Philip Ball in Nature:
Animals and plants prepare their cells for sex in very different ways — but no one knows why. A team of UK researchers now thinks that it has worked out the puzzle. Humans and animals set themselves up for sex well before the act will ever take place. At the earliest stages of life, in the embryo, our germ cells begin to develop. These are the cells that will go on to form the sperm and the egg, with half the usual number of chromosomes. In females, eggs are set aside and kept in arrested development until they are needed. After puberty, males produce sperm continuously throughout life, but a specialized germ line is created early on from which sperm are made. But corals, sponges and plants make no such cellular plans. They initially develop only body (somatic) cells, each with a full complement of chromosomes. When the time comes to mate, they produce their sex cells, or gametes, as needed by forming them out of stem cells from adult tissue.
Why the difference? According to biochemist Nick Lane of University College London, more complex animals create a devoted germline to preserve the quality of their mitochondria — specialized energy-producing structures in cells that sit outside the nucleus and have their own genes. In a mathematical model published on 20 December, Lane and his coworkers lay out their argument. According to the team, the problem for humans and other complex animals is that if cells were allowed to divide repeatedly and form adult tissues before some of them were turned into gametes, then their mitochondria would rapidly accumulate genetic mutations and errors. Some of the gametes might acquire a high load of these mutated mitochondria, leading to poor-quality tissues in the offspring. Producing all the eggs needed early on avoids this problem. The idea of ‘protecting’ mitochondrial DNA in quiescent eggs has been suggested previously1. But there’s a problem with that picture: some mutation is good for our mitochondria. Mutation is the engine of evolution, enabling advantageous mitochondrial genotypes to arise. Gametes made out of repeatedly replicated adult cells could therefore have useful variation. Evolution could preserve ‘good’ mutations and eliminate ‘bad’ ones, ultimately improving mitochondrial quality. There’s a delicate balance between the benefits and drawbacks of having a germline. How do you get enough variation between gametes for selection to act, without building up mutations that will impair an organism made from those gametes?