The Origin of Novelty

Why is it ridiculous to point out that chemical phenomena are formed by chemical processes? Do you know of any exceptions? Why is what we can readily observe ridiculous? Obvious to whom? The discussion is perfectly civil on my part. I thought you were aware of the examples of novel protein coding genes that I gave on the peanut gallery. There was one in the Douc Langur monkey and one in an Antartic fish. They are paralogs. I'll repeat them here if you really want me to when I've got time. There's nothing subjective about pointing out that natural processes are the best explanation for natural phenomena. The conclusion is based on observations we can all make.

[Copied from the peanut gallery on mindspawn's great debate].There are various theoretical models of how gene duplications can produce new function, and there's considerable evidence that this can happen in several different ways.One interesting way is the "Escape from Adaptive Conflict" model, known as "EAC". This is based on the fact that some genes perform more than one function. This could hypothetically cause "adaptive conflict", because the ideal allele for one function may not be the same as the ideal for the other. Duplication of such genes, says the theory, could lead to subfunctionalization of each paralog, and to enhanced or new function as each copy of the gene is free to perform only one of the original functions, thus ending the conflict.Here's a recent research paper which presents very good evidence of an example of neofunctionalization arriving in this way. AbstractArticle based on paper

quote:

---

Abstract

​

The evolutionary model escape from adaptive conflict (EAC) posits that adaptive conflict between the old and an emerging new function within a single gene could drive the fixation of gene duplication, where each duplicate can freely optimize one of the functions. Although EAC has been suggested as a common process in functional evolution, definitive cases of neofunctionalization under EAC are lacking, and the molecular mechanisms leading to functional innovation are not well-understood. We report here clear experimental evidence for EAC-driven evolution of type III antifreeze protein gene from an old sialic acid synthase (SAS) gene in an Antarctic zoarcid fish. We found that an SAS gene, having both sialic acid synthase and rudimentary ice-binding activities, became duplicated. In one duplicate, the N-terminal SAS domain was deleted and replaced with a nascent signal peptide, removing pleiotropic structural conflict between SAS and ice-binding functions and allowing rapid optimization of the C-terminal domain to become a secreted protein capable of noncolligative freezing-point depression. This study reveals how minor functionalities in an old gene can be transformed into a distinct survival protein and provides insights into how gene duplicates facing presumed identical selection and mutation pressures at birth could take divergent evolutionary paths.

---

Paralogs are identified by sequence similarity. Many paralogs with differing functions have been identified in many different species. Mindspawn faces the daunting task of demonstrating that all of these genes which look like functional coding paralogs are actually not (which is essentially what he is claiming).When something looks like a duck and quacks like a duck, the default is that it's a duck. The onus is not actually on RAZD to show that apparent ducks (or paralogs) are what they appear to be, but on mindspawn to support his extraordinary claim that they are not what they appear to be.Rather him than me!Note the significant added function of the new gene described in the article. "Unlike the SAS enzymes, which remain inside the cell, the AFP III proteins are secreted into the blood or extracellular fluid, where they can more easily disrupt the growth of invading ice crystals."

Scientists assume that what looks like paralogs are paralogs. They assume that the known process of gene duplication is responsible for pairs of genes that look exactly as if they are the results of that process. They assume that what looks like a frog is a frog, produced by the processes known to produce frogs.Now, would you like to demonstrate the existence of another process that produces apparent paralogs
or apparent frogs? Merely. Would you like to describe another known process other than duplication by which genes which appear to be duplicates can appear in the genome of a species. A known process.And having done that, as it's your claim that all apparent parologs in genomes aren't paralogs, how are you going to set about showing that this is true?

Yes. But only if you accept that the greatest diversity being outside the Middle-East falsifies your model. Yes. Try. Find out where the greatest genetic diversity is in the world.

The observed fact that duplication is a real phenomenon. No. Duplication can be detrimental, neutral or advantageous according to actual current observations. Message 35And "neutral" on arrival is all that would be required for subsequent neofunctionalization.You should be able to see that if child is born with a duplicate of CCL3L1, it has a potential advantage. Duplication of FCGR3B and AMY1 could also be advantageous if the individual has inherited low copy numbers. Therefore, you can figure out that there are known circumstances in which duplications can be advantageous. Also, with AMY1, you can see that duplication could be either advantageous or neutral depending on environmental circumstances and the number of copies already present in the individual in whom the mutation happens.There are other examples. Pfmdr1 amplification is known to be advantageous for the malarial parasites in developing drug resistance.Gene duplications can go to fixation in populations if they are advantageous or neutral, like all other mutations. There's no circular reasoning in direct observation of both present day duplications and of historic duplications. So, you don't know of a process that would produce apparent paralogs other than duplication. Go for the best explanation, then. You mean its anti-freeze gene? Evolution by gene duplication. The two genes look exactly as they should if that were the case.If you know of one process and only one process by which a phenomenon can be caused (two nearly identical genes in the same species in this case), then the best explanation for historical examples is that they were formed by that known process. Of course. Evolution is a demonstrably real process in biology. Gene duplication is a demonstrably real process in biology. Supernatural beings making things is not a demonstrably real process. Supernatural beings creating whole organisms like fish is not a demonstrably real process.I think you might be confusing creationist arguments about paralogs with creationist arguments about orthologs. Orthologs are similar genes in different species. That might be why you keep saying that we're assuming "evolution" (meaning speciation and common descent) in order to prove it.Paralogs could exist in your model of created kinds, because they could occur and go to fixation within one species, although on your time scale of 6,500 years there are unlikely to be that many.Orthologs could only exist in your model to the extent that you accept speciation. You presumably wouldn't accept them as such in anything excepting closely related species that could be regarded as the same "kind".What you should be arguing, in order to fit what we observe in genomes into your 6,500 year model, is that gene duplication followed by neo-functionalization can happen very quickly and frequently, and can go to fixation very quickly. You also need to argue that neutral and positive copy number variation can happen by both duplication and deletion, and can go to fixation quickly in groups.

On the subject of duplication: You haven't looked. There are plenty of examples of situations in which duplication can be advantageous or neutral on arrival. One of the things you could do to test this is to artificially duplicate genes in certain environments, and measure the effects on fitness. It's been done in E. Coli, and the researchers found 115 cases in which amplification alone could increase fitness in toxic environments. In most strains, there was no loss of fitness in the absence of toxins (the duplications would then be neutral). Yes. I was waiting for you to suggest it. Both can happen. Think of AMY1 in humans. Here's what's interesting for you. You say: That would be drift. It's a slow process. If you want a model of humans beginning 6,500 ya with the maximum known number of copies (15) so as to avoid any duplication, then you need a much higher mutation rate than we actually have, coupled with some positive selection on a decrease in AMY1 copies. You'd have the same problem with building up the number of copies by duplication on that time scale. No. The chances of an intelligent designer using an antifreeze protein encoded by a gene that looks like a duplicate of another are slim, given the options available. There are many other antifreeze proteins already in the life system, and our knowledge of artificial proteins indicates that the overwhelming majority of potential functional proteins are not even used in the life system. Evolution is constrained in what it can do in a way that designers aren't. The designer would have to be trying to make it look like evolution.You're still arguing that what looks like a frog could be something other than a frog. When you see an individual apparent frog, do you assume that it came about from the transformation of frogspawn into a tadpole, then a frog, or do you think it equally likely that it could be a Prince magicked into an apparent frog?Don't you understand that duplication events can be "read" on genomes, and that they happen regularly in labs? I'd be happy to, but you keep implying that supernatural beings can make things without presenting a single known example of this actually happening. It's a bit like having a conversation with someone who claims that kangaroos can speak French, but who cannot present any positive evidence of kangaroos speaking anything, let alone a human language, let alone French. Not quite, though, because at least that person could demonstrate that kangaroos exist! No. Natural explanations for natural phenomena aren't dumb. They are "plausible and realistic", as Bolder-dash would say. And just what he asks for in the O.P. I agree. What's that got to do with abiogenesis? Well, you made it! See above. And the original gene was not a good design for anti-freeze, hence the positive selection on the duplication.BTW, are all Zoarcid fish one Kind, in your opinion? And if so, what sort of environment do you think they were created to be in?

In a sense, you're nearly right. So "poorly" that "our side" isn't even being challenged. Your problem is that processes like mutation, selection and drift are demonstrably real. What you need to do in order to catch up with us is demonstrate the reality of your process, which is supernatural beings making things in general and biological features in particular. When are you going to start this attempt? For Creationism to be true, you need a supernatural being or beings that are 1. Demonstrably real. 2. Can make things. 3. Can and do make biological features 4. Can and did make all the complex features of all the organisms.We can demonstrate my 1,2 and 3 directly in the lab on behalf of the processes of mutation, selection and drift. You're asking us for detail on "4", which is historical, and cannot be directly proven. Yet you cannot even present a jot of evidence for 1,2 and 3 on behalf of your process, let alone dream of approaching 4.So, in your O.P. you ask for explanations to be plausible and realistic. We are clearly winning hands down on both realism and plausibility, aren't we?

Artificial gene amplification reveals an abundance of promiscuous resistance determinants in Escherichia coli.And a bonus! Adaption to warmth involving two similar but non-identical duplication events on two different cultures, and a deletion event on a third culture, plus other adaptions through point mutations. It should have occured to you by now that as positive and neutral duplications can occur, and positive and neutral point mutations can occur, you have no argument against neofunctionalization, which is merely a combination of duplication, then further mutation. What is there in duplicated genes that stops them mutating new function in exactly the way that non-duplicated genes do? No. You asked me whether I had thought of the possibility that there were high copy numbers in the "original population", and I said that I had. I had thought of it both in terms of an evolutionary scenario at some point in our ancestral group, and in terms of your 6,500 year old biosphere. That's why I knew you'd have problems with the idea of a supergenome and deletions going down less than 300 generations. So, anyone inheriting a lower number could duplicate up to a higher number without getting sick from too much dosage. Gone is the claim of duplications always causing problems. But now you're catching on to what your model would require. In reality, there has to be a lot of diversity in the population 6,500 years ago in order to fit what we see today. Have you tried finding anything out about Copy Number Variation in humans, and fitting the data into your model?And have you found out in which region of the world humans have the greatest diversity yet, as I suggested you should? It isn't the Middle-East. Says the man who keeps claiming that fairies can make genes. I have to point out that it is your claim that no evolutionary processes can increase the number of protein coding genes. It remains entirely unsupported. What I was pointing out is that there would be many ways that a designer could make an antifreeze protein that would not look like duplication. There is no need for a designer to design as if constrained to do things in the way that evolution does. Check out the history of anti-freeze in cars, and you'll see what I mean. No. The original gene had developed a secondary function that was relatively inefficient. It gave some protection to the eggs, but did not produce an antifreeze for the bloodstream. But it couldn't mutate away from its primary (and very different) function. Do you understand the idea of EAC (Escape from Adaptive Conflict)? The paper I thought you'd read before disagreeing with its conclusions.I can't give you more detail than the research team.

And the Ratites* would be flabbergasted.As for the poor confused penguin.....*They could fly before the Fall.....then they fell.

I'm not sure if you've quite understood the paper, but that last sentence of yours is correct. It produces them randomly all the time.It's producing useful duplications that we were discussing. You're welcome, and you're getting there! I don't know what you mean by "rare". Duplication + neofunctionalization wouldn't have to be an every day, every year, or every generation happening in order to account for the increase in number of protein coding genes in a population group from 1,000 to 20,000 (the scenario you were discussing in your debate with RAZD). The completion of such an event in one individual organism in the group every 10,000 years on average would get you there in 200 million years, and things have been evolving for far longer than that. Already when? In our hypothetical ancestral genome of 1000 protein coding genes? We wouldn't have been a starch digesting animal at that point, so I expect our AMY would have had a distant ancestor doing something else, and that this would be a distant ancestor of other genes we have now. Shall we look for relatives to test the hypothesis that genes, like organisms, come in families with nested heirarchies? Or do you mean high copy numbers in a created population 6,500 years ago? I'd expect there to be considerable variation 6,500 years ago in an evolutionary scenario, and before. 300 generations is not a long time to create much variation. A clue to another of the problems for your model is in the word "copy". In that paper about adaption to heat that you enjoyed, there were duplication events in 3 of the cultures that all included the same key genes. But the duplications were all different. When genes are duplicated, it's in this messy kind of way. If the AMY1 duplications look as though they are on messy randomly inserted stretches of DNA, wouldn't it be reasonable for you to ask yourself if your creator wasn't trying to make things look as though they were products of mutation? You won't find lots of neat little AMYs sitting in a row, looking pretty. Deletions and duplications don't look the same. And there are far too many human CNVs to have occurred in the last 300 generations of evolution. I think you need all the deletions and duplications that you can get! You also need a very high mitochondrial DNA mutation rate for a 6,500 year old Eve. Which brings me on to the next subject. The points made in that paper are absolutely fine, but they are not saying what you think they are, and their analysis and dating blows out your model, so I laughed when I read it.You're making a mistake about the haplogroup maps which are used to illustrate human population groups around the world.Ones like this: It shows the subgroups of L3 outside Africa, because the interest is in human population spread, but it doesn't show the equivalent subgroups of L3 plus other haplogroups within Africa.Here's L3
And:
L0
L1
L2
L4
L5
L6If you look at the true haplogroups, rather than just at those used to illustrate population spread outside Africa, you can see that the true ones are an indicator of diversity, although they can be misleading. As the paper you linked to mentioned, older haplogroups can have arrived in an area relatively recently.So, once again, which area of the world has the greatest diversity? Edited by bluegenes, : No reason given.

No. The "normal state" isn't amplified. They amplify all the known protein coding genes. From the paper, with my bolding:

quote:

---

The next logical step was to survey the entire E. coli proteome for its latent ability to confer genuinely new phenotypes (rather than to recreate old ones).

​

Here, we describe a comprehensive search for promiscuous proteins that can impart new phenotypes on E. coli. We provide experimental evidence that the overexpression of preexisting E. coli proteins can provide resistance to >80 antibiotics and toxins. Our results suggest that the evolution of novel traits is surprisingly likely, and that even the genomes of well-characterized bacteria harbor substantial reservoirs of latent resistance determinants.

---

quote:

---

Concluding Remarks.
We have used two tools from functional genomics (PM plates and the ASKA collection) to conduct a comprehensive search for E. coli proteins that can impart improved growth in the presence of toxic compounds. The resulting catalog provides a unique picture of a bacterium's latent evolutionary potential and emphasizes the high frequency at which novel traits can evolve. By cataloguing sources of phenotypic innovation, we have revealed the diversity of adaptive mechanisms that can be underpinned by overexpression mutations such as gene amplification. Our results suggest that the IAD model is a biochemically and evolutionarily feasibleand perhaps dominantmechanism for the birth of new genes under selection.

---

PaperIt certainly confers a new advantageous function. What happened was, firstly, at least two potentiating mutations. Then there was a duplication that formed a new hybrid gene. At this point the selection advantage was there, but still relatively weak. Then further duplications added copies (amplification) which greatly improved the new function. So, there was advantageous duplication upon advantageous duplication upon advantageous duplication.Now, didn't you started off claiming that duplication was always disadvantageous? Here's a pdf of the paper that describes the Lenski Advantageous Duplications.And the other one I showed you, with the Advantageous Duplications adaptive to increased heatAnd just for good measure, The malarial parasite regularly adapts to our attacks on it by both duplications (plural) and point mutations.Were you trying to make me laugh with that last sentence?. The mtDNA haplogroups that we were discussing are a good example of what might be called a short term hierarchy (see chart below). It's a nested family tree of mutations within a species.If you want a longer term one, what about the Elephantidae? They have nice long generations like us, so I'm wondering if you want to try to fit them into your 6,500 yr (about 260 generations) biosphere as one "kind"? All hard science sans philosophie so far. How many people survive this flood? Amplification has been observed to add to fitness. You may not realise it, but you're defeating your own arguments against an evolutionary scenario. If humans are perfectly healthy with high copy numbers of AMY1, there is nothing to stop them having evolved by duplication from one original.I entirely agree that there would have been copy number variation and high copy numbers present in the population 6,500 years ago (and before).Did you know that there are some genes with hundreds of copies in some individuals, and copy number can vary by more than 100 between individuals? And, moving from CNV to SNPs, did you know that there are some genes with more than 1000 alleles at the same loci, and at least one that is known to have more than 2000? That's interesting when you consider that your original population could only have 4 between them. Surely you agree. You would want Adam and Eve to have the maximum variation possible, wouldn't you? If they're like twins, you're in real trouble with your model. They have to have artificial different ancestry, just like they have artificial navels, and the first trees created have artificial tree rings, etc.Scientific creationism can be fun!And you've inadvertantly supported my statement earlier in the thread. You claimed that humans and chimps couldn't have 120,000,000 differences on the genome on a time scale of 5 to 7 million years based on mutation rates. Apply the same general principles to your model.You have a bottleneck 6,500 years ago (260 generations), and another 4,500 years ago (180 generations). From that point, all modern Y-chromosomes are ~180 generations away from that of just one man (Noah). So, we could test your model against mutation rates estimated from pedigree studies. (These are within species, so we avoid your issues with common descent).As you want figures, you can have lots of them. Example of a Y-chromosome pedigree studyA human phylogeny with some time estimates for Noah/Adam which uses the same mutation rate estimate concluded in the pedigree study above.So, if you read and understand those papers, you can see that we have a reasonable falsification of your 6,500 year old biosphere. It's stating the obvious. Here you can do the same as with the Y-chromosome above. Pedigree studies won't give us the real time of mitochondrial Eve for a variety of reasons, but they can give an indication of the most recent time possible. For example, this paper makes a <15,000 year old mitochondrial Eve seem extremely unlikely, and a 6,500 year old Eve essentially impossible. You haven't presented any "information". You've just made a mistake. You don't understand haplogroups or the maps, do you? African DNA is not any "older" than anyone else's. What you do find in Africa is slightly more general genetic diversity than elsewhere, both in terms of SNPs and CNVs. That's because there hasn't been a bottleneck there for a very long time, whereas everywhere else there has been at least one "founder effect" bottleneck. However, none of these founder effect groups seem to have been particularly small, so that even in America and Australia, where more than one founder effect has happened en route from Africa, people have retained most of human variation.Read the Y-chromosome phylogentic tree paper I linked to further up. The African haplogroups that get left out of "how we moved round the world" maps. Those maps mark the subgroups of L3-M and L3-N at the bottom right. Nearly all out of Africa people are L3 Africans in either the M or N subdivisions.

You could always try clicking on the link in the fifth sentence of the BBC article. The abstract you found (available in full here) is earlier research by same team, but no harm done, as it also looks interesting. Here's the 2013 paper.At a brief glance, processes include mutations on both coding and regulatory genes, plus my current favourite, increased protein expression due to selection on variable copy numbers of genes. That's how they harden their cuticles against our onslaughts. The kind of old tricks that rapidly reproducing organisms that exist in great numbers get up to. We do them all as well, but in relative slow motion.There's certainly "novelty", by any non-creationist definitions.EvCs own bug man Blue Jay might be able to help you, and, looking at the affiliations, might well know one or more of the authors. He might even be one of them!

"Latent" in this context means "potential" (look it up!). The genome has the potential to adapt by mutation (in this case, duplication leading to amplification) causing a new phenotype. That is evolution.Remember, I showed you this paper along with others (like the adaptation to warmth by duplication one) to show you that duplications can be advantageous on arrival as well as neutral and detrimental. You already know that point mutations can change the protein product of coding genes in ways that are advantageous or neutral. So, you have an answer to your question, which was how can evolution increase the number of protein coding genes from 1000 to 20,000. Combine the processes. Add a gene by duplication, then, like other genes, it is subject to change by point mutations. Voil. You've got a new coding gene. Why would the advantageous potential (latent) ability of self-replicators to adapt being favoured by nature over the hypothetical lack of that ability be "funny"? Static self-replicators would perish in an ever changing environment, so the survival advantage of strains that replicate with variation would be better described as " obvious" rather than "funny". You'd have noticed that there are about thirty amplifications of the new gene in the Antarctic fish paper which is mentioned in the subtitle above if you'd read it carefully. There are variations by point mutation between these, as well. They are, from memory, 97% to 99% identical. Read the paper carefully, and you will see that they have analyzed a historical sequence of events which happened entirely by common types of mutation that can be observed in the lab. There's a duplication, which enables one copy to mutate away from the primary function and form the anti-freeze protein, then further duplications of the new gene. How can a new copy already be there? And why can't the new copy mutate to produce novelty in the phenotype just as other genes do?If you read and understand the various papers I've shown you, you should be able to see very clearly that novel protein coding genes can be produced by well established processes. Duplication, then point mutation on one or both of the copies. It's not just a question of selection. Do you not understand that experiments like the adaption to warmth one and the Lenski experiment start from one original organism. The cultures derived from this are initially clones. The original genome is known, so that the researchers can identify what has arrived by mutation. So, novel features in the genotype and phenotype can be observed to arrive in the lab. Be careful. On the basis of known adaptations, you'll find yourself having to argue that a whole variety of modern pesticides were being used in the garden of Eden, and that Adam and Eve were wearing nylon and treating themselves with a range of antibiotics while also using modern anti-malarial drugs. I think you might have a few theological problems with all that, as well as the obvious historical ones. Remember, the Lenski adaptation required enabling mutations + the creation of a new regulatory gene by a duplication as well as the amplifications. As requested. I think you'll find that the young earth Baramin view will require extremely high levels of mutation to account for the differences within elephants. Deceptively, Asian elephants and the mammoth are closer to each other than they are to African elephants. What'll happen if the genomes are fully sequenced, and you find that the quantity of difference between African and Asian elephants is far too great for them to have come from a bottleneck 4,500 years ago? It certainly will be.Based on the genomes of two mammoths and some African elephants, the current estimates of the difference between the mammoths (+ Asian elephants) and the Africans is about half that of the differences between humans and chimps. Tens of millions. Does it? Why? But forget the hyrax. What I'm saying is that you'll require lots of elephant and mammoth pairs on the Ark (plus all the food they need for a year) in order to account for their current diversity. Remember your claim that it's impossible to get 120 million differences on the genome between humans and chimps in 5 to 7 million years? Well, you certainly won't get the differences between African and Asian/mammoth elephants (~60 million) from a tiny bottleneck 4,500 years ago, will you? These are different species with generation times like ours.For example, give the elephants 100 mutations per generation going to fixation along each lineage going back 180 generations back to your 4,500 yr old Ark. The fixed difference between any two groups separated by 360 generations should be about 36,000, not 60,000,000! The two mammoth I mentioned were from different groups, and they differ from each other by millions of point mutations as well. Then, in extant elephants, there are different breeds and sub-species within Africans and Asians, with some experts arguing for more that one species in Africa.Are you beginning to understand how your young earth model is easily falsified by genetics alone, without even talking about archaeology, paleontology, geology and cosmology? How do you decide what's "too different" to be related? Surely the limit should be set by the quantity of genetic differences possible in your time scale. That's so little that you'll not only have to separate the common chimps from the bonobos and us from Neanderthal, you'll have to separate Africans from Australian aborigines and have them separately created in different Edens. Does it? How? To whom? Experts in the relevant fields? You're forgetting your original point. The claim that duplication is always disadvantageous. If a duplication of AMY 1 occurs in one of your grandchildren, how can it be anything other than neutral or advantageous (depending on the kid's future diet)? I brought up the AMY1 gene along with the lab examples in bacteria and wild examples in the malarial parasite in order to demonstrate that your claim was clearly false. Protein coding genes only comprise ~1% of the genome. So, you're out by two orders of magnitude. At your mutation rate and with your calculations, one in 70,000 of the population would mutate on a particular coding gene. Then, if you understand population genetics and assume all the mutations to be close to neutral, only a tiny minority of the modern population would have variants in point mutations from the original 4 alleles of Adam and Eve, although there would be lots of these variants (any neutral mutation that occurred would remain in one in 70,000 of the total population with average drift luck). So, we have a prediction from your model. What we should see in the present population is the overwhelming majority with the 4 original alleles. Take a random sample of 100 people from around the world, and there won't be much variation, if any at all, from the original 4.Would you like that prediction to be tested?In addition, you have another prediction about the Y chromosome of Noah, which all men should have, without having much more than 60 point mutations difference from the original, and therefore not much more than 120 differences between any two individuals (from pedigree studies of Y-chromosome mutation rates like the one I showed you).Would you like that prediction to be tested? You're welcome. And thanks for the image of the Ark with a sizeable herd of genetically variable elephants on it, a big enough job for 8 zookeepers on its own!It's actually the research papers that are challenging to your beliefs, not my posts.Edited by bluegenes, : No reason given.Edited by bluegenes, : missing word

I know my posts require you to read and understand quite a few research papers, so I'm not surprised that it takes some time to reply to this: Message 751Part of what we're discussing (the increase in numbers of coding genes by successive mutations over time) is certainly relevant to a thread on the evolutionary origin of novelty. However, my falsification of your young earth model by genetics alone isn't really on topic, so I'll start a new one on that alone. It'll be called something like "Can the standard YEC model be falsified by genetics alone?". I'll show that it can, as a special present for you and any other YECs around.

Yes. But there's not much point in pursuing your young 6,500 year old biosphere model when it can be falsified by current observations in genetics, is there?