Mitochondria-Mediated Programmed Cell Death in Saccharomyces Cerevisiae Induced by Betulinic Acid is Accelerated by the Deletion of PEP4 Gene
Mitochondria-Mediated Programmed Cell Death in Saccharomyces Cerevisiae Induced by Betulinic Acid is Accelerated by the Deletion of PEP4 Gene
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PEP4 基因的缺失加速了桦木酸诱导的酿酒酵母中线粒体介导的程序性细胞死亡
DOI：
10.3390/microorganisms7110538
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发表时间：
2019-11
期刊：
影响因子：
4.5
通讯作者：
Chen Qihe
中科院分区：
文献类型：
--
作者：
Lu Hongyun;Shu Qin;Lou Hanghang;Chen Qihe
在这项工作中，使用酿酒酵母作为模型，我们表明，BetA可以抑制细胞增殖，并导致致命的细胞毒性伴随程序性细胞死亡（PCD）。有趣的是，液泡蛋白酶Pep4p在BetA诱导的S.酿酒酵母PCD。Pep4p的存在减少了BetA诱导的细胞的损伤。这一结果提示BetA可能诱导S. Pep4基因的缺失可能加速了细胞的PCD效应。本研究为深入研究Pep4p蛋白调控BetA诱导细胞PCD的复杂机制提供了初步的理论依据，为进一步研究Pep4p蛋白在动物模型中的作用奠定了基础。
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.
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影响因子：
3.5
作者：
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影响因子：
3.3
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