Proper homologue positioning required Rec8, McKay's group showed. In yeast, Rec8 is known to be essential for recombination and for the formation of the synaptonemal complex (SC), which first links the homologues. In mice lacking Rec8, however, the SC was still laid down—but between sister chromatids rather than homologues. Rec8 thus somehow prevents SC formation between sisters normally.
Chromosome pairing appeared normal in the mutant germ cells, but the pairs might not be presented correctly. “Early on in premeiotic prophase,” says McKay, “Rec8 may have a structural role in creating a competent core. With Rec8, you get two homologues presenting a nice unified core to the SC machinery. If you don't have it, maybe the homologues are never close enough together. The only thing left is the sisters.”
Sisters even underwent early recombination events, including DNA double-strand breaks. Later events were not seen, possibly because the unusual SC formation caused apoptosis before crossovers could be resolved. Germ cell death left the mice sterile, as expected. Less expected were the somatic effects, including growth defects, which could not be predicted based on the phenotype of yeast Rec8 mutants.