Reciprocal inhibition of autophagy and Botrytis cinerea-induced programmed cell death in 'Shine Muscat' grapes

文献类型： 外文期刊

第一作者： Xiang, Yizhou

作者： Xiang, Yizhou;Yuan, Hemao;Mao, Mengfei;Hu, Qiannan;Dong, Yingying;Wang, Lei;Luo, Zisheng;Li, Li;Wu, Bin;Wu, Bin;Luo, Zisheng;Li, Li;Luo, Zisheng;Li, Li

作者机构：

关键词： Vitis vinifera; Gray mold; Programmed cell death; Autophagy

期刊名称：FOOD CHEMISTRY （ 影响因子：8.5； 五年影响因子：8.2 ）

ISSN： 0308-8146

年卷期： 2024 年 460 卷

页码：

收录情况： SCI

摘要： Botrytis cinerea causes gray mold, decreasing the quality of table grapes. The berry response to B. cinerea infection was explored in present study, focusing on the relationship between presence of autophagy and programmed cell death (PCD). Results demonstrated B. cinerea infection decreased cell viability, triggering cell death, possibly resulting in PCD occurrence. It was further verified by increased terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL)-positive nuclei, heightened caspase 3-like and caspase 9-like protease activity, and elevated expression of metacaspase genes. Additionally, autophagy was indicated by the increased VvATG expression and autophagosome formation. Notably, the autophagy activator rapamycin reduced TUNEL-positive nuclei, whereas the autophagy inhibitor 3-methyladenine increased caspase 9-like protease activity. The PCD activator C2-ceramide inhibited autophagy, whereas the PCD inhibitor Acetyl-Asp-Glu-Val-Asp-aldehyde (AcDEVD-CHO) enhanced autophagy gene expression. Autophagy and B. cinerea-induced PCD in berry cells are reciprocally negatively regulated; and the rapamycin and Ac-DEVD-CHO could potentially maintain table grape edible quality.

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