Heterochromatin Protein Swi6 Suppresses Aberrant Gene Conversion at mat Loci by Adjusting the Balance Between the Two Pathways of Swi2 and Rad57

Abstract

Heterochromatin protein 1 (HP1) is a highly conserved, canonical factor involved in heterochromatin formation. HP1 has been shown to interact with proteins other than silencing factors and heterochromatin effectors. In fission yeast, the loss of the HP1 homolog Swi6 disrupts heterochromatin structure and affects mating type switching at the mat locus, where heterochromatin exists; however, cell growth is unaffected. In this study, we focused on the Swi6 dimerization domain, which provides a binding surface for various interactors. We isolated a distinctive swi6H321Q mutant that does not affect heterochromatin structure but causes variegation in growth defects and abnormal recombination at the mat locus. This mutation disrupts the interaction between Swi6 and Swi2, a mat locus-specific recombination protein. The AT-hook motif of Swi2, which is also required for chromatin localization at the mat locus, is necessary for growth inhibition, suggesting that mislocalization of Swi2 at the mat locus induces growth inhibition. Genetic analysis revealed that abnormal recombination at the mat region was independent of Swi2 but dependent on the Rad57-dependent homologous recombination pathway. These results suggest that Swi6 plays an important role in gene conversion at the mat locus by producing an appropriate selection of homologous recombination factors.