Okay, so there are like 20,000 polar bears left.
Meh, who cares, right? I mean, there are still some. 1,600 plus the ones in zoos. ‘Endangered’ animals are fine! Yeah… No. Minor problem with decreasing population numbers: Its more than just the numbers. Its genetic diversity within those numbers. If those 1,600 pandas are all we have left, and those 1,600 pandas are genetically similar, they are in big trouble.
Easy example? Tasmanian Devils. While there are still 20,000-50,000 Tasmanian Devils left, they are being slaughtered by an infectious tumor. An infectious tumor that is taking advantage of the fact there is very little genetic diversity in the remaining Devil population.
Ive talked about MHC molecules a couple times on this blag, but let me just post up a quick reminder– There are two kinds of MHCs. MHC I is on the surface of allll of your cells. It contains little bits of the proteins your cells are making, just as an ‘everything is normal’ flag. If the cell becomes infected with a virus, it will start throwing up viral ‘flags’ so cytotoxic T cells know to kill it. MHC II molecules are only on the surface of certain immune cells– ones that eat bacteria/pathogens. They put little bits of nommed up pathogen in MHC II to get other immune cells all riled up so they can clear the infection.
MHC I molecules are really, really important. Lots of viruses (including HIV-1) will down-regulate MHC I in the cells the infect in the hopes of ‘hiding’, but there are immune cells (natural killer cells) that recognize the lack of MHC I, and will kill a cell thats not sending up the ‘everything is fine’ flags.
MHC I are also important when it comes to transplants– there are >800 different MHC I alleles in humans. If the MHC I molecules of the donor and the recipient are different, the transplant will be rejected. Thats why its so hard to find the perfect donor for all the people in need of transplants, and why a close relative is usually your best bet.
And, MHC I are important when it comes to cancer. Cancer cells do not present ‘normal’ proteins in their MHC Is. CTLs recognize when cancerous cells are presenting mutated proteins, waaaaay too much of a ‘normal’ protein, or proteins that are only supposed to be expressed in embryos (embryonic cells are supposed to multiply really fast, normal cells arent).
So to get back to the Tasmanian Devils, they are currently dealing with an epidemic of a tumor. No, not a virus that causes a tumor, an actual tumor cell is passed from Devil to Devil via bites and fights (thus its usually found on the Devils faces, and is called ‘Devil Face Tumor Disease‘). The tumor gets so large that the little guys eventually starve to death… Im not linking to pictures. Too sad…
But what is really odd about this tumor is that the Devils immune systems ignore it. Now, from what Ive just typed about MHC I, we know of a few ways the Devils immune systems should be knocking this tumor down.
1– Tumors try to down-regulate MHC I. If this Devil tumor does the same thing, then it should be killed by natural killer cells.
2– The tumor is essentially a ‘transplant’. It is not self. The tumor should present non-self in MHC I and be killed by CTLs, just like if we gave someone who needed a heart transplant a baboon heart.
3– The tumor is a tumor. Its presenting all kinds of crazy proteins that the Devils, with their healthy, normal immune systems, should be clearing just fine!
But they arent. Infected Devils die in about a year.
Why??
No genetic diversity. Remember how I said humans have over 800 different MHC I alleles? Tasmanian Devils… their MHC I? Um, its all the same.
Transmission of a fatal clonal tumor by biting occurs due to depleted MHC diversity in a threatened carnivorous marsupial (free online!!)
They took white blood cells from Devils from all over Australia and mixed them all up. Normally when I do that with human white blood cells, they get all pissed off. Turns into an immune cell version of ‘Beat It‘ (which makes them easier to infect with HIV-1, for my experiments). Immunologists call it a ‘mixed lymphocyte response’. Devil white blood cells? They all had a tea party. They loved each other. No mixed lymphocyte response. Functionally, the MHC I molecules from the entire Devil population are identical.
What does this mean? From the authors discussion:
DFTD is a transmissible tumor that spreads through a population due to a lack of histocompatibility barriers. The disease has progressed rapidly due to low diversity at MHC loci and the propensity of devils to bite each other around the face and mouth during mating and fights for food.
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These findings reinforce the need for conservation biologists to focus on genetic diversity at functionally import ant loci that play a role in population fitness when designing conservation strategies. For devils, ensuring maximum MHC diversity in insurance populations is paramount. In light of the devils inability to recognize the clonal facial tumors as foreign and mount an immune response, the only course of action is the isolation of unaffected animals and the ongoing removal of affected animals from the population.
They also mention the lack of genetic diversity in cheetahs, seals, and a couple species of whales. There are, relatively, ‘lots’ of Devils left (maybe about 50,000). ‘Lots’ might not be enough to save them from extinction.
And there are 1,600 pandas.
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