The Evolution of Imperfection by Laurence D. Hurst

Author:Laurence D. Hurst
Language: eng
Format: epub
Publisher: Princeton University Press
Published: 2025-01-14T00:00:00+00:00

Why Doesn’t Everything Have the Same Mutation Rate?

Selection for increased mutation rates, we then think, is a second-order effect. The primary effect is to reduce the rate, as most mutations are harmful. Mutation rate theory is, in some regards, odd, as at first sight the prediction is that everything should be the same and (just about) everything should have no mutations. If you think of mutations as unwanted cellular accidents, you can see why. But as we have seen, while numbers are very low, there is lots of variation. As noted above, Paramecium tetraurelia’s mutation rate per base pair is 1,000 times lower than ours. We have 150,000 times more mutations per genome than Thermus thermophilus, a bacterium that lives near thermal vents and thrives at about 65oC (145oF). This equates to nearly 2,000 times the number of mutations in protein-coding genes. What can explain this variety?

For many years now there have been a series of ideas swirling around to explain the variation in mutation rates. It may well be the case that they all have some relevance. Nonetheless, as we shall see, the nearly neutral model seems to be the most important of these.

When we talk about the mutation rate per generation, this means something different for single-cell species than it does for multicellular ones like us. For the latter the “per generation” refers to the per sexual generation. In effect, our mutation rate is equivalent to the number of mutations from fertilized egg (your parents when they were each a single cell) to fertilized egg (you, when you were just one cell). These mutations happened at some time in the cell-lineage history of the sperm and egg in your parents. In this process, there are many cell divisions. In women, if we track back from any egg cell in a woman’s ovary to the initial fertilized cell (the zygote) that became the woman, we think there were about 30 cell divisions in between. In men, especially older men, there are quite possibly many more than that between any sperm a man produces and the fertilized egg that became that man. This is because in men, sperm are made from a sperm stem cell that keeps dividing—one of the daughter cells becomes a sperm, the other stays as a stem cell, capable of doing the same process repeatedly. The older the man, the more such divisions, the more chance for errors during cell division.

In single-celled species the mutation rate is defined per cell division. In yeast, for example, its single cells divide all the time. Here we consider one of the daughter cells and compare it, in principle, to the parent cell.

One problem is that this doesn’t look like a fair comparison. How could it ever be appropriate to label both measures—per cell division and per sexual generation—as “per generation”? Notice, for example, that the multicellular species have higher per-generation mutation rates (fig. 6.2). Could this not be a trivial consequence of having many more cell divisions contributing to each “per-generation” measure?

If you thought this, then you would have a point.

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