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By Nell Boyce DEVELOPING sperm cells are screened for genetic fitness before they are allowed to mature—but the selection process breaks down with age. These findings, from a study of mice, could explain why the children of older fathers are more likely to have birth defects. Biologists have known for some time that in mice, sperm cells tend to have fewer mutations than other cells. Some reasoned that this might be because cells in the testes were more efficient at repairing DNA. But Christi Walter of the University of Texas Health Science Center in San Antonio and her colleagues suggest another explanation. The team studied mice that had been given an extra gene which, when mutated, produces a protein that turns a gel blue. If the gene is not mutated it has no effect on the mouse. The mutations in the extra gene give a guide to the number arising in the mouse’s own genes. The researchers removed the animals’ testes and separated out sperm cells at different stages of development so that they could see how many cells with mutations were present at each stage. Cells that were at the earliest stage of development were the most likely to carry mutations, the researchers found. Cells that were committed to meiosis—cell division that halves the number of chromosomes in mature sperm—were less than half as likely to carry mutations (Proceedings of the National Academy of Sciences, vol 95, p 10 015). “There is a decrease in mutation frequency during the process of spermatogenesis,” says Walter. In old mice, the frequency of mutations is up to 10 times that in young ones—suggesting the protection mechanism breaks down with age. “This is completely new,” says Jan Vijg, a geneticist at Harvard University. The work implies the existence of a screening mechanism,
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