My latest Mind and Matter column in the Wall Street Journal is on
selfish DNA:
The theory of selfish DNA was born as a throwaway remark in the
book “The Selfish Gene” by Richard Dawkins, when he pondered why
there is so much surplus DNA in the genomes of some animals and
plants.
Perhaps, he suggested, our genomes are riddled with digital
parasites, sequences of code that proliferate at our expense and
aren’t there to help “us”-that is, the organism as a whole-at
all.
This theory has since explained a lot of puzzling phenomena. It
might be the reason that there are so many insect species on the
planet. Consider Wolbachia, a bacterium that lives inside the
cells of more than two-thirds of insects. This parasite is passed
through the female line, because insect sperm are stripped of their
cell contents when they enter the egg.
That means that Wolbachia in a male insect is in an evolutionary
dead-end. A gene trapped in a reproductive dead-end that mutates so
as to find a way to get into another generation will prosper-even
if it damages the interests of the creature it is part of. Indeed,
Wolbachia’s genes are so manipulative that they can convert male
insects to females, kill males, induce virgin birth in females and
even cause the offspring of males to die unless they carry the very
same strain of Wolbachia as the father.
The genes of insects respond by mutating to suppress Wolbachia’s
gerrymandering of sexual reproduction. A sort of arms race results.
But in the process, lots of different insect species emerge because
of the incompatibility of the Wolbachia strains. The Creator’s
“inordinate fondness for beetles” (a phrase attributed to J.B.S.
Haldane) may be caused partly by this parasite.
Wolbachia isn’t the only object inside the cell with its own
genes. Mitochondria, a cell’s electrochemical “batteries,” also
have genes, left over from when they were bacteria that set up shop
inside our distant ancestors’ cells. Mitochondria pass through the
female line too, and sure enough, their genes have a habit of castrating the male functions
of more than 150 species of hermaphroditic plants. (This
“cytoplasmic male sterility” is exploited by plant breeders seeking
to generate hybrid varieties, because it prevents
self-fertilization.)
Now it emerges that mitochondrial genes also can run amok in
animals. This month a new scientific paper discussed the finding that
small nematode worms of a certain species often carry a particular
mitochondrial mutation-the absence of 786 letters of code from a
crucial gene.
Experiments by scientists at Oregon and Portland State
Universities leave no doubt that this mutation puts its carriers at
a disadvantage. But they also show that, far from dying out, in the
lab the mutation increases in abundance by 1% per generation.
How can this be? Genes bad for organisms are supposed to die
out, not spread. The answer is that the mutation probably makes the
worms breed as self-fertilizing hermaphrodites, rather than as
males, so it thrives, selfishly, even as its owner suffers.
In recent years, some scientists have argued that such selfish
genetic elements serve the greater good in the long run by making
species more “evolvable,” like insects, and that this explains
their existence. Persuasive evidence against this, and in favor of
the idea that they are harmful parasites that generate greater
evolvability only as a side effect, comes from asexual species.
In asexual animals or plants, evolutionary diversification is
much slower because of the lack of genetic remixing that happens
during sex. So selfish elements should be welcomed in such lineages
if evolvability is a net benefit. Instead-as shown by some tiny
animals, called rotifers, that have not had sex for 80 million
years-selfish DNA is generally purged from the genomes of asexual
species as a nuisance.
Truly, the more we understand what happens within and between
genes, the more innocent the human world seems.