Valerie: Questions about TMR4A

But the measurements assume only 4 designed alleles right? :sweat_smile:

That link is way too technical for me.

Anyway, give me a couple of weeks at least to learn the basics…

Just please stop saying Jeanson should have figured out the pedigree rate of the whole genome, when the whole point of focusing on the y-chromosome is that it’s the only way to win the argument! :roll_eyes:

False. It assumed 4 alleles at each position, just like Sanford/Carter, but there are millions of positions, so it assumes millions of alleles.

You owe me an apology now. You made some personal claims that I’m not trustworthy, and it just comes down to your lack of understanding. Proverbs 4:7

I never claimed that. Rather I said his argument fails on a factual level, in part, because he ignores the high quality pedigree mutation rates on Y chromosome that are reported in whole genome studies. That’s still true.


Just please stop saying Jeanson should have figured out the pedigree rate of the whole genome, when the whole point of focusing on the y-chromosome is that it’s the only way to win the argument!

Do you have a timestamp of him saying this? Again, I watch these while doing other things in another tab, so I may have missed it, but I don’t recall this being his argument. It was more that Jeanson should have taken Y chromosome data from whole geneome pedigrees, since you can get individual chromosome pedigrees from their raw data. I think, anyways. Am I wrong, @swamidass ?


Exactly. Your understanding is right @Mr_Wilford.


Please link the studies he missed that reported a separate Y chromosome rate.

Here is one. Y chromosome rates are in the supplement. The authors emailed me even more detailed info when I requested it. I’m sure they would do the same for Nathaniel.

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I should add also that this isn’t what Nathaniel says. That would be cherry picking.

He says that he focuses on Y because it doesn’t recombine and recombination is hard to deal with. That was true before 2014, but not any more. There is no other reason he has given for focusing on Y, and I can’t imagine any reason to throw away 99% of the data to focus on the 1%, and further more restrict the analysis to poor examples of pedigree studies.

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He refers to raw data beginning here and a few more paragraphs if you look at the paper.

However, to test this hypothesis, a second aspect of Y chromosome sequence quality must also be considered. Regardless of the level of coverage, raw or unfiltered sequencing reads from Y chromosome sequencing runs are not useful for pedigree-based mutation rate analyses. Compared to autosomes, the Y chromosome has an exceptional amount of sequences classes that make sequence read mapping especially challenging for reads derived from next-generation (i.e., short read) sequencing technology. Palindromic sequences, repetitive sequences, and sequences that easily map (i.e., with 99% identity) to the X chromosome lead to high levels of ambiguity in sequence read placement (Helgason et al. 2015; Poznik et al. 2013; Skaletsky et al. 2003). Thus, any study that attempts to analyze the results of Y chromosome sequencing runs must account for this mapping challenge.

That text is not from me. @Mr_Wilford is asking you to find where I made the claim you assigned to me. I never did.

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So why not write up both of these things in a paper and give him a chance to respond? I don’t trust game-playing.

I have and he has not responded.

I’m not playing games, but taking time out of my life to explain this to you.


Please link the published paper or at the very least, blog post.

Are you serious? Here is the technical discussion, and I’ve already sent it to Jeanson: TMR4A.


I reject your analysis because your code was apparently written in python 2 instead of the clearly superior python 3.

(Note for observers: that was a joke)


That is not addressing any of his y-chromosome papers. I’m the one that introduced you to the second one earlier this summer.

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He has not addressed TMR4A, and we are discussing TMR4A. This is a clear evidential test of his model using 99x more data.


Well, I’ll go study up on alleles and their position and yours because unlike many men, I don’t play dodgeball. :neutral_face: This is way too important for that.

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Or you could just encourage Jeanson to have a conversation with me. I really do want to represent him correctly. I believe I am, and he is welcome to correct me.

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I missed what you were responding to earlier. No, you are not representing him correctly.

Because each side explain the nuclear DNA data in a different way, again Y-chromosome is the only way to win the argument. Again, if he looked at the whole genome, you’d explain the data based on your position - that is what he is saying. It’s not cherry picking for no purpose.

Because YE creationists explain the vast majority of autosomal differences by heterozygosity created in Adam and Eve (Jeanson and Lisle 2016; Sanford et al. 2018), and not via mutations since Creation, a direct molecular clock comparison is not possible for most nuclear DNA differences. However, the YEC model successfully explains the rare autosomal differences by post-Creation mutation (Jeanson and Lisle 2016). Conversely, since evolution explains all autosomal differences by mutation, evolutionists see the rare autosomal differences as stemming from the recent surge in human population growth (Coventry et al. 2010; Fu et al. 2013; Keinan and Clark 2012; Nelson et al. 2012; Tennessen et al. 2012). Consequently, at present, molecular clock analyses of rare human autosomal differences test—and appear to fit—both YEC and evolution.


The one human genetic compartment that has not received as much attention by all sides in the origins debate is the Y chromosome. For YE creationists, their expectations for Y chromosome differences today are easy to derive. Because males are XY and females XX, Adam would have been created XY, and Eve, XX. Therefore, a single Y chromosome would have been present at Creation. Consequently, unless God created Adam’s gametes with Y chromosome differences (Carter, Lee, and Sanford 2018; Sanford et al. 2018), all modern Y chromosome differences would be the result of mutations since mankind’s origin. Conversely, evolutionary expectations are also easy to derive. Because evolutionists explain all genetic differences ultimately by mutation, they also explain all Y chromosome differences by mutation. Thus, in theory, the Y chromosome differences and mutation rates could represent another direct test of the YEC and evolutionary timescales.

I looked in the supplements and didn’t find anything referring to y chromosome. If you have more information, then you may as well use it to prove his rate is wrong.

I read quite a few of the initial sections, but none of it actually rebuts this paper because you’re using evolutionary assumptions and don’t address any of the arguments here at all:

You either haven’t read this, or cannot read it with an open mind because something isn’t allowing you to.

Lastly, we examined the feasibility that God designed a unique
genotype for each gametogonium of Adam and Eve. Given the
premise of a miraculously created Adam and Eve, a logical way
for God to bless later generations with abundant “good” diversity
would be to create within Adam and Eve genetically diverse
gametogonia (the cells that give rise to gametes). Normally, a
woman’s egg cells form from her gametogonia while she is still
in her mother’s womb. In other words, women are normally
born with a vast number of eggs already formed in their ovaries.
However, assuming that Eve was created, not born, her eggs could
not have formed in the normal way – so each gametogonium
would have been miraculously formed and could potentially have
been genetically unique. Therefore, there is almost no limit to
the number of variant alleles and linkage blocks that could have
existed in Eve’s ovaries. Eve might have had a vast number of
designed SNPs in each egg. Similar logic would apply to Adam’s
gametogonia (giving rise to sperm). In addition, all those designed
gametic variants would logically have been created within linkage
blocks that were designed, specific, and functional. Our Designed
Gametes Model appears to not only help reconcile a literal Adam
and Eve with observed allele frequencies, but also with observed
linkage block patterns.
If there were individually designed gametes/gametogonia in
Eden, this would potentially constitute an enormous gene poo1,
comparable to the gene pool of a large human population. To
transmit a large fraction of the original genetic diversity to later
generations would require that the first family was very large.
Indeed, it is entirely feasible that Adam and Eve would have had
a very large family size, given the extreme longevity and vigor of
the early patriarchs (Carter and Hardy 2015). In such an extremely
large family, there could have been 100 or more different sets of
chromosomes, representing a very substantial sampling of the
primordial gene pool that existed within Adam and Eve’s gametes.
This means that the variants in that first human population could
have started with almost any initial allele frequency distribution,
in accord with God’s design for mankind. In the same way, the
initial population of gametes could have also started with a great
diversity of linkage patterns, as might have been in accord with
God’s design.