Carter: Response to TMR4A and Created Heterozygosity

[evograd (Blogging Graduate Student)]

@SFT

In a nutshell, if Africans have more recombination hotspots and the PRDM9 gene helps initiate recombinational hotspots, then logically that would mean Africans would have more recombinational events.

@SFT

Less recombination hotspots = reduced recombination.
More recombination hotspots and more functional PRDM9 genes = more recombination.

This doesn’t logically follow at all. Hotspots are regions of higher recombination rate, but the magnitude of recombination rate in each hotspot can also vary. It’s trivial to imagine a scenario where a population/species with more recombination hotspots has a lower average recombination rate per hotspot, resulting in an identical overall recombination rate compared to a population/species with a lower number of hotspots. That’s why I said in my original comment:

It’s true that Africans (notably West Africans) have more recombination hotspots in their genomes (see paper below), but I’ve yet to see any evidence that this results in a substantial increase in the overall genome recombination rate, rather than simply spreading out the same amount of recombination more evenly over the genome, as it were.

@SFT

Think about it…it should be obvious that the more broken or lost the PRDM9 gene is, the less enzymes there are to bind to different recombination hotspots. And so what we would be looking at is less overall recombination as time goes on. Therefore, it should be logical that going back in time to points where we have more and more fully functioning, or fully working PRDM9 genes, we would then have more recombination.

Nice hypothesis, do you have any data to support it? What makes the European allele of PRDM9 “more broken” than the African version? Can you point to which mutations degraded it, and show that they result in few recombination hotspots? You’re throwing out a lot of claims as though they’re facts, but very little data.

@SFT

This is why in Africa, where people clearly have more PRDM9 genes

More genes? Like more copies of the gene? Citation please. They have a greater diversity of PRDM9 alleles, and notably a higher frequency of the C allele compared to European populations (~13% vs ~1%), but not “more genes”.

@SFT

Non-Africans seem to be far more damaged when it comes to recombination than Africans.

Citation please.

@SFT

The activity of the PRDM9 gene is important enough to the point that if genetic erosion occurs at these sites, its essential function will be compromised. Over time, the function will become more and more compromised depending on how much mutation accumulation, inbreeding, etc, occurs.

Demonstrate that this has happened then.

@SFT

Mutation destroys binding sites.

Demonstrate that the binding sites have been destroyed by mutations.

@SFT

Well since PRDM9 controls activation of Mammalian recombination hotspots, it seems rather easy to test. We see more PRDM9 sites in Africans and more recombination hotspots. They also have more recombination (evolutionists interpret this as Africans being an older population). We can then look at non-Africans and see if they have a lower number of PRDM9 sites and fewer recombination hotspots as compared to Africans. It turns out they do. And it turns out they have experienced less shuffling.

This doesn’t distinguish between the two hypotheses. You’re using the fact that Africans have experienced more genomic shuffling as evidence that they have faster recombination rates, but this is also explained by the hypothesis that they’re an older population. You need to demonstrate that they have faster recombination rates, then you might be able to apply that to make inferences about timescales. That’s where you’re out of luck, because studies don’t show a substantial increase in overall recombination rate, more like a <10% increase in Africans relative to Europeans (as I pointed out before, again).

Talking big picture, African populations have ~47,000 recombination hotspots, while Europeans have ~43,000, and around 41,000 of these are shared between both populations (Manu et al). Combine this with the overall recombination rate data I mentioned earlier. Can you demonstrate that these relatively small differences account for all the observed differences between European and African linkage disequilibrium? I think not.

You’re forced to stick to this idea that recombination rates and distributions were substantially different just a few thousand years ago and that if only we knew those rates and distributions, all the data would neatly fall in line with YECism. Good luck with that.

@SFT

@evograd

Why are you so averse to discussing these issues in text,

I have a detailed book on this with plenty of sources to keep somebody busy for the next million years…this book is IN text lol

A book (using the term generously), especially one that isn’t free, isn’t a discussion. A discussion on a forum like this is a discussion.

@SFT

I also don’t do this for you guys, I do this for my audience. I do this for my brothers and sisters in Christ. It’s not a good use of my time to argue with people in blogs all day who won’t change their minds. If I see novel arguments, I bring it to my audience to show them how easily defended the biblical creation model is.

That’s the thing - by avoiding discussions like this the vast majority of the time, you fail to firmly grasp the arguments and data in question, and end up delivering a lot of faulty interpretations and incorrect data to your audience, and they can’t tell the difference. They lap it all up regardless. This topic is a perfect example. I haven’t watched your video yet, but if you made the claims you did here in that video, in your best confident and dismissive tone of voice, then I’ve no doubt that many members of your audience came away from the video believing exactly what you intended - that the YEC model is easy to defend. In constrast, when you actually engage in a discussion about the specific details, as you have here, if becomes clear that you don’t actually have the data to back up your confident assertions.

@SFT

Why do you think Dr. Jeanson or Dr. Carter don’t argue all day in blogs? It’s not good use of their time.

To a certain extent, sure. But there’s a big difference between arguing with random people in obscure forums and engaging with scientists with technical criticisms. The specific medium is largely irrelevant. A conversation where 3 detailed replies are made back and forth in the space of a day can be more useful in furthering the discourse than weeks spent writing independent blog posts to indirectly reply to criticisms.