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.