Y.E.C. Model: Was there rapid evolution and speciation post flood?

There seems to be a major point of disagreement amongst those proposing a Y.E.C. model of life's history. On the one hand, some propose wide spread and rapid evolution, including speciation (within "kinds") after the flood, while others deny that such things can happen. So, does the model require this speciation, especially considering that space on the Ark was limited? And how does it happen? Are beneficial mutations involved?

Let's discuss the model, which seems to be in need of a major update.

Anything relevant goes, including questions I like to ask like: how many giraffes were on the Ark and where did all the new Y-chromosomes come from?

Here's a modern YEC angle on rapid speciation within "kinds" after the flood from Answers in genesis

quote:

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Did Natural Selection Play a Role in Speciation?

How Species Arose after the Ark

by Dr. Nathaniel T. Jeanson on July 30, 2016

In our series, we’ve concluded that many new species have formed from the kinds that Noah took on board the Ark. We also observed that, when God created the kinds, He frontloaded them with genetic differences—with the potential to form all sorts of new species and varieties.

This fact alone completely transforms Charles Darwin’s “mystery of mysteries”—the origin of species.1 Darwin had no concept of our understanding of modern genetics, and the conclusions we have reached were entirely inaccessible to him. Specifically, with respect to how species change and the ultimate source of the visible varieties we observe, Darwin had no genetic insights. Conversely, since species are defined by their heritable traits, our modern genetic discoveries represent the first real, comprehensive answer to the central question Darwin pursued.

Our previous post left one significant detail unaddressed. While we carefully elucidated the origin of the vast majority of genetic varieties observable today, we didn’t quite connect the dots to how these varieties in individuals become distinct populations of new species.

From Genetic Differences to Visible Differences
In prior posts, we argued that, in individual members of the various kinds, God created the two copies of DNA different from one another. In technical terms, this is referred to as being heterozygous. For new visible traits to arise from this created heterozygosity, all that appears to be required is a shift from heterozygosity to homozygosity. The prefix homo- denotes “same,” and a movement towards homozygosity is a change from a DNA state in which the two copies differ toward a DNA state in which the two copies are more and more similar to each other.

To clarify, a shift from heterozygosity to homozygosity does not necessarily involve every chromosome. Though the image below depicts the most extreme examples (e.g., completely heterozygous and completely homozygous), a partially homozygous/partially heterozygous state can also exist. For example, if some of the chromosome pairs end up identical while other pairs remain different, this would represent a partially homozygous/partially heterozygous state. In fact, homozygosity need not even be at the whole chromosome level. Tiny chunks of a chromosome pair can be homozygous while other sections are heterozygous. Thus, a shift from heterozygosity to homozygosity can happen over a broad range of chromosome pairs and at multiple levels of chromosome organization.

Click to enlarge

Human DNA is inherited from both parents. Hence, the condensed forms of DNA (visible in the top part of this image as floppy, noodle-like structures called chromosomes) come in pairs—one of each pair is inherited from each parent. Because our parents are different, each member of a chromosome pair is different from the other, as under scenario #1 on the left part of this image. Since Adam and Eve were created directly by God without human parents, it’s possible that both members of each chromosome pair were created identical, as in scenario #2 on the right. Nonetheless, available evidence suggests that each member of a chromosome pair was created different from the other. Under this scenario, it’s very easy to explain the millions of DNA differences that exist among humans today.

Producing a more homozygous state is not hard. Gregor Mendel’s experiments with pea plants are instructive in this respect. At the visible level, Mendel observed that some traits can be hidden in one generation and appear in the next. For example, two pea plants that produce green, smooth-shaped pea pods can be crossed, and their offspring are a mix of 1) green and smooth-shaped pea pods, 2) green and rough-shaped pea pods, 3) yellow and smooth-shaped pea pods, and 4) yellow and rough-shaped pea pods. The information for yellow pea pods and rough-shaped pea pods was present in the parents, but it was masked. Green and smooth were dominant over yellow and rough.

Though Mendel was unaware, we now understand this phenomenon in more specific DNA terms. Since DNA is present in two copies (e.g., in chromosome pairs), even in pea plants, we can infer the DNA makeup of the green, smooth-shaped parental pea plants that gave rise to the same, as well as to yellow or rough-shaped pea pods. In short, for yellow or rough-shaped pea pods to appear consistently in the offspring of green and smooth-shaped pea pod parents, both parents must be heterozygous for the information for pea pod color and shape. In other words, in one pair of chromosomes, one copy of DNA in the parent must specify “yellow” and the other must specify “green.” Similarly, in another pair of chromosomes, one copy of DNA in the parent must specify “rough” and the other must specify “smooth.” When this heterozygous state exists, only green and smooth-shaped appear—they are dominant over yellow and rough-shaped.

In the process of crossing the pea plants, only one copy of the each DNA pair is passed on from parents to offspring. If one or both of the copies carries the information for green pea pods, then offspring will have green pea pods. However, if the copy from one parent contains the instructions for yellow pea pods, and if the copy from the other parent also contains the instruction for yellow pea pods, the DNA information in the offspring will be only yellow. Since no information for green is present, the information for yellow is no longer hidden or masked by the dominance of the information for green pea pods. Hence, when two heterozygous parents are crossed, visible changes in traits can appear in a single generation.

FOR A NEW SPECIES TO FORM, IN TECHNICAL TERMS, HOMOZYGOSITY MUST BE MAINTAINED.

For this process to lead to the formation of a new species, a new population must be formed. If a new population does not form, the yellow offspring might cross with green offspring, and the next generation will have the yellow trait hidden again. Under this scenario, no permanent change will have taken place. For a new species to form, in technical terms, homozygosity must be maintained.

How could a homozygous state be isolated and kept from being mixed with heterozygous individuals? How could yellow pea pod offspring be prevented from crossing with green pea pod individuals?

In Gregor Mendel’s case, he personally oversaw the breeding process. Similarly, in animals, human breeders keep desired offspring from mating with other individuals that lack the desired traits.

But in the wild, no human breeders exist. How could homozygosity be maintained?

Unlike plants, animals can move or migrate. Homozygous animal individuals can easily be isolated from heterozygous individuals by migration. Not surprisingly, many species today are geographically isolated from one another.

For example, as their names imply, the African and Asian elephants exist on different continents. As another example, the 7 wild species of horse-like creatures that exist today—including three different species of zebras—are spread out over Africa and Asia. In the cat family, tigers are Asian, lions are primarily African, jaguars and pumas are American. In short, on a globe as big as ours, geographic isolation is easy.

Notice that we haven’t discussed survival of the fittest. For homozygous individuals to be isolated away from heterozygous individuals, the death of the original heterozygous individuals is not required. Migration of homozygous groups away from heterozygous groups would do the job just fine.

Naturally and by chance, some individuals will die, and others will survive to reproduce.4 As we observed in a previous post, the vast majority of mammal kinds died permanently—they’re extinct. But repeated cycles of massive population death followed by survival of a few individuals to found a new population are not necessary for speciation. Once God created kinds with enormous genetic variety from the start, reproduction and migration were virtually all that were needed to produce a huge number of species.

Speciation from Start to Finish

WHEN GOD CREATED THE KINDS HETEROZYGOUS, HE VIRTUALLY GUARANTEED THE FORMATION OF NEW SPECIES.

Let’s put the pieces together one more time to understand how easily species formed post-Flood. When God created the kinds heterozygous, He virtually guaranteed the formation of new species. The statistics of reproduction ensure the appearance of new traits in one or a few generations, and simple population growth curves indicate that these offspring can found new populations in short order. As these populations moved away from one another geographically, new species could form.

Is this process still occurring today? Take the African Cape buffalo as an example. Its curved horns have become a symbol of African wildlife. Yet several subspecies of the Cape buffalo exist. These subspecies also happen to be geographically distributed across the African continent. In perhaps a few decades, it wouldn’t be surprising if scientists labeled these subspecies as separate species.

If this occurs, most people in the professional scientific community would probably view this as simply a bookkeeping change. Yet the process of speciation that I outlined above suggests that, in fact, what we’re observing right now is a bona fide formation of a new species.

Subspecies exist in many other species.6 Hence, speciation could be happening right now all over the planet. If we’re willing to consider the biblically consistent, scientifically justified model that I outlined above, I think we’d see a complete replacement for Darwin’s answer.

To underscore this fact, it should be clear from all that we’ve discussed that young-earth creationists are not evolutionists. We’re not a spin-off or an odd extension of Darwin’s principles. Instead, we postulate a very different source for the genetic variety we see today, and we explain speciation on a very different timescale.

UNDER THE PARAMETERS WE JUST LAID OUT, EVOLUTION AS DARWIN DESCRIBED IS NOT POSSIBLE.

Furthermore, this front-loading of genetic information at the creation event also naturally sets limits on the speciation process. Since most of the genetic variety we see today goes back to the Creation Week, formation of new kinds (i.e., higher categorizations, such as at the Family level, not species) would require a massive—miraculous—input of new genetic information. Under the parameters we just laid out, evolution as Darwin described is not possible. In contrast, formation of new species from the kinds on board is not only possible, it represents a scientifically superior explanation to any that Darwin or his scientific descendants have proposed to date.

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So, any thoughts? AiG seem to have given up the traditional species immutability in favour of massive rapid speciation within kinds.

Some YECs seem to disagree, and there are other models. I'll be adding links to YEC views as the thread goes on.

The model described above does make predictions, and would seem to create as many problems in relation to genetics as it solves (if not more).

It seems to be a reaction to modern genetic kinowledge, and perhaps to the realisation that the Ark would have been very crowded if there was no subsequent speciation.

Faith writes: In any case the allele count is Two Per Gene. Period.

One or two alleles for most, but some genes can have 100 or more, especially in immune systems. I've forgotten what the known record is in humans, but I'll look it up for you.

Adam and Eve would have had four, just 300 generations ago. That sounds like a dramatic increase in information to me!

Faith writes: As I said in my post, after giving the Bb example of a typical gene with two alleles, I suspect all those extra alleles people talk about are the result of mutations that don't change the function of the gene. Have you evidence of 100 different phenotypes from those 100 alleles in immune systems? How about a mere four? If you can't show actual phenotypic differences between those four then the best explanation is that two of them are normal built-in alleles that do specific identifiable things like produce blue eyes or brown eyes, and the others don't do anything different, making them "neutral" mutations.

Human blood types come to mind. That's actually three alleles producing four phenotypes and six genotypes. And I'm pretty sure that there will be lots differences in phenotype in the immune system, as it depends on these variations.

More to the point, what makes you think humans can have all these variants, regardless of function, when there were a maximum of four 300 generations ago? Are you proposing a super high and probably lethal mutation rate?

Faith writes: Bluegenes' example of blood types is all I know about so far of more than two alleles for a gene that actually change its function. (But some discussion is needed on this too since O and AB are sort of combinations of A and B(?)

A bit late for Easter, but here's some cute bunnies. They have four alleles on a gene that deals with colouring, and a lot of phenotypes can be produced from them.

Many of our immune system variant alleles will certainly have varying effects, because that's how they function - to combat many different foreign invaders.

There's a problem inherent with the model of building up the variation from a recent 4,500 yr old bottleneck.

And I haven't even got around to the Y Chromosome diversity yet!

Would you say that your views are fairly close to those of the Answers in Genesis guy who I quoted earlier in the thread?

Taq writes: bluegenes writes: Many of our immune system variant alleles will certainly have varying effects, because that's how they function - to combat many different foreign invaders. A good example is HLA-DRB1 which has hundreds to thousands of known alleles.

The interesting thing is, on most genes, as individuals, we shouldn't be varying from Adam and Eve's original 4, especially with the Noah bottleneck, because 300 generations of mutations shouldn't give a hit on an average sized gene per. person. So, if it's very easy to find a lot more than 4 alleles in a small sample of the population, our YEC model looks to be in trouble.

Quelle surprise

To further illustrate what I was saying about extreme polymorphism in the immune system:

The major histocompatibility complex (MHC) and its functions. NCBI

quote:

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Because of the polygeny of the MHC, every person will express at least three different antigen-presenting MHC class I molecules and three (or sometimes four) MHC class II molecules on his or her cells. In fact, the number of different MHC molecules expressed on the cells of most people is greater because of the extreme polymorphism of the MHC and the codominant expression of MHC gene products.

The term polymorphism comes from the Greek poly, meaning many, and morphe, meaning shape or structure. As used here, it means within-species variation at a gene locus, and thus in its protein product; the variant genes that can occupy the locus are termed alleles. There are more than 200 alleles of some human MHC class I and class II genes, each allele being present at a relatively high frequency in the population. So there is only a small chance that the corresponding MHC locus on both the homologous chromosomes of an individual will have the same allele; most individuals will be heterozygous at MHC loci. The particular combination of MHC alleles found on a single chromosome is known as an MHC haplotype. Expression of MHC alleles is codominant, with the protein products of both the alleles at a locus being expressed in the cell, and both gene products being able to present antigens to T cells. The extensive polymorphism at each locus thus has the potential to double the number of different MHC molecules expressed in an individual and thereby increases the diversity already available through polygeny

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It is important that the alleles have slightly different products because it helps give variety to our immune system.

This same variety can be observed in other species of mammal. They do not appear to have been through a tight bottleneck in the last few thousand years. I coloured the sentence and bolded the last part because the fact that each allele is present at a high frequency in the population should mean something to anyone attempting to build a YEC model. The model needs to be compatible with this diversity.

Faith writes: bluegenes writes: There's a problem inherent with the model of building up the variation from a recent 4,500 yr old bottleneck. Not if you assume much greater genetic diversity among those on the Ark, especially much higher heterozygosity for more genes than we see today.

I'm assuming the maximum heterozygosity for Adam and Eve, but the point is that for Noah + family, and even for us, the original 4 alleles would predominate at all loci. You cannot get the effect of easily finding lots at one locus. There wouldn't have been enough mutations to get the effect we see in the immune system.

Faith writes: More genes too. This is where I keep coming back to the idea that junk DNA is dead genes that used to be functional and contributed greatly to the greater genetic diversity, from which all the different species we see could easily have evolved since the Ark.

We can look at stone age genomes, and they're just like ours, so that probably wouldn't be a good suggestion for our model (it would be too easily falsified).

Faith writes: Not if they are all neutral or deleterious mutations.

Over 300 generations, we would have a mutation of some kind on about 1 to 2% of our coding genes. The rest would be identical to those of Adam and Eve. So how come we can easily find hundreds of alleles on some of them without searching a great number of people?

Faith writes: Can. But only as an accident, a fluke, and so rarely as to be of no use to the organism. Besides which, again, this is far more an article of faith than it is a demonstrated reality. And meanwhile mutations are known to have produced thousands of genetic diseases, and in the best scenarios they simply don't change anything.

You're making a mistake in arguing strongly against beneficial mutations and positive selection, because your Y.E.C. model requires them. On the loci where we find multiple alleles, neutral evolution (drift) will not account for what we can observe.

Consider. There can only be a maximum of 4 original alleles per locus. But on some genes we easily find many in a small population sample. The rate of occurrence of new variants on any given gene, and the 300 generation timespan, mean that, although there could be many variations on a gene scattered throughout the population, all the new ones would be rare on drift alone.

However, with strong positive selection on the new variants, we might be able to move your model closer to the actual observed results, that many of the new variants are common (because far more than 4 alleles are common on many of these loci). It's necessary that new variants on the extremely polymorphous MHC genes were beneficial on arrival and faced positive selection if there were only 4 alleles at these loci 300 generations ago.

So, in order to get the best possible Y.E.C. model, the one that best fits the evidence, beneficial mutation and strong positive selection are necessary. Seriously.

Faith writes: I'm going with two alleles per gene

But that's demonstrably false. Or do you mean originally (Adam and Eve)?

Faith writes: More than one gene for some traits

Certainly.

Faith writes: No beneficial mutations, they are all an interference Strong selection isn't needed, nor drift, just migration + isolation

Then why are so many alleles in the MHC common?

Edited by bluegenes, : redundancy removed

Faith writes: You haven't shown that those alleles actually do anything. You think they do, but it's all an assumption from what you've said.

We'd all be dead if they didn't!

But you're missing the point. They are there. The mutation rate and drift (including the effects of migration etc) will not give us the observed pattern.

Perhaps you mean to suggest that the variants don't have different functions? Did you look at the paper I linked to earlier?

Message 26

bluegenes writes: To further illustrate what I was saying about extreme polymorphism in the immune system: The major histocompatibility complex (MHC) and its functions. NCBI quote: Because of the polygeny of the MHC, every person will express at least three different antigen-presenting MHC class I molecules and three (or sometimes four) MHC class II molecules on his or her cells. In fact, the number of different MHC molecules expressed on the cells of most people is greater because of the extreme polymorphism of the MHC and the codominant expression of MHC gene products. The term polymorphism comes from the Greek poly, meaning many, and morphe, meaning shape or structure. As used here, it means within-species variation at a gene locus, and thus in its protein product; the variant genes that can occupy the locus are termed alleles. There are more than 200 alleles of some human MHC class I and class II genes, each allele being present at a relatively high frequency in the population. So there is only a small chance that the corresponding MHC locus on both the homologous chromosomes of an individual will have the same allele; most individuals will be heterozygous at MHC loci. The particular combination of MHC alleles found on a single chromosome is known as an MHC haplotype. Expression of MHC alleles is codominant, with the protein products of both the alleles at a locus being expressed in the cell, and both gene products being able to present antigens to T cells. The extensive polymorphism at each locus thus has the potential to double the number of different MHC molecules expressed in an individual and thereby increases the diversity already available through polygeny It is important that the alleles have slightly different products because it helps give variety to our immune system. This same variety can be observed in other species of mammal. They do not appear to have been through a tight bottleneck in the last few thousand years. I coloured the sentence and bolded the last part because the fact that each allele is present at a high frequency in the population should mean something to anyone attempting to build a YEC model. The model needs to be compatible with this diversity.

You have to argue for positive selection, otherwise only the original Adam and Eve alleles would be common (only 4 common alleles, or 2 if you like).

Faith writes: I did read that but since it is hard for me to read anything of any length I may have missed something. the question I have is whether there is really any difference among the alleles since "neutral" mutations don't change the function. So when function is described -- the codominant function of two alleles -- isn't it possible most or all of the alleles do the same thing?

Again, you seem to be missing the point. If the changes are neutral, then new variants wouldn't be common after 300 generations, so you should want the common ones not to be neutral in order to fit a YEC model. The view expressed in the paper, that variation is useful, is better for your model than "neutral".

Faith writes: I don't think so. Just random recombination of Adam and Eve's two genes with two alleles per gene for skin color could produce in one generation all the different skin colors. There is no lack of diversity in this system. Diversity is all a matter of the many possible combinations of the two alleles per gene.

Again, the extreme variation at certain loci is there, whether or not 2 alleles would perform the function.

Faith writes: But my main argument is for a random selection anyway, the random favoring of certain alleles over others in the simple migration of a part of a population to another location where it has reproductive isolation. You get new gene frequencies that way, that bring out new phenotypes, others decreasing and even eventually disappearing from the new population. The original two alleles per gene now seems to me to be completely sufficient for all the diversity of life we see, including the formation of every species including some exotic or strange ones.

Then how have many, many "new" alleles in the MHC become common in 300 generations? Mutation and drift certainly won't give that result. Almost all the mutants would be very rare.

The only thing that might (possibly) explain this is strong selection. Apart from that we would need humans and other mammals to have been around for far longer than 300 generations..........

So, which is it?

Edited by bluegenes, : missing s

Percy writes: It is worth mentioning again that eye color is determined by at least 6 genes, and skin color by at least 10.

And it's also worth mentioning that the human MC1R gene (one of the above) has more than 30 known alleles. Adam and Eve? Maximum 4.

Also, as most board members are of European ancestry, many will have visible phenotype features that owe their existence to mutants of this gene.