Now, Richard Buggs replies,
Now to look in more detail at the points you raise about allelic diversity. This is where I think your argument is strongest, so I would like to examine it in some detail. To do this full justice, I want to start with what you say about this in your book chapter. One of your most explicit statements about this in your book chapter is as follows:
…scientists have many other methods at their disposal to measure just how large our population has been over time. One simple way is to select a few genes and measure how many alleles of that gene are present in present-day humans. Now that the Human Genome Project has been completed and we have sequenced the DNA of thousands of humans, this sort of study can be done simply using a computer. Taking into account the human mutation rate, and the mathematical probability of new mutations spreading in a population or being lost, these methods indicate an ancestral population size for humans right around that 10,000 figure. In fact, to generate the number of alleles we see in the present day from a starting point of just two individuals, one would have to postulate mutation rates far in excess of what we observe for any animal.
As I note in my blog, you give no citation to the scientific literature to back up this point, so it is hard for me to interact with you on it. I would invite you again to make such a citation so that we can discuss this point further.
In your recent blog you have now made a similar claim, and given more detail:
So, a bottleneck to two individuals would leave an enduring mark on our genomes – and one part of that mark would be a severe reduction in the number of alleles we have – down to a maximum of four alleles at any given gene. Humans, however, have a large number of alleles for many genes – famously, there are hundreds of alleles for some genes involved in immune system function. These alleles take time to generate, because the mutation rate in humans is very low. This high allele diversity is thus the first indication that we did not pass through a severe population bottleneck, but rather a relatively mild one (estimated, as we have discussed, at about 10,000 individuals by current methods).
Would I be correct in assuming that this statement in your blog is intended to illuminate the passage I quoted above from your book chapter? If so, this is helpful as you give a link in the blog to an online primer about Human leukocyte antigen (HLA) genes, suggesting that your argument relates to these genes. But the online primer has nothing in it about models of past human bottlenecks. I would invite you to make a more explicit argument on this point, as I think this is the strongest argument that is available to you against a bottleneck of two. As you mention HLA genes in your blog, it sounds to me as if your argument may rest on Ayala et al (1994) but this paper was published before the human genome project, so I assume you must have a more up to date source that you drew on for your book chapter. Please could you let me know what it is so that I can follow up your argument?
I realise that some of your non-biologist readers may think I am being rather pedantic in asking for a citation when you are making what appears to be a very straightforward case from allele numbers. But biologist readers will know that very few things in this area are straightforward, and without a citation I have to treat your claims as unsubstantiated. More.
Over to Venema.
See also: Adam, Eve, Richard Buggs, and Dennis Venema: Could Adam and Eve have existed?
Geneticist defends possible Adam and Eve in Nature: Ecology and Evolution
Geneticist: Adam and Eve could have existed