Rad52 phosphorylation by Ipl1 and Mps1 contributes to Mps1 kinetochore localization and spindle assembly checkpoint regulation

Abstract

Significance Rad52 is a well-known factor in homologous recombination. In this study, we discover functions of Rad52 in spindle assembly checkpoint (SAC) regulation and Mps1 localization for chromosome biorientation. Deletion of RAD52 leads to various phenotypes of inaccurate chromosome segregation that are not observed in another homologous recombination-defective rad51 Δ mutant. Furthermore, we find that Rad52 is a substrate of mitotic kinases Ipl1/Aurora and Mps1 and that Rad52 phosphorylation by Ipl1 and Mps1 contributes to Mps1 kinetochore localization and SAC regulation. From these findings, we suggest that Rad52 functions as a mediator between Ipl1 and Mps1 in the regulatory pathway of mitosis. Our results provide detailed insights into the molecular basis of chromosome segregation and SAC regulation.