Msh-2 is a highly conserved protein required for eukaryotic repair of mismatches in DNA. We have deleted the Neurospora msh-2 orthologue in a number of strains. Of 43 octads from an msh-2 deletion homozygote, 6 displayed non-Mendelian segregation at his-3, lys-4 or cot-1. In all cases the marker segregated 5:3, confirming the requirement for Msh-2 in Neurospora mismatch repair. Among 192 random progeny of a mutant cross all 16 genotypes were detected, including those that arose from double or triple crossovers, extremely rare events in a wild type cross. Msh-2 may thus have an unexpected role in crossover interference. Although an msh-2RIP null allele was shown to increase his-3 allelic recombination, we have found this to be true only for his-3 alleles of different wild-type origin, suggesting Msh-2 may regulate recombination between dissimilar sequences. In contrast, preliminary data suggest crossing over in intervals flanking his-3 is unaffected by deletion of msh-2, even when the sequences are known to be substantially divergent.

This work was supported by a grant from the Australian Research Council.