Biology, always more complicated

[nancylebov]

Genetics of passenger pigeons

The hypothesis is that they were strongly selected for living in huge flocks, which is why they all died off instead of surviving in small groups.

I’m not sure that the strong immune systems which make sense for large flocks would make it hard to survive in small groups, but there might be something else.

This caught my eye:

“When a beneficial mutation spreads through a population, it carries along with it adjacent stretches of DNA, so subsequent generations carry not only the good mutation but entire sections of identical DNA. These regions of low diversity can be broken up by recombination, the process in which paired chromosomes exchange sections of DNA during the formation of eggs and sperm (which explains why parents don’t pass on exact copies of their chromosomes to their offspring).

“Recombination tends to happen less frequently in the middle of chromosomes than at the ends, a tendency that is especially pronounced in birds. In the passenger pigeon genome, the researchers found that areas of low genetic diversity were in the middle of chromosomes, while higher diversity regions were at the ends.”

I’d assumed that genes are selected for individually, but apparently not.

Comments

it's always more complicated, as <user name="oursin"> likes to say

[redbird]

If I understand correctly (which I may not; if you have a biologist to consult you probably should) sometimes genes are selected individually, or might as well be (selection for one gene that brings along a chunk of adjacent noncoding DNA), but some things are stuck together, more or less literally. Sometimes that combination is an actively useful (in that context) gene or genes combined with something that seems to make no difference to survival or fitness (the ABO blood types come to mind here, but I don't know if they're actively linked to anything). And sometimes it may be one useful/selected for gene along with something mildly harmful, or something irrelevant at the time but useful or harmful generations later (like greater susceptibility, or resistance, to a newly emerging disease).

That seems to be one of the things that happened with the Neanderthal-derived genes in Eurasian humans. (The latest on that is that we're not as different genetically from humans entirely of African descent as people were saying a few years ago, because some of those "Neanderthal" genes are the ancestral hominin condition: Africans had them, they got lost somehow (randomness and a genetic bottleneck?) when some of our ancestors left Africa, and then reacquired from mixing between H. sapiens and Neanderthals.

[siderea]

The hypothesis is that they were strongly selected for living in huge flocks, which is why they all died off instead of surviving in small groups.

I’m not sure that the strong immune systems which make sense for large flocks would make it hard to survive in small groups, but there might be something else.

OMG.

Allow me to reframe that for you: living in high population densities may give rise, through natural selection, to high rates of genetic autoimmune disorders, and other genetic disorders of overactive immune response.

If the hypothesis in this article is correct, one might see a burst in immune disorders in very-high-population species just a few generations after a major communicable infectious disease challenge.

You know, like massive upticks in asthma, lupus, rheumatoid arthritis, etc a few generations after a global influenza pandemic.

[thnidu]

Ummm... OMG, that's painfully plausible.

[nancylebov]

Your theory is plausible, but we might know enough to check on it-- at least something is known about whether people's forebears were living in cities before antibiotics, and that could be checked against auto-immune disorders.

[siderea]

Hmm, not quite; the issue isn't "living in cities" vs autoimmune disorders in descendents, it's surving epidemics vs autoimmune disorders in descendents. [ETA: because I don't know that the population densities of most non-city areas are actually low enough to make a difference. I'm assuming we have to treat pretty much all human civilization as pretty high density, epidemiologically, at this point.]

My theory says that the pandemic of 1917 would have killed off a bunch of people who didn't have sufficiently sensitive immune systems*, leaving the part of the population with more sensitive immune systems more able to reproduce. That is, people today are statistically more likely to inherit their immune response from people who survived the pandemic (duh) which includes those whose immune responses are touchier – more given to Type 1 errors.

People with immune systems more given to Type 1 errors are more likely to develop an autoimmune disorder.

* However! IIUC, most of the deaths from the Spanish Flu pandemic of 1917, were, unusually for influenza, the product of excessive immune reaction (fever?), not the infection itself. It gave the pandemic the perverse property of hitting the healthiest the hardest, with young adults having the worst survival rates, and infants and the elderly doing better than them. So I am distinguishing between how quickly a body identifies a protein as a pathogen, and how vigorously the body responds to the identified pathogen. It sounds like the right response to the Spanish Flu was to recognize it as influenza as quickly as possible, but not mount too vigorous an immune response.

What we'd need to test this hypothesis is epidemiological data about autoimmune disorder rates in geographical areas (ideally isolated, with largely non-migratory population) that had previous deadly epidemics a couple generations back.

(Um. I hate to say this, but somebody should check on the rates of asthma, rheumatoid arthritis and lupus in Madagascar in 60 years.)

[nancylebov]

Would it follow from your theory that Native Americans should have an unusually high rate of immune disorders?

I'm not sure that there should be a difference between descendants of survivors of pandemics and descendants of survivors of less dramatic background of infectious disease in cities. Or maybe you'd include both?