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FERONIA通过雷帕霉素靶蛋白(TOR)发挥作用,对自噬进行负调控。

FERONIA functions through Target of Rapamycin (TOR) to negatively regulate autophagy.

作者信息

Wang Ping, Clark Natalie M, Nolan Trevor M, Song Gaoyuan, Whitham Olivia G, Liao Ching-Yi, Montes-Serey Christian, Bassham Diane C, Walley Justin W, Yin Yanhai, Guo Hongqing

机构信息

Department of Genetics, Development and Cell Biology, Iowa State University, Ames, IA, United States.

Department of Plant Pathology and Microbiology, Iowa State University, Ames, IA, United States.

出版信息

Front Plant Sci. 2022 Aug 23;13:961096. doi: 10.3389/fpls.2022.961096. eCollection 2022.

Abstract

FERONIA (FER) receptor kinase plays versatile roles in plant growth and development, biotic and abiotic stress responses, and reproduction. Autophagy is a conserved cellular recycling process that is critical for balancing plant growth and stress responses. Target of Rapamycin (TOR) has been shown to be a master regulator of autophagy. Our previous multi-omics analysis with loss-of-function mutant implicated that FER functions in the autophagy pathway. We further demonstrated here that the mutant displayed constitutive autophagy, and FER is required for TOR kinase activity measured by S6K1 phosphorylation and by root growth inhibition assay to TOR kinase inhibitor AZD8055. Taken together, our study provides a previously unknown mechanism by which FER functions through TOR to negatively regulate autophagy.

摘要

FERONIA(FER)受体激酶在植物生长发育、生物和非生物胁迫响应以及繁殖过程中发挥着多种作用。自噬是一种保守的细胞循环过程,对于平衡植物生长和胁迫响应至关重要。雷帕霉素靶蛋白(TOR)已被证明是自噬的主要调节因子。我们之前对功能缺失突变体的多组学分析表明FER在自噬途径中发挥作用。我们在此进一步证明,该突变体表现出组成型自噬,并且通过S6K1磷酸化和根生长抑制试验检测TOR激酶活性时,FER是TOR激酶活性所必需的,该试验使用了TOR激酶抑制剂AZD8055。综上所述,我们的研究提供了一种此前未知的机制,即FER通过TOR负向调节自噬。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1422/9446147/9ed7289687d9/fpls-13-961096-g001.jpg

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