Phylogeny of Lactase Persistence

[Tabaccus Maximus]

Here's a post by Maju regarding the phylogeny of LP genes associated with certain populations.

Here we see that T-13910, G-13915 and G-13907, being variously responsible for Lactase Persistence, have a genetic relationship. Moreover, given the phylogeny, these relationships seem to suggest that Euroesque T-13910 is slightly -or more- basal than the other two.

It would also appear to me that LP in the Arabian peninsula derives from the NE African highlands where pastoralism was practiced, not the other way around. (Maju suggested)

I would go a step further and suggest that all three genes were introduced in the late Neolithic by cattle herders from the Near East, via North Africa, those such as the Naqadans of Upper Egypt and the people that crossed the Tassili pass in Southern Algeria, Mali and into Northern Cameroon.

Maju posted a phylogenetic tree which gives it a little more perspective.
http://forwhattheywereweare.blogspot.com/2014/03/lactase-persistence-genetics-in-africa.html

First of all, it is edifying to know that my previous hunch is confirmed, that LP has it's origins with a single Neolithic population and not the ridiculous notion that it has been
developing independantly everywhere, because it obviously has not. C-14010 is the only mutation that falls outside of this scenario (possibly), but it is less understood and may not necessarily have any sort of causal relationship with LP in the first place. The age of C-14010 may shed some light on this, if it is a gazillion years old instead of 10,000 years old then that should tell us a lot.

I've mostly resisted the super-duper selectability argument like LP is some sort of "super gene", because it is not. This is evidenced by the fact that the overwhelming majority of humans on earth have no problem having fifty kids without the LP gene. Having a gene that gives me the ability to digest tree bark might improve my survivability, but probably not, since steak and salmon are more appealing to me. Milk drinking is niche practiced by a particular group of people in ancient history.

Even those peoples long, long exposed to LP genes through genetic drift, such as the Subcontinentals or Chinese, did not develop this "super trait" in any measure or at all. That is because it is not a super gene and in the case of C-14010 may not have any meaningful expression at all. The upper branch of LP, at least, is a gene that a single, Near Eastern, cattle-based population confired on its founding descendants and roughly in proportion to its genetic descendants. (cattle; not goats, mice or cats)

I would be interested to know more about LP in Balochistan and the Indus Valley since it appears much higher there than the surrounding areas. Also given that the earliest attempts at cattle management happened around modern Turkmenistan or Khazahstan, I would think more studies would focus on this area.??

http://www.eupedia.com/forum/thread...P)-in-Europeans?highlight=lactase+persistence

 

[LeBrok]

First of all, it is edifying to know that my previous hunch is confirmed, that LP has it's origins with a single Neolithic population and not the ridiculous notion that it has been
developing independantly everywhere, because it obviously has not.

If it happened in middle East Arabs and Europeans would have same LP allele, or at least both varieties, one Middle Eastern and one African.

I've mostly resisted the super-duper selectability argument like LP is some sort of "super gene", because it is not. This is evidenced by the fact that the overwhelming majority of humans on earth have no problem having fifty kids without the LP gene. Having a gene that gives me the ability to digest tree bark might improve my survivability, but probably not, since steak and salmon are more appealing to me. Milk drinking is niche practiced by a particular group of people in ancient history.

You can't compare lactose digesting gene, which already existed and needed only one mutation to become persistent (possibly blocking methylation), to bark digesting gene. Actually to digest bark we would need to get many mutations, completely new genes, at the same time from stomach structure, to new enzymes, to appetite for bark, and who know what else. We know that once people started herding at least 3 mutations showed up for LP within 6 or so thousand years. Meaning that it was rather an easy process. In big contrast to bark digesting genes, when getting many and complicated mutations would take probably a million years or more. So long that it didn't happen yet, although as you pointed out would have being extremely beneficial for humans.

Let's keep in mind that mutations, which happen blindly, need to occur first, before natural selection can determine if they are beneficial or not. You can't eat bark and encourage/make mutation to happen, just because you want and wish it to happen. It is a completely blind process. Therefore, the more it means, that if LP allele is so widespread in some areas, the benefit of it was very substantial to the populations.

 

[Tabaccus Maximus]

If it happened in middle East Arabs and Europeans would have same LP allele, or at least both varieties, one Middle Eastern and one African.

Well first, LP does have, apparently, a single phylogenetic origin, so that happened somewhere. Founder events most likely explain why there are differences among populations.
But also, there are multi-variety LP genes where two or three are found in West Africa or East Africa, for example.

You can't compare lactose digesting gene, which already existed and needed only one mutation to become persistent (possibly blocking methylation), to bark digesting gene.

I did not mean tree bark eating to be taken literally, rather to point out that Lactose Tolerence doesn't necessarily advantage a population more than another. In fact, you could equally make the case that un-pasturized milk was responsible for as many deaths.

My point being that Lactase Persistence rates are best explained my migrations of people that already had them for a long time, not through relatively recent super-selection.

 

[LeBrok]

My point being that Lactase Persistence rates are best explained my migrations of people that already had them for a long time, not through relatively recent super-selection.

Than I have no idea how can you explain 90% LP in Denmark for example. Did they all migrated from Middle East, as you suggesting LP started there? Autosomal DNA doesn't agree with it.

Secondly, if LP in Denmark is local, you still need to explain why it is so popular their. Over few millions inhabitants with LP in Denmark alone. You don't want to say it is coincidental?

Cows, grass, long winter, lots of hay, little anything else to eat, thousands extra calories from milk per person from dry grass. If this is not important in this equation of LP then I don't know what is?

 

[Orillion]

I don't understand the need to try to explain LP with convoluted population migration theories when it's obvious that it's a huge selective advantage.
Like LeBrok said, milk is an endless concentrated energy source, available at all times provided there is a mid-sized or a large mammal around, without the need to even kill said mammal. Being able to assimilate milk provides super useful when food is scarce, and it's completely plausible to say that LP spreaded all over Europe along with early shepherds and their flocks. After all, if R1b and other haplotypes did, why couldn't LP?

Also, let's not forget that sometimes, the exact same mutation can appear sporadically (i.e. deltaF508 in cystic fibrosis), there's not always a need for a single ancestor.