Lipopeptide induces apoptosis in fungal cells by a mitochondria-dependent pathway

文献类型： 外文期刊

第一作者： Zhu Fayin

作者： Zhu Fayin;Yu Ziniu;Zhao Xiuyun;Du Peng;Yang Xiufen;Qiu Dewen;Chen Jingyuan

作者机构：

关键词： Lipopeptide;Fungi;Apoptosis;ATPase;Cytochrome C

期刊名称：PEPTIDES （ 影响因子：3.75； 五年影响因子：3.389 ）

ISSN： 0196-9781

年卷期： 2010 年 31 卷 11 期

页码：

收录情况： SCI

摘要： Bacillus amyloliquefaciens WH1 inhibit the growth of fungi by producing a new surfactin called as WH1fungin WH1fungin plays an anti-fungal role by two models high concentration to elicit pores on cell membrane and low concentration to induce apoptosis WH1fungin can also inhibits the glucan synthase resulting in a decreased synthesis of callose on fungal cell wall Further detection revealed that classical apoptotic markers such as reactive oxygen species (ROS) accumulation phosphatidylserine (PS) externalization DNA strand breaks and caspase-like activities could be found in fungal cells after treated by WH1fungin Oligomycin was used as an inhibitor to block the mitochondria-dependent apoptosis in fungal cells and results showed it could not inhibit but enhance the apoptosis induced by WH1fungin After isolation by affinity chromatography WH1fungin was found to bind with ATPase on the mitochondrial membrane and result in a decreased ATPase activity in fungal cells This was further verified by treating fungal cells with FITC-labeled WH1fungin which could bind to the mitochondrial membrane showing green fluorescence in fungal cells After that cytochrome C was released from the mitochondria which then acted with caspase 9 to induce apoptosis by an intracellular pathway High caspase 8 activity was also detectable in apoptotic fungal cells indicating that an extracellular pathway might also be responsible for apoptosis induced by WH1fungin Taken together we report that lipopeptide can induce apoptosis in fungal cells and induction of apoptosis by lipopeptide might be a common anti-fungal mechanism of Bacillus in the natural habitat (C) 2010 Elsevier Inc All rights reserved

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