Genetics: Asymmetric breaks in DNA cause sterility.

Abstract

The part that the mouse gene Prdm9 plays in generating double-strand breaks in DNA has now been linked to its putative role in speciation, thanks to experiments that use a 'humanized' version of the gene. See Article p.171 PRDM9 is a DNA-binding protein that controls the position of double-strand breaks in meiosis, and the Prdm9 gene that encodes it is the only known example of a mammalian speciation gene, being responsible for hybrid infertility between closely related mouse species. These authors show that hybrid infertility in mice can be eliminated by introducing the zinc-finger domain sequence from the human version of the gene, thereby altering the position of double-strand breaks. PRDM9 may therefore have a general but transient role in the early stages of speciation.