文献类型： 外文期刊

作者： Zhu, Xin ¹ ; Zhang, Kunxi ¹ ; Gong, Peijie ¹ ; Riemann, Michael ¹ ; Nick, Peter ¹ ;

作者机构： 1.Joseph Gottlieb Kolreuter Inst Plant Sci, Karlsruhe Inst Technol, Mol Cell Biol, Fritz Haber Weg 4, D-76131 Karlsruhe, Germany

2.Henan Agr Univ, Coll Hort, Zhengzhou 450000, Henan, Peoples R China

3.Jiangsu Acad Agr Sci, Inst Plant Protect, Jiangsu Key Lab Food Qual & Safety, State Key Lab Cultivat Base Minist Sci & Technol, Nanjing 210014, Jiangsu, Peoples R China

关键词： Cis-3-hexenal; Hypersensitive response; Metacaspase; Programmed cell death; Tobacco BY-2; Vitis rupestris

期刊名称：PLANT CELL REPORTS （ 影响因子：4.5； 五年影响因子：6.1 ）

ISSN： 0721-7714

年卷期： 2025 年 44 卷 8 期

页码：

收录情况： SCI

摘要： Key messageVitisrupestris metacaspase 5, tethered to microtubules, drives grapevine. Hypersensitive response via calcium-dependent auto-processing, linking cytoskeletal dynamics to defence activation by elicitors.AbstractMetacaspase 5 is a key player for the hypersensitive response of grapevine against biotrophic pathogens and must be activated rapidly as to prevent colonisation. This activation is likely to occur through changes in protein activity. By expressing a GFP fusion of metacaspase 5 from Vitis rupestris in tobacco BY-2 cells, we can show that this protein is bound to microtubules and that the overexpressors are more responsive to the cell-death-inducing elicitors, cis-3-hexenal and harpin. The disruption of microtubules and actin filaments by these elicitors can be blocked by inhibitors of dynamic turnover and stabilisation. Stabilisation of microtubules by taxol can mitigate cis-3-hexenal induced mortality. Mutations of the catalytic or the putative microtubule-binding sites of metacaspase 5 can suppress auto-processing of this enzyme in biochemical assay. Likewise, the response to cis-3-hexenal (cell death, induction of salicylate-related gene expression) is suppressed in cells, whilst the cytoplasmic remodelling is retained. Calcium and the sites for catalysis or microtubule binding are required for both auto-processing and enzyme activity. We arrive at a model, where metacaspase 5 is inactive when tethered to microtubules, but becomes unleashed for auto-processing upon defence-mediated microtubule breakdown.