We are exploring the role chromatin structure plays in the segregation of chromosomes during the first meiotic division. To this end, we performed an RNAi feeding screen to identify chromatin-associated factors that influence the rate of recombination. The gene associated with the strongest effect on recombination was
gak-1 (germline AT-hook protein), which was previously reported to function in X chromosome segregation. We have established that deletions of
gak-1 result in increased recombination on the autosomes, but decreased recombination on the X chromosome. Furthermore,
gak-1 mutants exhibit a HIM phenotype and reduced brood size, with
gak-1 individuals displaying variability in both phenotypes. We raised antisera against the GAK-1 protein and used it to stain dissected gonads from N2 worms. The staining pattern of GAK-1 is striking: it coats the autosomes, but is excluded from the X chromosome.
gak-1 mutants show premature separation of the X chromosome, which we believe is the result of reduced meiotic crossing over on the X chromosome. This idea is supported by our observation that the HIM phenotype of
gak-1 mutants is rescued by gamma-irradiation. We propose that GAK-1 functions to reduce access to the autosomes by the double strand break machinery, thereby increasing access by this machinery to the more highly condensed X chromosome; the result of GAK-1 function then is to permit sufficient double strand breaks on the X so that it can undergo homologous recombination, which is required to maintain homolog pairing throughout meiosis I. Our initial characterization of the
gak-1 gene product suggests that GAK-1 has a novel and unique function in X chromosome segregation.