Data from: Hybrid sterility locus on Chromosome X controls meiotic recombination rate in mouse

Meiotic recombination safeguards proper segregation of homologous
chromosomes into gametes, affects genetic variation within species, and
contributes to meiotic chromosome recognition, pairing and synapsis. The
Prdm9 gene has a dual role, it controls meiotic recombination by
determining the genomic position of crossover hotspots and, in infertile
hybrids of house mouse subspecies Mus m. musculus (Mmm) and Mus m.
domesticus (Mmd), it further functions as the major hybrid sterility gene.
In the latter role Prdm9 interacts with the hybrid sterility X 2 (Hstx2)
genomic locus on Chromosome X (Chr X) by a still unknown mechanism. Here
we investigated the meiotic recombination rate at the genome-wide level
and its possible relation to hybrid sterility. Using immunofluorescence
microscopy we quantified the foci of MLH1 DNA mismatch repair protein, the
cytological counterparts of reciprocal crossovers, in a panel of
inter-subspecific chromosome substitution strains. Two autosomes, Chr 7
and Chr 11, significantly modified the meiotic recombination rate, yet the
strongest modifier, designated meiotic recombination 1, Meir1, emerged in
the 4.7 Mb Hstx2 genomic locus on Chr X. The male-limited transgressive
effect of Meir1 on recombination rate parallels the male-limited
transgressive role of Hstx2 in hybrid male sterility. Thus, both genetic
factors, the Prdm9 gene and the Hstx2/Meir1 genomic locus, indicate a link
between meiotic recombination and hybrid sterility. A strong
female-specific modifier of meiotic recombination rate with the effect
opposite to Meir1 was localized on Chr X, distally to Meir1. Mapping Meir1
to a narrow candidate interval on Chr X is an important first step towards
positional cloning of the respective gene(s) responsible for variation in
the global recombination rate between closely related mouse subspecies.