Mitochondria-Mediated Programmed Cell Death in Saccharomyces cerevisiae Induced by Betulinic Acid Is Accelerated by the Deletion of PEP4 Gene

Abstract

In this work, using Saccharomyces cerevisiae as a model, we showed that BetA could inhibitcell proliferation and lead to lethal cytotoxicity accompanying programmed cell death (PCD).Interestingly, it was found that vacuolar protease Pep4p played a pivotal role in BetA‐induced S.cerevisiae PCD. The presence of Pep4p reduced the damage of BetA‐induced cells. This work impliedthat BetA may induce cell death of S. cerevisiae through mitochondria‐mediated PCD, and thedeletion of Pep4 gene possibly accelerated the effect of PCD. The present investigation provided thepreliminary research for the complicated mechanism of BetA‐induced cell PCD regulated by vacularprotease Pep4p and lay the foundation for understanding of the Pep4p protein in an animal model.