Asexually-reproducing organisms, like many bacteria and protists, some plants and fungi, and a handful of animals, have the advantages that it's fast, and only requires one parent. There's a major downside, however; a genetic phenomenon called Muller's ratchet. Muller's ratchet has to do with the fact that the copying of DNA, and the passing of those copies on to offspring, is not mistake-proof. Errors -- called mutations -- do happen. Fortunately, they're infrequent, and we even have enzymatic systems that do what amounts to proofreading and error-correction to take care of most of them. A (very) few mutations actually lead to a code that works better than the original did, but the majority of the ones that slip by the safeguards cause the genetic message to malfunction.
It's called a "ratchet" because, like the handy tool, it only turns one way -- in this case, from order to chaos. Consider a sentence in English -- space and punctuation removed:
TOBEORNOTTOBETHATISTHEQUESTIONNow, let's say there's a random mutation on the letter in the fourth position, which converts it to:
TOBGORNOTTOBETHATISTHEQUESTION
Now, suppose a second mutation strikes. There is a chance that it would affect the fourth position again, and purely by accident convert the erroneous g back to an e, but that likelihood is vanishingly small. This is called a back mutation, and is more likely in DNA -- which, of course, is what this is an analogy to -- because there are only four letters (A, T, C, and G) in DNA's "alphabet," as compared to the 26 English letters. But it's still unlikely, even so. You can see that at each "generation," the mutations build up, every new one further corrupting the message, until you end up with a string of garbled letters from which not even a cryptographer could puzzle out what the original sentence had been.
Sexual reproduction is a step toward remedying Muller's ratchet. Having two copies of each gene (a condition known as diploidy) makes it more likely that at least one of them still works. Many genetic diseases -- especially the ones inherited as recessives -- are losses of function, where copying errors have caused that stretch of the DNA to malfunction. But if you inherited a good copy from your other parent, then lucky you, you're healthy (although you can still pass your "hidden" faulty copy on to your children).
This, incidentally, is why inbreeding -- both parents coming from the same genetic stock -- is a bad idea. It doesn't cause problems in brain development, which a lot of people used to think. But what it does mean is that if both parents have a recent common ancestor, the faulty genes one of them carries are very likely the same ones the other does, and the offspring has a higher chance of inheriting both damaged copies and thus showing the effects of the loss of function. It's this mechanism that explains why a lot of human recessive genetic disorders are characteristic of particular ethnic groups, such as cystic fibrosis in northern Europeans, Tay-Sachs disease in Ashkenazic Jews, and malignant hyperthermia in French Canadians. It only shows up in the children when both parents are from the same heritage -- which is why "miscegenation laws," preventing intermarriage between people of different races or ethnic backgrounds, are exactly backwards. Mixed-race children are actually less likely to suffer from recessive genetic disorders -- the mom and dad each had their own "genetic load" of faulty genes, but there was no overlap between the two sets of errors. Result: healthy kid.
Horizontal gene transfer in metazoans has been documented in only a few species and is usually associated with endosymbiosis or parasitism. By contrast, in bdelloid rotifers we found many genes that appear to have originated in bacteria, fungi, and plants, concentrated in telomeric regions along with diverse mobile genetic elements. Bdelloid proximal gene-rich regions, however, appeared to lack foreign genes, thereby resembling those of model metazoan organisms. Some of the foreign genes were defective, whereas others were intact and transcribed; some of the latter contained functional spliceosomal introns. One such gene, apparently of bacterial origin, was overexpressed in Escherichia coli and yielded an active enzyme. The capture and functional assimilation of exogenous genes may represent an important force in bdelloid evolution.
What shocks me most about this is how the hell this doesn't muck things up further. I mean, it's a little like finding some typos in a book you're reading, and trying to solve the problem by tearing pages out of other books and inserting them into your book in random places. Okay, maybe you now have fewer overall typos in the book than you did before, but what's the chance you picked up something you can actually use?
Apparently this point is still being studied.
So a peculiar little pond creature somehow makes no-boys-allowed parthenogenesis work by pilfering genes from all and sundry. Which I have to admit is ingenious, but it's also just strange. Darwin didn't know how right he was when he talked about "many forms most beautiful and most wonderful." Can you imagine how gobsmacked he'd be if he could see what we know about biology today?







