Creation vs. Evolution: DNA Under Cross-Examination | Y Chromosomes & mtDNA

[00:00:00]My question to kick it off for those I'm assuming Estabbon believes in apeto man evolution or common ancestry between humans and chimpanzees. And so my general question would be this and then Esabomb feel free to unmute introduce yourself and then kick off the discussion.

[00:00:21]Here in this image this is from the conventional literature.

[00:00:25]We've got [clears throat] humans and chimpanzees. This is their Y chromosomes and I want to make it bigger so we can the audience can see it better.

[00:00:36]So it's all colorcoded uk chromatin heterocchromatin. This is densely packed DNA largely comprises repetitive sequences like satellite DNA. It's essentially absent in your pan lineage. This is chimpanzees and bonobos. They're said to go back to a common ancestor roughly two million years. Human and chimpanzee chromosomes are half the size.

[00:01:03]Gene content totally different.

[00:01:05]Palindrome amplon amplonic sequences are uh different. So when you consider overall size differences, architecture and gene content, your human Y, you can see this here in this visual from a paper in 2024.

[00:01:23]your human Y and chimpanzee Y are less than 30% the same. So 26.2% to be exact. I can pull that up again if we need to. So the question I think is pretty obvious. If humans and chimps are related through common ancestry and go back to a common ancestor roughly six to nine million years, how do you account empirically for these massive dissimilarities where it's less than 30% the same in the Y chromosome between humans and chimps?

[00:01:55]Estabbon and welcome to the program.

[00:01:58]Just make sure to unmute before you speak.

[00:02:01]>> Hi, good to have you Estabbon.

[00:02:05]>> How are you?

[00:02:06]>> Hi. Hi, my name is Stean or Stean if you want to call me. If you want to call me Steve, I'm I go by Bio Steve on YouTube.

[00:02:14]>> Okay, >> so >> I see Yep, I see you in the chat.

[00:02:18]>> Yep. What >> I appreciate you having the guts to join. We We appreciate anybody, right, Sam? Anybody who's willing to >> jump in into the debate dojo and engage.

[00:02:27]I I appreciate that. I respect that.

[00:02:29]>> Thanks. Uh before I go further, I want to um I want to clarify what I do, who I am, um what I want to talk about, where I come from, a bit of that.

[00:02:44]Um so, uh my name is Stean. Uh I come from well, Mexico.

[00:02:50]I am a biology student. I am an undergrad doing my thesis. And I want to talk about generally the similarities between chimps and humans and why you think they're significant and why of course you you don't think they are significant, but I want to talk about why they don't fit the common design model as you propose it.

[00:03:19]>> Okay. Well, I I think I just put out if we could do more of a free flowing discussion, that'd be good.

[00:03:25]I'll say this, >> it's the differences that make all the difference. And then Sam, feel free to jump in anytime as we're having a free flowing discussion here. It's the differences that make all the difference. Okay? So, yes, we both agree there are similarities. It is interesting that even in similar sequences though, and we can discuss this between humans and chimps, there's differences in the way those genes are regulated and expressed, especially in the brain. So, even in the similarities, there's differences. But I say it's the differences that make all the difference because it's in this world that's going to help us answer this question of ancestry. Do we have separate ancestry where humans and chimps are not related or do we have common descent or universal common ancestry that says at least in this case humans and chimpanzees are related through common ancestry. Okay. So if it's the differences that make all the difference, I feel like that's where we need to focus. And in the Y chromosome, when you consider everything, gene content, architecture, size differences, I can put it up on screen again. They are less than 30% the same. So you just said, Estabbon, that yes, and I appreciate you laying out your position. You believe humans and chimps are related, >> go back to a common ancestor. How can that be the case if their Y chromosomes here are so massively different?

[00:04:47]>> Well, depends how much change are we allowing here. Because if you want to take a look at all of the great ape Y chromosomes u they differ significantly all of them even within species. For example, the human white chromosomes are highly variable especially in all of those palindroic regions. the applonic sequences, the copy number of genes is different. The structure, the relative orientation of these elements, >> well, they're not that different. I just want to say this, Esban, because notice here, human.

[00:05:22]>> No, >> the human on the Y, they're nearly >> that that's that's not a different human. That's the same. All of these are aligned to the same Y chromosome.

[00:05:32]They're not different individuals.

[00:05:34]>> I understand that. But I'm saying if you take worldwide Y chromosomes, okay, and you were to look at the human male Y chromosomes, then you would have 99% the same. But are are you saying that if if you look at the the variable sections like amplons, heterocchromatin, palendromes, you might get some instances of what 85% 84% >> much less than that. Depends on how you compare those genome. Well, the sequence of those chromosomes. The difference in size of course is massive. Some Y chromosomes in humans are 45 million base pairs long and others can be up to 85 million base pairs long. Not just that, the number of copies of specific genes vary quite a lot between humans and also the sequence in alignable regions of both of two diverging Y chromosomes can be as low as 80 something%.

[00:06:32]>> But those reasons would be due to intraspecies. of humans where generally I mean I could show you papers and excerpts that I have in my slideshow presentations where they say that human Y chromosomes have very low variation 99% the same okay so you might be able to find some outliers >> where there's been some some significant gene deletions in amplons or structure or whatever and so in those rare >> anomalies or outliers because of those massive gene deletions but if we're looking at humans and chimpanzees. I mean, you're looking at both gene gene loss, gene gain, the loss of entirety, uh the entirety of certain uh gene uh genetic content like the heterero chromatin. We don't find that level of difference between within humans, do we?

[00:07:26]>> We do find we do find a really high level of difference, higher than any chromosome in fact. And that applies to humans of different ethnicities. Of course we you will find that between two humans of course of course or within two humans that live within the same region two humans of the same same ethnicity you'll have well a higher degree of Y chromosome similarities but but as you go and find people from different cultures you will find that the more distantly related they are to you the more different the Y chromosomes will be and this applies in all metrics >> okay is there any two humans where you could point to what we're seeing because even between chimpanzees and bonobos this could be accounted for largely due to gene loss. I mean they both lack the type of heterocchromatin that we see in humans right here. So are you able to point me to any two humans in between any two cultures or countries where one lost the entirety of its heterocchro heterocchromatic arm and the other one retained it?

[00:08:36]Well, um, two different humans.

[00:08:42]I'm looking at the study. There's a study that was conducted by nature well by in nature was published in nature conducted by several scientists publish published in August 2023 where they compare the sequences of multiple Y chromosomes between humans and they found that there is a considerable degree in for example between two >> the paper can can you link it to me.

[00:09:13]Estabbon, I closed the screen share so I could check it out.

[00:09:16]>> Of course. Oh, I can >> the live chat or is it in the private chat?

[00:09:22]>> I am doing that through my computer and I'm talking through my phone. So, I will tell you the the title of the paper.

[00:09:30]Assembly of 43 human Y chromosomes reveals extensive complexity and variation >> that was published in 2023.

[00:09:50]>> Now are they going to conclude that so let's see extensive structural complexity structural variation size differences. Okay. So, are they concluding that this is largely due to massive gene loss in certain >> not just content?

[00:10:06]>> I don't [clears throat] think it's gene loss. It it's a lot of that is duplications. It's inversions.

[00:10:14]>> Um, it's se it's transposition of elements. There's a lot of changes that occur within these Y chromosomes that don't typically occur between two normal chromosomes. Like if you compare chromosome 22 between two humans, you will never find this degree of v variation. Same thing as between human and chimp for example X chromosomes. They are fairly identical.

[00:10:42]They're incredibly similar in both gene content, structure, um, sequence identity.

[00:10:51]And so I find it fascinating that the chromosome, the Y chromosome, which is the most variable even among individuals, is also the most variable within species.

[00:11:02]So is that a coincidence? That seems like it or it suggests that Y chromosome just changes at a rate greater than any chromosome.

[00:11:18]>> Okay, I'm looking at the paper right here.

[00:11:21]So 43 human Y chromosomes, >> there's high structural variation.

[00:11:28]>> They're structurally dynamic.

[00:11:32]And and so how does this as I move through this and I appreciate you bringing this up. How does this resolve the substantial human to chimp why chromosome differences though reported in papers like Hughes Adal which and then the the the more sophisticated paper in 2024 the telomeir to telmir human to chimp comparison because if you want to are you extrapolating that okay we find a lot of variation in Y chromosomes within the human species so we're going to extrapolate that to now Humans and chimps have Y chromosomes when you consider everything that are less than 30% the same. Well, those changes can now happen in the 6 to9 million years. Are you extrapolating that or are you able to >> provide a quantitative model where we can actually look where these changes happened over the 6 to9 million years? I don't think there's yet a quantitative model that explains how how exactly these sequences have changed over the past 16 well I'd say 7 million years but what we know of the Y chromosomes in humans is that not only they vary a lot they change very rapidly they change in length of heterocchromatin they change in copy number of the sequences they change in structure complete loss but no complete loss of I'm still going through the papers >> there there's loss of course of regions >> complete loss of the heterocchromatic arm >> no but reduction there is depending on which chromosome you're talking about >> for example some chromosomes are 45.2 2 million bases long and some other chromosomes are 85 million bases long and a lot of that length is heterocchromatin. Most of it in fact is heterero heterocchromatin.

[00:13:28]So either one of the the human wise gained a lot of heterocchromatin or one or the other lost or there was a lot of change of gain and loss.

[00:13:39]>> Yeah. Well, I would say it's easier to break a gene. It's much easier to >> Yeah. But it's simple duplication >> deletion >> which duplicate regions >> which means you would probably argue then that since the split humans and chimps go back to a common ancestor six or nine million years ago. Would you say that the pan lineage lost >> a lot point all of it? Well if you look at the if you look at the visual and then read the telomeir to telmir paper it looks like it lost the entirety of its heterocchromatic arm. So, so would you say that that occurred since the split in the pan lineage?

[00:14:14]>> Yep, pretty much.

[00:14:15]>> Okay. And so my argument would be or my response would be what's the evidence for that? I I'd be looking for a quantitative model. You said that currently that doesn't ex because I get what you're saying. Okay. There's variation in human Y chromosomes. But if if you take a percentage, just take all human male Y chromosomes on the planet.

[00:14:34]Okay.

[00:14:36]you you can uh look at a number of papers where it says there's low variation, incredibly low variation, okay? Uh really just a few hundred differences on average separating people.

[00:14:48]But within some outliers, >> that's if you count alignable regions.

[00:14:53]But if you count >> everything, gene content, size differences.

[00:14:58]>> No, there's a lot more differences between any two humans if you count all of the differences. In fact, if you try to align two human genomes, there will be large sections that don't match.

[00:15:09]>> No, I understand that. Well, and that's why depending on what methodology you use, if you're using just alignable regions or nucleotide by nucleotide versus everything, then you could get either a 97 98% number, >> which would get an 84 85% number.

[00:15:26]>> The same applies to humans.

[00:15:28]>> Well, yeah. No, and gorillas too. Within gorillas.

[00:15:30]>> Oh, gorillas. bury a lot in their their genome structure% right but a lot of that same thing is is due to gene deletions I mean you can have >> and duplications >> okay well if you go g how are you going to be able to differentiate between what's a duplicated region and what's a deleted region >> oh if you compare different genomes of different individuals you will find that x individual has 20 copies of these element most individuals have 10 so that's typically frequency, >> right? So, so you'd put frequency. Yeah, that makes sense. If if 90% of the the population have 40 of this gene, >> but then only a small number have 20, then obviously >> that's adion.

[00:16:15]>> Yeah, that would be deletion other way around duplication.

[00:16:18]>> So, okay. So, I see what you're saying.

[00:16:22]The next step for the evolutionists then since this is a whole another level, you have humans and chimps considering everything less than 30% the same.

[00:16:33]So we would need a quantitative model.

[00:16:35]We would also because we're looking at human to human. So we could be able to model out like you're saying where the duplications took place, where the deletions took place in amplons, palendromes, heterocchromatin.

[00:16:49]This is really in observable time. We can do some uh real-time experiments, >> of course.

[00:16:54]>> But humans and chimps, well, that's a totally different time scale. So, humans and chimps go back to a common ancestor 6 to9 million years. It's going to be more difficult now to quantify and to tell us which lineage lost the palendromes, which lineage lost or gained the amplons, how was the heterocchromatin lost or gain. So now it's more it's going to be more difficult to model that out, won't it?

[00:17:20]>> Of course.

[00:17:21]>> For scientists when they do these kinds of genomic comparisons between different species, we they generally take a look at the genomes of many species within what we consider a taxonomic family. For example, gorillas, humans, orangutans, chimpanzees. And we look at all of these regions and align them to each other.

[00:17:42]And we see that for example the gorilla and the human have the same number of copies of this element. The chimp has an extra copy and vice versa. There are regions where the chimp has fewer copies. The human has the same amount or a s more similar amount to gorillas. And when you put all of the data together, you can see that the chimp has the fewest amount of copies of all of these repetitive elements in its Y chromosome.

[00:18:13]And not just the chimp, the bonobos as well. They all got they got the most reduced Y chromosome.

[00:18:20]>> Okay. So you're saying that the chimpanzeee and bonobo the pan lineage is the outlier essentially the odd man out >> that's experiencing these. Okay. So, since we're on the same page, let's address this. And Erica's in the chat apparently. So, even though we're on the same page here, like we're >> Oh, we're modeling this out now. And Erica's look at us getting slaying on getting slayed on this. No, actually, we're we're digging into the meat now finally because >> I don't like to refer to it as that. I want I want it to be a conversation, not a win.

[00:18:53]>> No, exactly.

[00:18:54]>> thing. I I don't want to win anything.

[00:18:56]>> No. Well, and it's a compliment to you, Estabbon, because typically we we don't get past first base or step one with with the evolutionist that we debate, but now we are past step one, which I appreciate with you. And step two would then be modeling it out. And that's where we're at right now. And that's what I've been looking for. and perhaps if you can engage a couple of these questions and I won't press you too hard on them because you've already helped to kick off an opportunity for us to have a a quantitative model on this to to make it science. So how would you address this? For example, now we're looking not just within human variation, humans and chimps. So which lineage lost? And I I'm not expecting you to know all this at the top of your head. So if you can site papers and things like that for me to look at afterwards that's cool too. So which lineage lost what then Estabbon?

[00:19:56]What specific amplons palendromes or gene families were supposedly lost in each lineage? As in you have the split 6 and nine million years ago can lineage one way human or hominin lineage the other way.

[00:20:12]>> How would you how would you quantify this?

[00:20:15]>> So I would look well I don't know the answer of course. um because well I haven't delved deep into these differences. This is not the topic I am currently studying but I would look at all of the shared amplons and paling and gene families that are shared between the apes and I would find those that are most commonly found and if they are not found in the chimpanzeee well that's what they lost of course.

[00:20:44]>> Okay. And if you take a look at the the structure of the Y chromosome yet is yes it is different between the chimpanzeee and the human but it is actually more similar between humans and chimps than it is between chimps and gorillas still >> right >> in fact not just that the sequence identity in the regions that are directly aligned is about 97% in those in those regions that directly align between the chimpanzeee and the and the human Y chromosomes the the identity is really high. It is higher than between between them than it is between them and gorillas. So >> well but again I I'm looking at this I'm taking a holistic approach because we can look to variation within humans. We can look at various ancestral sequences. we can map out pretty good I think uh an empirical quantitative model but now when we're looking to two species like humans and chimps that would be separated by more time well now we bring in the question it begs the question are humans and chimps related in the first place so I am going to have a viewpoint you're going to have a viewpoint and one major aspect or difference within our viewpoints is you as as a proponent of common descent that would argue that the vast majority if not all DNA differences or DNA variety is due to mutations.

[00:22:21]That's why we're talking about duplications here and we're talking about gene delete. But let me just finish this. But we as creationists, >> we would argue that the vast majority of DNA differences or DNA variety is due to design diversity or created hetererozygosity. So now I think it's important and then Esa I know you're going to say something so I'll give you uninterrupted time again.

[00:22:43]>> The second question and I do appreciate you addressing one would be where is and if we don't have it how do we formulate how do we design an ancestral Y chromosome reconstruction? From my understanding the 2010 paper explicitly states that that it cannot be determined at that point. It's been years since then.

[00:23:05]>> Yeah. Because what you're saying is okay, we're going to look at the, you know, palendromes in this lineage, amplons over here in this lineage, and we're going to now we're model building which lineage lost what, which lineage gained what. [snorts] But without that ancestral Y chromosome reconstruction, how can we determine empirically that that really is the case in order to move us away from storytelling and into the realm of true science? Estabbon go ahead.

[00:23:35]>> Okay. So, okay. What we what we are looking for is how do we determine which why would you say that? No, I want to formulate this correctly because you're claiming that this is due to design diversity. So, how do we difference design diversity between mutations?

[00:24:03]Right. It's a good question. Are you asking me that >> when we Oh, okay. Let me go on a little further and >> yeah, take your time.

[00:24:11]>> Let you answer me. So, because all of the changes we see between the Y chromosomes of different species like humans, chimps, orangutans, gorillas, they are all within the range of what we know mutations can achieve. So if we look at all of the regions, we see how closely related, how closely associated the Y chromosomes of all of these species are.

[00:24:37]And we have a plausible path. We will have several possible pathways for how the differences between these chromosomes could arise. And we know that Y chromosomes are already pretty mutable.

[00:24:54]So in that in this case I think it is the safest inference not only the safest but the most scientifically sound inference to simply conclude that the variations that exist between the Y chromosomes are due to mutations that we observe happening >> but if if you're looking at the var >> I understand what you're saying if you're looking at the v well a couple things if we've been if roughly 100 to 200,000 years ago you have Y chromosome Adam and then you have the out of Africa dispersal event where people spread to all parts of the globe. That means for thousands of years you'd have people groups separated, isolated. I understand today we live in a world where we can travel and migrate and things like that.

[00:25:41]But I would argue and you can push back on it in a second that [snorts] in light of what you're saying that the Y chromosome does mutate fast, which it does. I mean the the rate is roughly one to three per person per uh generation paternally of course and but with overall low low variation. I find it interesting that in roughly 200,000 years there isn't more differences within uh the human Y chromosome. So, so let's say within those outliers, you want to extrapolate it and say, well, then the best inference is that the 70% difference between humans and chimps is that they're related and those differences accumulated since the split rather than a lot of them being due to design diversity. But then my push back is I want to see the quantitative model then >> I may work on that one day. But okay. So if >> unless it has been worked on I mean you know I'm not I I I think probably the most upto-date picture of this issue that we have is the 2024 Makova paper.

[00:26:53]Is that right? Do you think?

[00:26:54]>> Um I haven't read it so I I don't know.

[00:26:59]>> I I'll ask this. How would we go about if if you like you said you you'll work on it one day and clearly you know this stuff this is good how would you as an evolutionist deriving or formulating a quantitative model laying out all these different changes and I've been speaking a lot so feel free to take as much time as you need on this one how would you derive an ancestral Y chromosome reconstruction because as you can see in my slide I say if loss is invoked which you're doing not only loss I understand duplications then you must show the ancestral state without an ancestral reference. Loss is just speculation. You're arguing, well, it's more than just speculation because of the variation in Y chromosomes anyways that we see within humans. But I want you to convince me that that that is not just an extrapolation fallacy.

[00:27:49]Estabbon, >> I don't think extrapolations are bad in science. But okay, we will the first thing that I would do to reconstruct the well the ancestral Y chromosome is to look not just at the human and chimp. I would look at the the human chimp, bonovo, gorilla, orangutan and also maybe given Y chromosome and see the elements that they share in common and the elements that they have lost. that are duplicated, the elements that are are deleted, and would probably find the elements that are most likely ancestral, the ones that have diverse that are most well conserved and would probably make a mesh of them to predict more or less what the ancestral state of that chromosome would be. So what is more present in other apes? Well, and what is more variable?

[00:28:54]So what is more present in among apes is a medium size for the Y chromosome. So I would say it's a mediumsized chromosome.

[00:29:02]Well, a smaller size, but but given that not as small as the chimps, but not maybe not as big as as the gorillas on average. So I would say that a relatively small chromosome I would look at all of the genes that all of the Y chromosomes of apes and would say well that those are probably the genes that were present in that ancestor.

[00:29:30]>> Okay.

[00:29:31]>> So yeah that that's about it. That that's not much which I can >> and now you got to get to work.

[00:29:39][laughter] >> Yes, of course. Because my assertion would be I get it. We we're going to sit here and discuss all day. When [snorts] you consider everything, it's less than 30% the same.

[00:29:55]>> There's a lot of differences. Okay.

[00:29:57]You're you're pointing to I understand you're looking to point uh differences and outliers within >> human Y chromosomes on this planet today.

[00:30:06]>> Okay. So with a 70% difference and I'm talking overall architecture, gene content, size differences, now we now we need to model it out quantitatively.

[00:30:16]Which lineage lost what? Which lineage gained what? When, how, where, and why was the entirety of the heterocchromatic arm lost? How, well, here's my next question then, and I'm sure you got a simple answer. How was fertility made?

[00:30:32]all these massive changes are occurring within uh the pan lineage since the >> and how is fertility maintained?

[00:30:39]>> How is fertility maintained with such a a high mutational load?

[00:30:43]>> So that's a pretty interesting question and it actually has a pretty interesting answer and that is that is simple selection because when you have a multitude of Y chromosomes only the functional ones are passed on. It's simple. If you have a lot of laws of these elements that are redundant, but you have a conservation of the elements that are strictly needed, then if those ele if the loss of these elements of these repetitive elements is not is is not detrimental to the survival, then they're probably not going to be preserved. If if sperm with smaller Y chromosomes are more easily produced, then and those smaller Y chromosomes still have their main their core genes intact, which if we look at the chimpanzeee and the human genomes, the human Y chromosomes, they have most of the same, in fact, pretty much the same core genes. And all of those score genes that are the most vital for fertility, for reproduction, for all of those things are preserved.

[00:32:02]They are and they are highly identical among chimps and humans. In fact, I have compared the SRY utilizing blast between humans and chimps and it's about in the regions that we can directly align, which is most of it, they are like 98% identical. So the genes that are most essential for the function of the Y chromosome they [snorts] there's a strong selection against losing them because if one individual loses them if one Y chromosome loses them then you have no no kid you know what I meanction right >> there's that's a lot of you have a lot of loss of elements that are not essential not vital they may help but If if they are not vital and they are how do you put it? They are they are not essential. Okay, they are not essential.

[00:32:59]So when you have reproduction you they m they aren't m maintained over time and you can find this between human Y chromosomes. most humans. In fact, if you take a look at different human populations, the more distantly related you are, the more the more variation you find in the non-essential genes, the more in the copy numbers of the non-essential genes, but the more essential genes are highly conserved.

[00:33:30]And this happens >> well in light of chimps as well.

[00:33:34]>> Well, and I get your answer and and I appreciate that. It's a a good story of of how fertility could be maintained. I would still hold true to the argument that says, okay, in light of how fast we understand the why chromosomes mutate in humans, one to three per person per generation, uh massive deletions that could uh take place, some duplications within 4,500 years since the flood. It makes sense of the differences in variation that we see. But within 200,000 years in the out of Africa scenario, one would wonder why we don't find more divergence or more differences.

[00:34:18]>> Are you saying that the amount of variation that we find is consistent with 200,000 years?

[00:34:24]>> Yes. In fact, the estimated divergence time between the Y chromosomes of the individuals in the same study that I am citing, the 43 Y chromosomes, the divergence between the two most variable chromosomes is 183,000 years.

[00:34:44]>> Okay. But how come when we map it out on a I'm going to get to a slide here and get your thoughts on it as we start to wind down. This has been fun. Um, I I would say this is a general rebuttal to to what you've been saying so far, and I like that we're kind of brainstorming here. And my arguments are getting you to think on how to provide a a quantitative model. And so my challenge has been to evolutionists, where is the ratebased population genetic model?

[00:35:15]You're saying uh something you'd like to work on. That'd be great. Show the duplication, deletion, recombination of mutation rates required to produce new human specific palendromes, restructured amplons, loss of the entire heterocchromatic regions in pan, a large size golf.

[00:35:35]>> That's 30 megabases.

[00:35:39]30 million base pairs of difference >> within and and I you know you gave the story about breaking male fertility and again the brainstorming is good and explaining to me how that could be done is one thing but actually doing it and providing the the model is another thing.

[00:36:01]>> Find your phoggenetic tree feel free to respond. Go ahead. So, two humans that are distantly related can bury in size of their Y chromosomes about 40 million bases.

[00:36:15]So, that's a lot of hetrochromatin that is lost, >> but not the entirety of it.

[00:36:22]>> Well, no, but that it's not the case either with with the human and chimp.

[00:36:28]They don't lo the the gems didn't lose their whole heterocchromatic structure. They just lost one arm.

[00:36:36]>> Well, look at this figure. I mean, here's a heterocchromatin within humans.

[00:36:40]>> Yes. But that is also variable between humans.

[00:36:44]>> Is this a general picture of the human Y?

[00:36:47]>> That's probably of some human wise of the average human Y, but there's a lot of variation >> with some outliers. But what I'm saying is the average human Y and the average Chimbe and Z Y are just totally different.

[00:37:07]>> Can you hear me?

[00:37:09]>> Yes. Yeah.

[00:37:10]>> Oh, okay. We might have lost. So that's not some outliers that that's that's the variation we see naturally between humans between human populations. In fact, the most distant depends on how distant the human population is to you. You will find more differences. For example, you will find that Asians, I think, I think it was Asians, they have shorter Y chromosomes on average than your than some than most Europeans, for example. And you will find that there the differences in are in the millions of base pairs of length. Tens of millions of base pairs of magnitude. So >> yeah and and and those changes >> uh can accumulate in in the young earth model. And which brings me to this question because I know you'll contest that. Why when we map out why chromosome differences in a phoggenetic tree Dr. Rob Carter did this. Why can we trace worldwide malewide chromosomes back to a single man based on the observed mutation rate 1 to three per generation roughly 4,500 years ago? Why not 200,000 years ago worth of mutation accumulation estab?

[00:38:28]>> Oh, I'm still wait I got lost. Can you repeat that?

[00:38:34]>> Yes. How come when we map out worldwide Y chromosome paternally inherited as we all know but for the audience sake passed on on the father's side why when we take worldwide malewide chromosomeal variation and map it out on a phoggenetic tree like Dr. Rob Carter did here.

[00:38:56]Why does it go back to a single man based on one to three per generation just 4,500 years ago and not 200,000 years ago like you're saying?

[00:39:06]>> Well, that's where where you getting that information because as far as the conventional scientific model is concerned, the last Y chromosome ancestor of all humans lived about 200,000 years ago.

[00:39:19]>> Yeah. But aren't they calibrating the data? They're not using observed rates to get that, are they?

[00:39:25]>> They are. Oh, we we're getting into the Y mitochondrial chromosome territory, which I am really fond of. But okay, so >> well, you can do the same with the Y chromosome.

[00:39:36]>> I understand what you're saying with the mitochondrial chromosome, which we have here, >> but just with the Y chromosome, you can do the same. [clears throat] >> But that's that's the thing. The variation between individuals does not reflect how these mutations accumulate over time in populations. Is that the same thing that happens in in mitochondrial mutation rates?

[00:39:57]>> Okay. Well, if you want to if you want to go to mitochondrial mutation rates, how come in these studies like Parsons, Hguson, Howell when they're looking at neutral neutral rates like in the Dloop, the control region, which you said you're fond of. So that's good.

[00:40:14]>> Oh, this is very interesting. Well, so right here, Parsons, [laughter] I almost wish Estabbon, you would have joined at first because we could discuss. I I feel like you and I need to set up just a one-on-one discussion in the future, but what we'll pack this on as as a bonus segment for the audience.

[00:40:32]>> Well, I think this has been pretty much a one-on-one, but I Yeah.

[00:40:35]>> No, no, I know. I mean, but I mean like where we could just sit down for three hours because you joined, you know, two hours.

[00:40:40]>> I would love to. In fact, uh I all almost need to go. So, let's get this over quick.

[00:40:47]>> Okay, good. Well, we'll consider this a bonus section and then uh you know what?

[00:40:51]Email me or message me on Facebook. You can find me either standing for truth or Donnie Biddinsky. And then I'll let you know when our next open hangout is and we'll have you join.

[00:41:02]>> And so, okay, Parsons right here, 10 substitutions were observed, empirical rate one out of 33. Obviously, you know all this already. You're fond of it.

[00:41:12]20fold higher than estimates of phoggenetic uh rates. We could look at Howell Helguson is is a deeprooted multi-generational one that corroborates what we find in Parsons from what I've read. Okay. So those mutations occurr which are neutral.

[00:41:28]>> So they're not subject to selection. So if they say in the paper you're going to look to background selection. I know just one side. So so uh link selection is maybe the technical term for it. So if the neutral rate approximates the fixation rate as Fatuma said, I got slides on that. So yeah, you can extrapolate the neutral mutation rate in the mitochondrial DNA and it goes back as they say here 6,500 years. Why not 200,000 years? Estabon.

[00:41:56]>> Well, that's just we I think we just answered that which the answer is pretty pretty simple. It is background selection. Of course it is because if you >> Okay. Can you take 30 seconds to explain back? I could I could explain it. Let's have you explain.

[00:42:13]>> Yeah. The D explain it >> may be neutral.

[00:42:17]The mutations that go there may be neutral but as far as mitochondrial variation goes the they are tied to the regions that are not >> that are not neutally evolving. In fact the mitochondrial genome has very few regions. that dloop is actually relatively small compared to the region that codes for proteins. So that region since the Y chromosome the Y white Y chromosome the mitochondrial genome is not recombining.

[00:42:49][snorts] So when you have these variations but okay sorry I am getting nervous because there's only a few seconds left.

[00:43:00]So let me rewind a little bit. These mutations may be not select maybe not selectable but the mutations that occur in the >> in the protein coding region do are selectable. So >> okay >> even if you have so even if you have variation that that mean that variation will not all be passed down because those regions are still tied to the selection indirectly.

[00:43:30]>> Okay, I see what you're saying. too long to say a very simple thing, but I am not working right now.

[00:43:36]>> And and that's why we're going to have a three-hour discussion on this. So link selection or background selection, you have >> the mitochondrial chromosome and it's one unit passed down as one unit. So yeah, you have the dloop, these >> famous mitochondrial genome.

[00:43:52]>> Yeah, the mitochondrial genome 16,500 letters. The dloop is a smaller region like you said, but it's important. It's why Parsons and Howell and and these researchers like that region because they're largely neutral and so they can accumulate unchecked. They're not subject to selection. But you're >> of course >> but you're saying okay that's linked though. So you have the coding regions the protein codings they're more essential. So if they're hit with a delterious mutation then there's not going to be reproduction in a lot of those cases. Selection weeds those individuals out. Problem is though, uh, linked selection or background selection, it's wiping out lineages, but mitochondrial DNA mutations have accumulated worldwide. So, it's it's nothing. It's not doing anything to prevent the accumulation of these mutations in the Dloop.

[00:44:50]>> Oh, there are various >> You're just removing lineages.

[00:44:54]>> Yes, they are worldwide. But if you look right the probability that those mutations will keep accumulating >> over the next and next and next generations will be lower. So >> you will have >> Yes, of course it will.

[00:45:11]>> It won't be significantly lower Estabbon because according to your model the out of Africa model and this is where we get technical you have an extended period of time. You know, if I had a pencil, I could the pencil for the evolutionary model, a picture of a pencil and the tip that you write with. That's known history. That's roughly 6,000 years. The the rest of the pencil, the rest of the length >> is the evolutionary model, which has human beings existing in Africa, tens of thousands of years in smaller isolated populations broken up into tribes. overall population lower as well 10,000 maybe 30,000. Okay. So you'd actually have if evolution were true you'd have faster rates of fixation for the majority of history. That's why today fixation is basically zero. But for the majority of evolutionary history, fixation is fast and therefore there's a counterbalance where even with linked selection and background selection, mutations are still accumulating in a manner where they where the observed pedigree rate approximates the fixation rate because you have so much time in your model where fixation's fast. So there's a counterbalance.

[00:46:27]>> So what makes you think fixation is fast? It's well it's not fast today because people we there's eight billion people were spread out around the globe.

[00:46:37]Okay. So it's basically zero. Like if if if uh somebody in Australia random guy well it wouldn't be a guy a girl gets a mutation in the mitochondrial DNA to pass it on because people are spread out about 8 billion people. That alil is not going to get stuck in place. Right? But here's the thing. The last 6,000 years of human history, it's just that tip of the pencil. For the majority of human history in the evolutionary model, you have humans existing in smaller populations. They're isolated. That means you have a fast mutation rate acting upon a smaller isolated population. That means fixation is faster. So fixation is fast. Boom boom boom for the majority of history. Only until recently it's slow. That's why the neutral rate even in light of link selection still approximates the long-term accumulation rate.

[00:47:32]>> Yeah. But that's even if if fixation is faster, you still have a lot of selection to work with. So lots of most of those mutations that occur to the white to the mitochondrial. What?

[00:47:46]No, because there's really only a few that we'd have to account for anyways in the I'd recommend checking out Dr. Rob Carter's paper in the conventional literature, mitochondrial diversity in in human peoples. At a later time, we can pull it up. We don't have enough time right now, but uh you can see how much diversity separates people from uh the EVE consensus sequence. Anyways, there's really only a few to account for in the coding regions, which is where the selection's occurring, and only a few in the dloop. So it doesn't take much time at all to accumulate that even with some linked background selection estab to without most mutations that occur in the white the mitochondria.

[00:48:41]>> Most mutations are nearly neutral and unselectable.

[00:48:46]Yes, that's true. That's mainly of course in protein coding in non-coding regions. In coding regions, there are many ways in which those genes can be broken. So there will be a very strong selection not just >> it would have to be a large mut. It would have to be a large mutation though. It would have to be a highly delotterious one because you can you can get all kinds of mutations that have you know slight effects but not big enough to stop reproduction.

[00:49:15]You'd have to stop reproduction for for that individual or lineage to be wiped out. So my question would be this or and I understand what you're saying but you need to give us enough background selection to take the Eve that we're seeing in these papers Parsons Howell Helgus deeper rooted one where if you take the empirical observed pedigurate you got 6,000 years okay but you need to extend that >> when you need to extend that with background selection to 200,000 years How you going to do that? How you going to do that? That's a lot of background selection.

[00:49:53]>> You say that the rate of selection today is is well the rate of fixation today is which is way lower due to a larger human population, >> right?

[00:50:07]>> But that's that would be the case if all of the human populations were all intertwined. But we have today living populations that are more or less isolated. And we could look at the substitution rates of the Y chromos of their mitochondrial genomes and we can find that they are not significantly different in that >> like who are you talking about like Trista Duna study and Canary Islands Richard III.

[00:50:34]>> Yep.

[00:50:34]>> Yeah. But here's the thing that these are demographic distortions because now you have different assumptions that this is not a good global representation of the mutation rate because what we see in Parsons and Howell and Helguson and Santos to a degree. Okay, this is a good global representation. These are pedigrees. Those like Trista Duna as far as I understand and Canary, those are not pedigrees. They're looking at when these islands were settled. Well, now you got island populations. So they're going to be more isolated. So they're going to be artificially slower because if you have populations, >> they should be faster. Well, yeah, but if you're inbreeding, then you could have uh enough degeneration there where selection could be acting upon at least those individuals on those populations because >> so for the most of human history when the model of the model of human origin suggests that populations weren't that big. At least not >> Yeah. But were they all localized on one area? Don't you have in the out of Africa model you have? Oh, there were several populations that were localized in different areas >> spread out to a great degree in in Africa. Correct.

[00:51:49]>> Yes.

[00:51:51]>> Now, so are these other studies Tristuna, Canary Islands, are they pedigrees?

[00:51:57]>> If I I don't remember correctly because I haven't read them. What I read is that we can extrapolate the we can extrapolate the substitution rate of these populations by counting the differences in their mitochondrial genomes and comparing them and estimating how much estimate how much time has passed since they established their >> I understand >> yeah substitution rate the thing is why I would argue that studies pedigree studies like Parsons how >> they are indeed pedigrees it seems >> well yes but they're directly observing mutation transmission through known maternal lineages with fewer assumptions than what we would see in studies based on Trista Duna the Canary Islands or historical lineages estimating the long-term substitution rates okay because now we have other assumptions at play founder facts drift lineage extinction.

[00:53:04]There's other assumptions at play in those studies as compared to what we're seeing in Parsons and Howell and Helguson.

[00:53:12]>> Oh, it seems >> a better global representation of the overall rate.

[00:53:16]>> I got an answer in the chat. It seems that these studies that looked at this the mutation rates in these the control region they they they did not prune somatic mutations. No is a really good pro really bad problem for for them.

[00:53:33]>> No, they did somatic mutate. Like for example, we'll start to wind down here because we could talk about this now for an hour. Like a skin cell. Okay. Yeah.

[00:53:41]If when I go outside and I'm getting sun and getting hit with rays, I could get a a a somatic cell mutation. That's not going to be passed on.

[00:53:52]>> But inherited mutations, we're going to see those at a high frequency. and Parsons they talk about heteroplasm they talk about somatic mutations if you get an inherited mutation from the germ cell line that mutation is in every cell of that person's body but if it's a somatic mutation again you could see in the parson's paper they charted this out blood cells skin cells they're going to be able to tell that these are occurring at such a low frequency that actually if they considered if they would have not filtered out or they would have not considered hetereropplasm in the in the way that they did or somatic mutations the rate would have been even faster. So yeah, it's pretty easy to figure out what's somat like making sure that we're dealing with inherited mutation. Plus it doesn't even matter because we have helen which is a a multi-generational pedigree and it actually matches with parsons. Was that >> are they comparing are they counting mutation rates or substitution rates >> pedigree?

[00:54:54]Yes, but they are >> substitution. Yeah, I mean substitution mutations.

[00:55:00]>> I don't think so because substitution rates are population level. So not all mutations will pass on and that's of course due to selection. So >> but several generations >> I'll I'll say this and then and then we'll wrap up because I got to get some food in me and we've been doing this for a few hours and this has been fun. Okay.

[00:55:22]Paper that studies like Parson's Howell I know Parsons for sure they talk a lot about hetereropplasm they understand mitochondrial bottlenecking right the sampling that takes place in fertilization with the woman passing on mitochondrial DNA to her daughters her kids somatic mutations all of this is considered but again an inherited mutation is going to be at a higher frequency than a somatic mutation. So it's pretty easy to figure out, yeah, this here, this is somatic.

[00:55:58]This is not inherited versus a germ cell mutation that will be passed on. And and Parsons does discuss this, but other studies, strong studies like Helguson, they they corroborate what we find in Parsons. But I I would encourage you Well, I talked a lot. Go ahead, Estabbon. feel free to respond.

[00:56:21]>> Oh, as far as I'm concerned, they did not distinguish the mutation rates of somat of somatic cells between the substitution rates in the germ lines.

[00:56:34]So, well, I'll do more research on those papers. Can you provide them for me?

[00:56:39]>> Yes. Yeah, I can. I've got them all. But yeah, they they Parsons considered these issues. They're well aware Parsons at all well aware of hetereropplasm maternal transmission dynamics in the Parson's paper if you go through it I'll send it to you hetereropplasm is one of the central topics discussed in that paper and so they've done a good job at showing why the the rate that we see in the dloop is more or less accurate they're not adding in somatic mutations I don't why people use that argument. I mean, again, they can look at the frequencies because your inherited mutations, you're inheriting them in every cell of the body. They're going to be at a higher frequency. A somatic mutation that I'm going to get in my lifetime in a skin cell. It's really only going to be localized there. It's not going to be at a high frequency. They can figure that stuff out. So even with length selection, even with background selection, the challenge for you is how do you take that 6,500year date, how do you take that to 200,000 years in light of the fact that the majority of your history people are existing in smaller isolated populations.

[00:57:59]>> Yes, smaller isolated populations are >> all spread across the globe. So you will find you over many generations.

[00:58:12]Okay, we find actual isolated populations today and we can extrapolate their how much time has passed by observing their actual mutation rates, their actual substitution rates more like it.

[00:58:28]>> I mean, >> yeah, but again your neutral rate that they're observing in the dloop, the control. Yeah, but that's only a few generations, like three, isn't it?

[00:58:37]>> Well, they're they're accumulating >> if you look at these studies and you can corroborate it with >> the thing that's not that's just a single line. That's not a whole population thing. If you look at a whole >> it's more than just a single line and it corroborates Parsons. Parsons you have 99% of them, if I remember correctly, mother to daughter, mother to daughter, mother to daughter. One of them I believe is grandmother, mother daughter, but even that one they calculated as grandmother, grandmother to mother.

[00:59:12]Check the differences, mother to daughter. So yeah, it is it is single, but they're looking through the FBI blood bank. They got a good variety, a good sample of people and nationalities.

[00:59:23]And then other studies, other future studies like Helguson actually corroborated with that faster rate and Parsons discusses things like heteroplasm somatic cell mutations are certainly not an issue but Estbon I'm getting pretty tired and hungry here. We've been at this I'm going to give you tired and hungry. So >> yeah.

[00:59:46]>> Oh so >> that's why you take the last word because you've been so cordial and >> last word. Thank you. Um so okay we can look at actual isolated populations today and see how much their substitution rates vary comparing compared to larger populations though I don't think that's an issue for the whole because selection is well while drift is yes greater in smaller populations we can see that selection is still at play especially because the the genome of the well the mitochondrial genome is so packed with protein coding genes so that even in smaller populations we'll still see a lot of a lot of selection for those regions so I don't think that's really a problem for the model at all >> well would you agree and you're still going to get the last word don't worry would you agree that the smaller populations that would have the the demograph graphics and the way people were spread out and existed in the out of Africa model, you would have had genetic drift acting more stronger genetic drift >> in smaller populations.

[01:01:09]>> Well, in your out of Africa model, if you have a smaller effective population size in your out of Africa model, are you going to have stronger?

[01:01:16]>> Not so much. mainly because the the mitochondrial genome is not the same as the automal genome. It is far more packed with protein coding genes. So selection is a lot stronger with it than drift. So yes.

[01:01:32]>> So would you agree agree that smaller effective populations like uh out of Africa by drift?

[01:01:42]>> Yeah. that they would experience stronger drift making neutral fixation more likely and generally faster essentially.

[01:01:48]>> I don't think so. I don't think so because if because the mitochondrial genome is not like the whole like the arsonal genome so it's not drift is not as strong with it even in smaller populations.

[01:02:03]Well, no. I think it's pretty well established that if early human populations and most of the models that I've seen, they had relatively small effective population sizes, that means genetic drift would have been stronger than in today's global population where people parts of the >> not strong enough to change the substitution rate significantly like it does for example.

[01:02:28]>> Well, you need to read Fatuma. I I could show you a bunch of slides right now where where fatuma is very clear and I know people like Dan say well mitochondrial chromosomes hloid we can consider uh somatic mutations we can consider link selection background selection all of these different things because of the way your model is for the majority of human history. Okay, these neutral variants are going to become fixed a lot faster in the past. Making the neutral rate in the dloop approximate the fixation rate. So the challenge is still out there. You got to quantify. Show me the model that has the selection at play. Taking a 6,500year mitochondrial Eve to 200,000 years. I think it's pretty I think it's interesting when you look at the genomes of bacteria and compare it to the mitochondrial genome and you see how much drift and selection play a role and you can find that selection is much stronger for bacteria than it is for well larger genomes like the ukareotic genome. So the same thing applies to the mitochondrial genome which is even smaller than the bacteriums.

[01:03:43]So I even with the added genetic drift you will still have a lot of effects from selection in smaller populations to the and especially because mitochondrial genomes that are passed on in the germ line they are they pass two events of selection. One is when gamut is gamts are produced. So even if you have a smaller population, you still have millions and millions of gamts per individual. So >> I understand, but I don't think any of that's going to help you establish.

[01:04:25]We've been able to touch on a lot. This is now in three days. We've done two open mics, six hours. We've given uh all the opportunity in the world for critics to join. That includes good old Dr. Dan Stern Cardinell. Why he didn't join, I'm not sure, but we were sitting here waiting for him. Estabbon, you were brave enough to to join and have a really good discussion. I think we'll get some good clips from this and also hopefully some good future conversation.

[01:04:54]So, Esban, thank you so much uh for joining us. Message me on Facebook, please. We'll set up some discussions.