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PeFtsH5 negatively regulates the biological stress response in Phalaenopsis equestris mitochondria

文献类型： 外文期刊

作者： Wu, Yiding 1 ; Meng, Yang 1 ; Zhang, Long 1 ; Yang, Zhenyu 1 ; Su, Mingyang 1 ; Jia, Ruidong 3 ; Ming, Feng 1 ;

作者机构： 1.Shanghai Normal Univ, Coll Life Sci, Dev Ctr Plant Germplasm Resources, Shanghai 200234, Peoples R China

2.Shanghai Normal Univ, Coll Life Sci, Shanghai Key Lab Plant Mol Sci, Shanghai 200234, Peoples R China

3.Chinese Acad Agr Sci, Inst Vegetables & Flowers, Key Lab Biol & Genet Improvement Flower Crops Nort, Minist Agr & Rural Affairs,State Key Lab Vegetable, Beijing 100081, Peoples R China

4.Shanghai Xinchang High Sch, Shanghai 201314, Peoples R China

关键词： Phalaenopsis equestris; Mitochondria; FtsH5; Virus induced gene silencing (VIGS); Cell apoptosis

期刊名称：JOURNAL OF PLANT PHYSIOLOGY （ 影响因子：4.3； 五年影响因子：4.5 ）

ISSN： 0176-1617

年卷期： 2024 年 292 卷

页码：

收录情况： SCI

摘要： Mitochondrial homeostasis plays a crucial role in determining cell fate by direct influence on cell apoptosis and autophagy. The ATP and Zn2+-dependent protease FtsH are of paramount importance in maintaining mitochondrial homeostasis. In Phalaenopsis equestris, three mitochondrial FtsH proteases were identified, one of which was encoded by the PeFtsH5 gene. This gene encoded a distinctive mitochondrial protein featuring a unique domain within the FtsH family. Down-regulating the expression of the PeFtsH5 homolog in Nicotiana benthamiana resulted in elevated expression levels of SA synthesis-related genes, leading to enhanced disease resistance. However, this down-regulation also caused cellular damage. Similarly, in P. equestris, the down-regulation of PeFtsH5 expression promoted the expression of defense response genes, leading to accelerated apoptosis and increased ROS levels. Nonetheless, this down-regulation also positively influenced plant resistance to biotic stress. Notably, the PeFtsH5 (i-AAA) protein, as revealed by dual membrane experiments, could form homopolymers exclusively, as it did not interact with the other two mitochondrial FtsH proteases. Consequently, this mitochondrial FtsH protease functioned as a homopolymer within P. equestris cells. The findings of this study elucidated the role of PeFtsH5 in responding to biological stress and provided new insights into its potential molecular mechanism. The result presented in this study hold promise for future research endeavors examining the regulatory effects of mitochondrial proteases on mitochondrial homeostasis and the development of stressresistant P. equestris varieties through breeding programs.

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