Conserved domains of meiosis-specific CHK2 protein in budding yeast contribute to its kinase activity

Abstract

Programmed double strand DNA breaks in meiosis can be repaired as inter-homologue crossovers and thereby aid the faithful segregation of homologous chromosomes. Biased repair mechanisms enforce repair with the homologue. Further, DNA breaks left unrepaired lead to checkpoint activation. Meiosis-specific Chk2 kinase in budding yeast mediates the biased repair of meiotic DSBs using homologue partner but also enforces the meiotic checkpoint. Here we investigate Mek1 kinase activity in budding yeast by analyzing novel point mutants derived from an EMS mutagenesis screen. The point mutants in different domains of Mek1 abolish its activity that cannot be rescued by complementation in transheterozygotes. Our findings lend insight on the mechanism of Mek1 function during meiosis.