Bmh1/Bmh2 Redundancy in the Control of the Spindle Assembly Checkpoint in Yeast Cells

The spindle assembly checkpoint (SAC) monitors errors in chromosome attachment, but the regulation of the SAC is not fully understood. Previous research shows that the budding yeast 14-3-3 protein Bmh1 serves a sequestering function for Fin1, which prevents the kinetochore recruitment of Fin1-PP1 and prolongs the SAC. After chromosome segregation, Bmh1 detaches from Fin1, allowing the Fin1-PP1complex to bind to the kinetochore and remove SAC proteins from the kinetochore. bmh1 mutant cells show chromosome missegregation and early dephosphorylation of SAC proteins in the presence of tension defects, which indicates premature anaphase entry. We found that Bmh2, a homologue of Bmh1 that is less prevalent within cells, has some redundant function with Bmh1. By creating a bmh1 GAL-BMH2 cell line, we were able to overexpress the Bmh2 protein in the absence of Bmh1. This new strain grew poorly on glucose medium when Bmh2 expression is suppressed, which confirmed the synthetic growth defect of the bmh1 bmh2 double mutant. When this strain was grown in galactose medium to induce Bmh2 overexpression, we observed suppressed sensitivity to microtubule poison and decreased Fin1 kinetochore localization. Therefore, we concluded that Bmh1 and Bmh2 play redundant roles in cell cycle regulation.