The cysteine-rich receptor-like kinase CRK10 targeted by Coniella diplodiella effector CdE1 contributes to white rot resistance in grapevine

文献类型： 外文期刊

第一作者： Liu, Ruitao

作者： Liu, Ruitao;Tan, Xibei;Lin, Feng;Li, Peng;Rahman, Faiz Ur;Sun, Lei;Jiang, Jianfu;Fan, Xiucai;Liu, Chonghuai;Zhang, Ying;Liu, Ruitao;Zhang, Ying;Wang, Yiming;Lin, Feng

作者机构：

关键词： Effector; grapevine; Coniella diplodiella; cysteine-rich receptor-like kinase (CRK); grape white rot; disease resistance

期刊名称：JOURNAL OF EXPERIMENTAL BOTANY （ 影响因子：6.9； 五年影响因子：8.0 ）

ISSN： 0022-0957

年卷期： 2024 年 75 卷 10 期

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收录情况： SCI

摘要： Grape white rot is a devastating fungal disease caused by Coniella diplodiella. The pathogen delivers effectors into the host cell that target crucial immune components to facilitate its infection. Here, we examined a secreted effector of C. diplodiella, known as CdE1, which has been found to inhibit Bax-triggered cell death in Nicotiana benthamiana plants. The expression of CdE1 was induced at 12-48 h after inoculation with C. diplodiella, and the transient overexpression of CdE1 led to increased susceptibility of grapevine to the fungus. Subsequent experiments revealed an interaction between CdE1 and Vitis davidii cysteine-rich receptor-like kinase 10 (VdCRK10) and suppression of VdCRK10-mediated immunity against C. diplodiella, partially by decreasing the accumulation of VdCRK10 protein. Furthermore, our investigation revealed that CRK10 expression was significantly higher and was up-regulated in the resistant wild grapevine V. davidii during C. diplodiella infection. The activity of the VdCRK10 promoter is induced by C. diplodiella and is higher than that of Vitis vitifera VvCRK10, indicating the involvement of transcriptional regulation in CRK10 gene expression. Taken together, our results highlight the potential of VdCRK10 as a resistant gene for enhancing white rot resistance in grapevine. The fungus Coniella diplodiella , a causal agent of grapevine white rot, secretes an effector protein to suppress grapevine immunity through manipulating the resistance protein cysteine-rich receptor-like kinase 10.

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