evidence from ancient DNA contradicts your claims.Edited by Admin, : Typo.Edited by Admin, : Grammar.

Yes, of course. My examples using specific values for the number of genes and alleles were intended to make clear just what an increase or decrease in genetic diversity is. However difficult actual quantification might be in the real world, it can be an aid to hypothetical thinking to consider specific values.Let me state it another way. If a population's genome should acquire an additional gene, that's an increase in genetic diversity. Or if it should lose an existing gene then that's a decrease in genetic diversity. And if a gene of that population's genome should acquire an additional allele then that's an increase in genetic diversity. Or if it should lose an existing allele (meaning no individual of the population possesses that allele) then that's a decrease in genetic diversity. Sure, but wouldn't that definition be more appropriate to a different discussion? People are trying to help Faith understand that genetic diversity can increase through mutation. Mutation can add and subtract both genes and alleles, and when that happens across a population it is obvious that genetic diversity increases or decreases.Now of course mutation directly affects proportions of polymorphism and heterozygosity, but it seems more difficult to talk about genetic diversity in those terms. For example, varying heterozygosity of a specific loci helps measure the genetic diversity of a population. Fundamentally the type of genetic diversity this is measuring is how much variation there is across individuals in a population.But I think what we're really interested in this discussion is the fundamental genetic diversity of a species. We don't really care to what degree a specific allele is distributed across a population. If that allele becomes more common or less common in the population it has absolutely nothing to do with mutation. All we care about is that that allele exists and continues to exist. Only if it should cease to exist in that population would it be a change in genetic diversity that this discussion would care about. And of course if that allele should experience a mutation then its gene now has one additional allele that it didn't possess before, and that means the population's fundamental genetic diversity has increased, which this discussion would also care very much about.Perhaps that I'm finding myself forced to modify the term "genetic diversity" by adding the modifier "fundamental" up front means that what's really important to this discussion is not genetic diversity but something different though similar.Edited by Admin, : Wordsmithing in 2nd para.

So this is all about the size of the creature.The original chart gives what sound like the names of locations on the left margin. Were these fossils found scattered in many locations, or in roughly the same geographical area or even in a column one layer above another? Or do the names designate the layers themselves. And does it matter how many fossils were found in each layer?I'm going to have to comment as I go if only because I interpret this sort of thing differently than you do. so I can't just let evolutionist interpretations stand. OK, but that of course is evolutionist theory. A simple description of the phenomena would be something like: "Such and such number of this fossil were found in such and such layer at such and such geographical area. This layer is usually dated to such and such MYA. The many collections of these fossils found in various layers appear to differ in average size from one layer to the next. The measured sizes are such and such." And the dates each was found could be handy, as well as who found them etc.Instead of simple description we get theory. Why is that? No problem with superposition of course, tells the order they were buried in which might have something to do with their size though it might not; but geological time is always problematic. Again this is of course evolutionist theory. If they were simply buried all at once in a one-time catastrophe the only continuity would be that they are clearly the same species that got sorted into different burial locations for one reason or another. Did anyone differentiate between adult and young individuals or male and female? It could. Since four subspecies/races are noted the sizes could reflect the range of genetic diversity for size in each population, which I think is what you have in mind. But again I'd like to know if the size could be related to age or sex and if that was taken into account. OK, I'm getting that now, thanks to your writing it out more clearly this time. First, of course I dispute the whole evolutionist interpretation that says the populations genetically diverged from each other over time as represented by the layers, which I guess would make P. ralstoni the ancestral population. My interpretation is that they are certainly all related and may be different subpopulations but that they would have been contemporaneous with each other, probably inhabiting different locations. If some are subpopulations of others there is no reason to think they lived in different time periods anyway, or that the higher in the strata are necessarily the offspring of the lower: it could be the other way around.But for the sake of argument, accepting the evolutionist interpretation that the higher descended from the lower over time, and that size was the main variable from population to population, while there should always be a trend to loss of genetic diversity as a new subpopulation develops its new gene frequencies, there's no way to know, especially from fossils, whether the alleles for the other trait completely disappeared from the new population. If they still exist in the collective genome, further population splits could select those alleles, and two separate populations branching off could select alleles for each end of the spectrum, which would be reflected in the size differences between the two groups at the top. Or those two populations could reflect incompletely inbred genes, since the first stage of the expression of new gene frequencies is likely to bring out a motley collection of traits, possibly including the extremes, which would work through the population through many recombinations over time until a general phenotype emerges.So there would have been a reduction in genetic diversity if these really were subpopulations formed over time, but complete loss of alleles for different traits doesn't necessarily always occur. It's a TREND I'm trying to highlight, that only becomes expressed in complete genetic depletion at the end of a series of subpopuloations.I don't think that is what happened though because of course I don't accept the whole evolutionist interpretation that these fossils represent different populations that formed at separate times from the one lower in the strata. Edited by Faith, : No reason given.

Let's see what I have provided until now:

• E. coli experiment demonstrating genetic innovation by mutations in conjunction with selection is occurring and adding to phenotype diversity
• other experiments on prokaryotes showing the same
• Dachshunds and the like have short legs due to genetic mutations, empirical studies showed
• the fossil record (without even having dated it) shows a constant emergence of new life forms with completely new and different genomes and phenotypes
• several empirical studies on eukaryotes (fruit flies, yeast, beetles), demonstrating genetic innovation by mutations in conjunction with selection is occurring in sexually reproducing animals as well.

"No evidence provided" you did say? RIGHT.But also I substantiated that the one single occasion (correct me if I am wrong on it being the only attempt until now) where someone (Sanford) tried to provide scientific and empirical arguments for the idea of genome deterioration, he was found to fail in all respects.ALL of my core points have no been addressed until now.
Basic questions like how would it be possible that we now see genes in humans galore with more than 4 alleles, are still awaiting their answers.And until now, despite being requested by me and others here on several occasions, you didn't provide a single shred of evidence for any of your claims.If you don't mind, I will continue to build my case, adding more.So you think that the original genetic diversity in the genomes of the species, created by God for the first time, is now lost due to deterioration as demonstrated by junk DNA?I already pointed you out to the difficulties of this position:

• it should have been a lot of genes that turned into junk DNA, even when we know that not all non-functional DNA is pseudogenes. Because whatever definition you accept for "junk DNA", the proportion of pseudogenes in it must represent thousands of genes that were lost (according to your scenario). So I was wondering what all those genes were for in the original super genome. No satisfactory answer was given by you until now.
• you claim the genetic bottleneck occurring during the Flood was the main cause for the loss of genetic diversity. It completely escapes me how a genetic bottleneck could cause a loss of genes. For alleles that would make sense, but genes? So there were thousands of genes active in the rest of the human population (or any animal at those days) that got extinct by the death of their owners? So we have a population of the very same species where a substantial proportion of the genes are present in some individuals but not in others? Gee, normally only a few percent of genes differ BETWEEN different species and you are implying that a major chunk of the genes WITHIN the very same species are differing???? Weird.

Anyhow, consider this: in their 2006 paper, Thewissen et. al. investigated the genetic basis for hind limb loss in cetaceans. To be found here: Just a moment....In this study Thewissen unravels how genetic mechanisms that cause the development of hind buds in cetacean embryos, arrest and causing already developed hind limb buds to degenerate in 5th week of gestation. It turns out that cetaceans still have the genetic outline for developing hind limbs but one crucial Hox gene Sonic Hedgehog (Shh) has been disabled by mutations. It plays an essential role in the molecular cascade that controls limb development in vertebrae.This also is backed up neatly by the fossil record of cetaceans. Basilosaurids and Dorudontae were extinct cetaceans that still grew hind limbs and pelvises. But they couldn't walk with those. First of all those hind limbs were very tiny: not much bigger than an extant house cat's ones - while Dorudon weighted some estimated 600 kg or more. But even more telling is that the pelvis was detached from their spinal cords. Now what would a fully marine animal do with legs and a pelvis that were not suited to walk.That is what I call a pseudogene!
But, unfortunately for you, it is not the remnant of the kind of genetic deterioration you assume. It is an evolutionary remnant.
And last decades, geneticists are digging them up abundantly - in nearly every species that has been examined:

• genes that once made tooth enamel found in toothless animals
• platypuses lack a stomach. But not the genes that normally code for enzymes related to digestion
• all mammals still have three genes that code for vitelogenin, a protein that fills the yolk sac in egg laying reptiles and birds. All three are silenced by mutations. But not in monotremes which still lay eggs: one of those gene is still functioning in these mammals
• humans carry a lot of olfactory genes. About 400 out of 800 olfactory genes in humans are silenced. In dolphins even 80% of the olfactory genes are disabled
• many primates including humans do not manage to synthesize vitamin C themselves out of their food. But still those primates have the L-gulano-g-lactone oxidase gene for that
• chickens still have the gene set for growing teeth
• the same applies to genes for growing teeth in baleen whales. moreover, comparing the differences in the mutational errors in different species of baleen whales, made it possible to establish their relationships with phylogenetic consensus (that it, these result match the phylogenetic relationships established in other ways
• genes controlling the development of the tail in other vertebrates, Wnt-3a and Cdx1have been found in the human genome. This is confirmed by the development of tail structures in human embryos in early embryonic gestation. The precise process in which the Wnt3a gene is suppressed, is identified.

I could expand the list endlessly.Indeed there are pseudogenes. But these tell a quite different story. the story of evolution.Edited by Denisova, : Solving some linguistic problems....

All bacteria have to do to adapt is generate one mutation that is then copied many times and becomes the characteristic of a new population. It's pretty specialized at that point though, having lost all its other genetic information, which doesn't sound like it's even particularly a good thing for bacteria. I'm sure this is way too simplistic but I'll have to come back to it later if it's too far out of the ballpark.In sexually reproducing creatures a mutation has to occur in the right place at the right time with the right characteristics even to get passed on, and then you'll only have this one mutation that can only affect the phenotype if it's dominant; if it's recessive it has to continue to get passed on until it pairs up with another copy of itself in order to be expressed in the phenotype. I don't think there is really any valid comparison with bacteria and in fact I think even if beneficial mutations did occur the chances of their contributing anything to the organism is pretty iffy. Again I'm sure this is way too simplistic but I'll have to come back to it some other time. OK, I'll spell it out. Death started at the Fall, and all the disease processes, but we can tell from the fact that people normally lived hundreds of years up until the Flood that there was still a great deal of vitality in the genome of human beings; and most likely animals too since they were also taken onto the ark in very small numbers, from which all species since then descended, showing enormous genetic diversity and vitality compared to now.But the Flood was a one-time catastrophic death of human beings and animals both. a massive fulfillment of the effects of the Fall which would have wiped out not only the creatures but their genetic information. But I barely have the hypothesis worked out and where is the evidence going to come from? I can offer reasoning to support the hypothesis but how on earth could I prove it beyond that, especially since genetic studies are always interpreted through evolutionist theory. Emphasis on "interpreted" because it really isn't any more evidence for evolution than for Flood theory, it's mainly a difference in interpretation.I think the fact that it's a reasonable interpretation of junk DNA that fits the known facts ought to be treated as evidence.So where is the evidence for the evolutionist interpretation of the fossil record? It's all interpretation of facts that are open to other interpretations. RAZD just spelled out the typical evolutionist interpretation of different populations of species being found in separate layers, treating it as known fact. It's not, the Flood offers a whole other interpretive system. Other "evidence" includes nested hierarchies. But this is based completely on subjective assessment of similarity of traits. Similarity of traits can bei\ interpreted as design factors; there's no actual evidence for descent, it's simply assumed. I've also offered a whole other interpretative system for new traits emerging from microevolution: Darwin and followers explain it as environmental pressures or natural selection changing the organism to accommodate to the envifronment. You find this even in discussions of speciation where simple random migration with subsequent change in gene frequencies is taken seriously. But actual natural selection is really quite rare. Pocket mice and peppered moths come to mind. But Darwin's Galapagos turtles that look different from their mainland progenitors don't fit the natural selection model; they fit the migration model which brings out new traits simply through the new gene frequencies in the Galapagos population. Same with Darwin's finch beaks. Migration is enough to explain these variations through simple change in gene frequencies too, and natural selection would be enormously costly since all the "wrong" or unfitted beaks \for a particular food would have to be eliminated from the population; but when the new beak is there first the finch simply finds the food it's suited for.Then a couple years ago on another thread there was the example of the surprisingly rapid evolution of a lizard that was isolated on an island in Croatia, that was found after thirty years of isolation to have developed a very large head that fitted it to a different diet from its ancestral population. In a mere thirty years did the food bring about the change in the head size? More likely didn't the head size emerge as a result of the new gene frequencies caused by the smaller numbers of individuals inbreeding for thirty years, and then finding new food that it could now handle? There is no more EVIDENCE for the random gene frequencies theory than the evolutionist natural selection theory, except the time factor and common sense. And then there was the example of the Jutland cattle that developed four completely different subpopulations in a very short period of time, not time enough for natural selection to change them, besides which it was supposedly genetic drift and no change in the environment that made the difference anyway.There's no EVIDENCE for natural selection in these cases, but there is again reason or common sense that supports the random genetic change theory over natural selection. In other words you are asking me for a kind of evidence that isn't even available for evolution. Almost any particular offering of evidence for evolution can be interpreted from a completely different but just as reasonable a point of view, and more reasonable in many cases. Well I've thought about this and have the beginnings of a reasoned argument, but not hard evidence if you insist on that.Genomes are "specialized" to use Denisova's term, for the trait combinations of the subpopulations they govern. If a trait is governed by ten different genes then the different combinations of the alleles for those genes will determine differences between races or breeds; and if there are many alleles for those genes as well, which is still in question, the combinations can vary almost astronomically. So the people and animals on the ark would have carried their own particular combinations of genetic material and that's what would have survived to generate all further subspecies from then on. They would not have had junk DNA except perhaps a tiny percentage reflecting death since the Fall, but as these few humans and animals started reproducing after the Flood, some of the limited availability of alleles would start pairing up and becoming fixed loci and some of those would eventually find nothing to pair up with and the gene would die, and the dead gene would continue to be passed on and that's the source of junk DNA. Again I'm being terrifically simplistic and I'll have to work on it more. I've been clearer on this at least to myself. Based on bogus dates but yes. So if you want to demand evidence of a kind I can't produce and a coherent statement of an alternative hypothesis and different system of interpretations isn't enough I'll have to leave.Edited by Faith, : No reason given.