Evolution Requires Reduction in Genetic Diversity

In the first place he didn't suppose that. I've read his book "Why Evolution is True" very well. There he explains genetic drift quite extensively. So basically a straw man here. Not "by" the reduction of genetic diversity but resulting in dispersion of genetic diversity.Do you happen to have actual EVIDENCE for your supposition that any of the subspecies actually have more or less genetic evidence?We can suppose EVERYTHING, even most reasonable and even evidently - but in the end you have to provide the empirical evidence.

Yes I WILL correct your opinion when it's WRONG. That's debate for.
The correct way to conceive evolution in ring species is NOT "....you are getting a series of subspecies by the reduction of genetic diversity from subpopulation to subpopulation rather than "speciation" at any point as evolution defines it. "BUT: "....you are getting a series of subspecies by the dispersion of genetic diversity among the subpopulations and eventually resulting in "speciation" as evolution defines it."THAT is what REALLY happens.I explained that the genetic dispersion among subspecies or breeds of the original diversity is the RESULT, not the MECHANISM as you falsely conceive it.And my arguments on it HAVE NOT BEEN ADDRESSED until now.
And I am awaiting for 8,9 posts by now. I beg your pardon but SINCE when do I have to back up the evidence FOR YOUR CLAIMS????????And in case you didn't notice: I actually am the only one of both of us who comes up with empirical evidence. Like the Lenski experiment. Discarded by you without any ado let alone a sound argument.So pony up INDEED.Edited by Denisova, : No reason given.Edited by Denisova, : No reason given.

You can't tell that until you find genetic innovation in one of the O. aries' breeds (subspecies). If you find such examples, Faith's opinion is stone-dead.Faith's supposition is that all species some 6,500 years ago (at the moment of creation by God) had super-genomes, those since then deteriorating, leaving ever greater parts of the genome ruined in the shape of junk DNA.Furthermore, Faith does not accept genetic innovation to happen.
Because genetic innovation would replenish the gene pool and thus compensate for possible genetic deterioration. Faith thinks the phenotype variation we spot in O. aries, is solely the result of activating already (or should I say STILL) present genetic diversity or just of Mendelian mechanisms.The whole debate here, boils down to these two crucial points.That's also why it is difficult to get in the same line with her (implicit) definitions of concepts like speciation, as well as her ideas about the differences between phenotype and genotype and the sort.Faith's position on O. aries versus O. orientalis also rests on these two basic suppositions. As soon as anyone can prove that any of the traits of any of the O. aries ones are caused by fixed mutations, her whole position will be falsified. Or, for that matter, in any other bred species. SO LET'S HAVE THE EMPIRICAL EVIDENCEI asked Faith several times to provide empirical evidence for her suppositions. Until now nada. Accompanied by just refusing to face or address the contra-evidence provided.Now, by absence of Faith's own evidence, let's test her supposition of phenotype variation in breeds or subspecies to be solely the activation of genetic diversity still lurking in the genome or by Mendelian mechanisms. In other words, "no genetic innovation allowed".Let's have a look at the Dachshund, that fierce and proud little creature..... (...sorry, I was distracted a bit by my weak-spot for these utterly lovely quadrupeds, pardon for this little whim).

The beer belongs to my master

In their genetic analysis geneticist Ostrander and her team looked for the genetic factor causing the short, stumpy limbs of Dachshunds and other stump-legged dog breeds. They found out that a mutation in the gene FGF4 (short for fibroblast growth factor 4), which plays an important role in bone growth, was copied and reinserted into a new site in the dog genome.Ostrander examined 835 dogs across 76 different breeds, including 95 short-legged individuals, and found the genetic signature to be unique to these stunted animals.Source: Researchers Discover Evolutionary Event Underlying the Origin of Dachshunds, Other Dogs With Short Legs | National Institutes of Health (NIH).Now that's not an old luring gene getting expressed, nor Mendelian reshuffling of alleles. It is mutation by gene duplication and frame shifting.I was wondering how high the odds were for such genetic change also to occur in O. aries breeds. Let me have a guess: VERY HIGH. AS LONG AS this question is not answered, we are just manoeuvring in the dark.I also pointed her out to the Lenski experiment which unequivocally demonstrates genetic innovation occurring in E. coli bacteria. For any unknown reason Faith refuses to address it. Well, actually, I have a hunch.... EVIDENCE FOR DETERIORATING GENOMESI also asked Faith to provide her evidence for deteriorating genomes.
Until now, no answer.But by default of any attempts by Faith, let me elaborate myself on that too.
Actually someone actually did try to substantiate the supposition of deteriorating genomes scientifically: John Sanford with his concept of genetic entropy.Now there is not much left of Sanford's concept in current genetics. the reasons are plain: a lack of empirical foundation, an abundance of empirical evidence for the opposite and, unfortunately common among creationists, major misinterpretation of what evolution theory actually has to say and implies as well as, even worse, distortions of the work of others.A neat and decisive article on Sanford is to be found here, written by Scott Buchanan: STAN 4 | Letters to Creationists, the "JOHN SANFORD’S GENETIC ENTROPY AND THE MYSTERY OF THE GENOME" section down the page after the Behe section.First, Sanford backs up his claim of genetic entropy by referring to an empirical study by Kimura. Kimura there skips the beneficial mutations out of his observations. Sanford would have his readers believe that Kimura was so dismayed by the evolutionary implications of having only small numbers of beneficial mutations that Kimura did not dare treat the subject. But, actually, he reason Kimura omitted beneficial mutations was not that they have too little effect (as Sanford implies), but that in his model they would have TOO much effect. He just ruled them out as a bias to his actual methodological aims: when one wants to study the relationship between A and B, factor C which may also take part as a causal factor, needs to be sorted out.This was the distortion part.Secondly, the actual evidence for beneficial mutations. I quote the article: "The literature is rife with examples of helpful new mutations becoming fixed in a population which is exposed to a new environment". Buchanan refers to the studies no. 4 - 9 in the References section of his article. Many of those involve studies on emergence of resistance against antibiotics or pesticides and most of them find genetic change due to mutations.Thirdly, Sanford claims that natural selection does not have enough "selective power" to counterbalance the accumulation of deleterious mutations. In his reply Buchanan provides a series of empirical studies showing Sanford to be factually wrong. among those Lenski's long term experiment on E. coli (in that very long term one should observe deterioration in fitness which didn't happened - on the contrary), as well as several mutation accumulation experiments with eukaryotes, including Drosophila melanogaster, yeast and beetles. Those studies are also listed in the Reference section of his article.Buchanan ends up this section with the inevitable conclusion of all these experiments: "when natural selection is not operating, the population genome deteriorates, and when natural selection is operating, the average genome of the population does not deteriorate", as well as:
"This is so simple and so obvious, that we must ask: How can Sanford possibly claim what he claims, when decades of experimental studies clearly show the exact opposite? As a genetics researcher, he was certainly familiar with MA studies and their implications. This is another example of deceit in Genetic Entropy, and it is a whopper."Fourthly, Buchanna also directly addresses Sanford's claim of genome deterioration by mentioning several empirical studies which indicate this to be incorrect. see his Reference list again for those. FINAL CONCLUSIONSIn other words, the one occasion when one creationists tried to empirically substantiate claims for genome entropy, it actually ended up in being made minced meat out of it. If anyone here knows other attempts, of course be free to introduce it.The empirical evidence does not favour deteriorating genomes. It falsifies that notion.Until Faith doesn't solve these problems with her claims, we are all making feints and diversions in the shimmery realm of unsubstantiated propositions, discussing all kinds of neat details but evading the core points.Edited by Denisova, : No reason given.Edited by Denisova, : No reason given.

I know that - but my point was that finding examples of genetic innovation will falsify Faith's supposition that breeds in O. aries are only exhibiting phenotype variance because of Mendelian mechanisms and already existent genes re-expressing and no genetic innovation is involved. And until that moment, any discussion about taxonomy and speciation makes no sense and only leads to manoeuvres in the dark.

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.

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....

I know and agree. Ask Faith, it's her vehicle and also read the thread first.
I also assume that at least a substantial part of the junk DNA are pseudogenes.
What proportion exactly is not very relevant here. I'm only driving Faith's assumptions to their logical consequences - that is, implding under its own weight. Ask Faith, it's here vehicle.
She is assuming that all the original genetic diversity was deteriorated or collapsed by the Flood or the Fall. I have no idea what proportions. Faith doesn't specify it. How could she because she has no empirical evidence to substantiate that or to calculate those proportions anyway. So I take her argument and bring it to its logical consequences and see what happens.Speciation is not in Faith's vocabulary.My opinion on speciation and its relationship to genetic diversity is spelled out numerous times in my previous posts, if you don't mind, i am not going to repeat that here again. Every individual can carry a maximum of 2 alleles for each gene.
When there were a population bottleneck of the Flood proportions (only leaving 8 people alive, 3 of them being sons of 2 other ones), the maximum alleles per any gene cannot exceed a total of 10 (3 X 2 in the wives of the sons, max. 4 in Noah and his wife and therefore the same ones in their sons).Hence, that number of 10 alleles would evidently have been much lower than the number in a much larger, pre-Flood population.The number of alleles cannot drop to nil because there are 8 persons still surviving, thus this implies some alleles will always survive in such circumstance.In the animals the situation is even worse because of many of them only two specimen, 1 male and 1 female, were taken on the Ark. So the maximum number of alleles for any gene in those genomes is 4.But the number of genes cannot drop that much. Because all individuals in questions are of the same species. Species do not vary genetically much. Max. 1, 2 or 3% genetic diversity. Otherwise you would get a different species!So the number of alleles after such severe population bottlenecks will drop dramatically but the number of genes only very slightly. Off go Faith's notions. Well, if you compare species mutually, you will see that they share a lot of proteins. The more phylogenetically they resemble, the more proteins they share. But they do not share all proteins. So there must be at least some protein sequencing having occurred in the course of evolution. On the other hands, proteins are biochemically very redundant. Cytochrome C in algae may differ considerably in biochemical composition from the variant found in, say, bacteria or animals. But its functional part is biochemically spoken exactly the same among all known species. They even did transplant the cytochrome C from an alga (if I recall well) to an bacterium, two very distant life forms. Normally their cytochrome C differs considerably in chemical composition. But yet nothing happened with the bacterium. I could well do with the alga's cytochrome C.So the picture is a bit complicated. But yes, much evolutionary change would be due to altered Hox genes and the like. But not all!

Percy,Is it normal in this thread that you get no answers on the questions you pose?I get posts by Faith in which she endlessly addresses unimportant details leaving the core and import unanswered.I came here from Topix in the hope I would be spared from dodging and evading but it is not different here.

The move the discussion forward it would also and particularly very helpful when Faith starts to answer questions and address the things we put forward. In the first place.

All those pesky scientist doing science, how annoying isn't it.
A very miserable argument frankly.
So basically you are saying that the whole scientific community within the life and earth sciences are collectively biased towards an empirically unsubstantiated paradigm?YOU MUST BE KIDDING.
Are we here on a scientific forum??????????In other words THERE IS NO empirical evidence for a deteriorating genome.I tell you a little secret: THERE IS NO SUCH THING.As you may not recall, I dedicated a part of one of my post to the work of John Sanford who actually tried to substantiate the claim for a deteriorating genome. Due to distortion of the work of others, a lack of own empirical evidence and severe flaws, this is basically made minced meat.A lack of evidence does not need evidence.So, OFF goes your propositions. They not only lack evidence but the instance where it tried to substantiate empirically, it failed. NOW I will come back to my old saying: DO YOUR HOMEWORK.
I will NOT fulfil YOUR obligations here. I WON'T spell out the evidence FOUR YOUR CASE.
Please DO YOUR HOMEWORK."Well on to the next dodge and evading".

Percy,I complain about the dishonest way Faith is debating here.
See her Message 488.What may I expect from the scientific import of the debate here?
As I wrote, i moved here from Topix in order to find decent scientific debate. It's hardly there.Edited by Denisova, : No reason given.

A lack of evidence does not need evidence.
WHERE is the empirical evidence for your concept?No evidence?
NEXT.

The problem here is that in debate - even within the scientific realm - but certainly on sources like Wikipedia and else, the concepts used are highly blurring.We have:
- junk DNA
- non-coding DNA
- non-functional DNA
and even more terms of use, all hopelessly muddled as mere mutual synonyms.If you google "non-functional", you mainly get articles with "non-coding" and vice versa.Purely on semantic grounds, non-functional DNA would be the best term.
Because much of the DNA that is non-coding, actually STILL is functional, including the transcriptional and translational regulation of protein-coding sequences, centromeres, telomeres, scaffold attachment regions (SARs), genes for functional RNAs, and many others.So, if geneticists say 98% of the human is "non-coding" that DOESN'T say it is "junk" as well.ENCODE claimed that 76% of the human genome's noncoding DNA sequences were transcribed and that nearly half of the genome was in some way accessible to genetic regulatory proteins such as transcription factors. And off went the common people in utter chaos. Because not every DNA sequence that is transcribed or accessible by transcription factors is FUNCTIONAL.So, yes, we still can say that the very most of our genome is non-functional or, as the ENCODE team neatly admitted "the larger proportion of genome with reproducible but low biochemical signal strength and less evolutionary conservation is challenging to parse between specific functions and biological noise". And THAT part already is 70% of the documented transcribed coverage.After all the noise in the aftermath of the ENCODE debates, the human genome, according to ENCODE, is left with 12-15% "under functional constraint".In my language this reads that ENCODE implies 75-78% of the human genome to be non-functional. You may call it "junk".ENCODE still contends that the 12-15% figure may still be an underestimate.
Nothing wrong with that prediction.
Just let's see what their or other research will bring.
Let the facts speak!Edited by Denisova, : Typo...Edited by Denisova, : No reason given.

In the first place your answer does no relate to the point I made. I was not talking about junk DNA in that particular point. I was saying that in a population bottleneck it is impossible for the number of genes to drop dramatically.Now let's examine what happens when the vast majority of a population gets extinct by such an alleged event like the Flood. You imply that the great majority of the genes are silenced or just passed away along with their owners, leaving only the small subpopulation of Noah and his crew with their subset of genes and alleles.Such an extinction event will delete many alleles from the original, common genome, without any doubt. They will be GONE because all the unfortunate ones that died throughout the flood took those alleles with them to their inundated graves.That means that there will be NO REMNANTS of THOSE alleles in the genomes of Noah and his crew. Noah can't just take away with him the alleles of OTHER persons who just died. Not even in the junk parts of his genome.Now what about the genes themselves?
Are there genes within individuals who belong to the very same species that may not exist in other members of that species? Without any doubt they will. But not much I think. Because too much of non-shared genes will imply interspecies rather than intraspecies differences.When, as you imply, most of the original genes are silenced by an extinction event, it must be those ones that disappeared along with their deceased owners. In that case, again, Noah and his crew just can't "take over" those genes. When their owners died due to the Flood, those genes will be lost for eternity.In other words, junk DNA in extant humans CANNOT be explained by extinction events by definition and sheer logic.Moreover, when MOST of the genes ("95% junk DNA") are lost, the original human genome must have comprised thousands of genes more than today. BECAUSE all these genes originally were in the individuals that were killed during the Flood, there must have been an ENORMOUS genetic divergence between the unhappy mortals that died and the surviving Noah crew. I don't think that ANY definition of a biological species can be compatible with such an ENORMOUS genetic diversity within just the very same species.Edited by Denisova, : No reason given.Edited by Denisova, : No reason given.Edited by Denisova, : Language issues.