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

In this work, using Saccharomyces cerevisiae as a model, we showed that BetA could inhibit cell 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 implied that BetA may induce cell death of S. cerevisiae through mitochondria-mediated PCD, and the deletion of Pep4 gene possibly accelerated the effect of PCD. The present investigation provided the preliminary research for the complicated mechanism of BetA-induced cell PCD regulated by vacular protease Pep4p and lay the foundation for understanding of the Pep4p protein in an animal model.