Mitochondria-Mediated Programmed Cell Death in <i>Saccharomyces cerevisiae</i> Induced by Betulinic Acid Is Accelerated by the Deletion of <i>PEP4</i> Gene
In this work, using <em>Saccharomyces cerevisiae</em> as a model, we showed that BetA could inhibit<br />cell proliferation and lead to lethal cytotoxicity accompanying programmed cell death (PCD).<br />Interestingly, it was found that vacuolar protease Pep4p played a pivotal...
| Main Authors: | , , , |
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| Format: | Article |
| Language: | English |
| Published: |
MDPI AG
2019-11-01
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| Series: | Microorganisms |
| Subjects: | |
| Online Access: | https://www.mdpi.com/2076-2607/7/11/538 |
| Summary: | In this work, using <em>Saccharomyces cerevisiae</em> as a model, we showed that BetA could inhibit<br />cell proliferation and lead to lethal cytotoxicity accompanying programmed cell death (PCD).<br />Interestingly, it was found that vacuolar protease Pep4p played a pivotal role in BetA‐induced <em>S.</em><br /><em>cerevisiae</em> PCD. The presence of Pep4p reduced the damage of BetA‐induced cells. This work implied<br />that BetA may induce cell death of <em>S. cerevisiae</em> through mitochondria‐mediated PCD, and the<br />deletion of Pep4 gene possibly accelerated the effect of PCD. The present investigation provided the<br />preliminary research for the complicated mechanism of BetA‐induced cell PCD regulated by vacular<br />protease Pep4p and lay the foundation for understanding of the Pep4p protein in an animal model. |
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| ISSN: | 2076-2607 |