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RD21通过促进自噬介导的病毒沉默抑制因子P6蛋白降解来增强对草莓脉带病毒的抗性。

RD21 enhances resistance to the strawberry vein banding virus by promoting autophagy-mediated degradation of the viral silencing suppressor P6 protein.

作者信息

Yang Xianchu, Feng Jiying, Xu Kai, Han Jincheng, Zhang Minghui, Cheng Aiwen, Wang Zhanqi, Wang Fang, Zhou Xueping, Jiang Lei, Jiang Tong

机构信息

School of Plant Protection, Anhui Agricultural University, Hefei, China.

Key Laboratory of Vector Biology and Pathogen Control of Zhejiang Province, College of Life Sciences, Huzhou University, Huzhou, China.

出版信息

Plant Biotechnol J. 2025 Sep;23(9):3597-3611. doi: 10.1111/pbi.70168. Epub 2025 Jun 8.

DOI:10.1111/pbi.70168
PMID:40483578
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12392972/
Abstract

Responsive to desiccation 21 (RD21) is a papain-like cysteine protease (PLCP). PLCPs are involved in plant growth and development, as well as stress and plant immune responses. Currently, few studies have reported on the involvement of PLCPs in defence against viral infections. Here, we show that RD21 of strawberry (Fragaria vesca) interacts with the strawberry vein banding virus (SVBV) P6 protein. SVBV infection induces FvRD21 expression. Subcellular localization revealed that FvRD21 and P6 colocalize in the perinuclear and cytoplasmic regions. Further analysis showed that FvRD21 overexpression induces the autophagy pathway that degrades the P6 protein, destroys the function of P6 as a viral suppressor of RNA silencing (VSR), inhibits the pathogenicity of P6, and confers resistance to SVBV in strawberry plants. Moreover, mutant FvRD21 lost its ability to interact with SVBV P6 and did not affect P6 accumulation and VSR function. Additionally, abscisic acid (ABA) pretreatment of strawberry plants promoted FvRD21 upregulation and inhibited SVBV infection, and FvRD21 overexpression activated the ABA pathway. In summary, FvRD21 inhibits SVBV infection by degrading SVBV P6 through the autophagy pathway. Hence, this study provides a novel report on the defence strategy of strawberry plants against SVBV infections.

摘要

响应干燥21(RD21)是一种木瓜蛋白酶样半胱氨酸蛋白酶(PLCP)。PLCP参与植物的生长发育以及胁迫和植物免疫反应。目前,关于PLCP参与抵御病毒感染的研究报道较少。在此,我们表明草莓(Fragaria vesca)的RD21与草莓叶脉束带病毒(SVBV)的P6蛋白相互作用。SVBV感染诱导FvRD21表达。亚细胞定位显示FvRD21和P6共定位于核周和细胞质区域。进一步分析表明,FvRD21过表达诱导自噬途径,该途径降解P6蛋白,破坏P6作为RNA沉默病毒抑制子(VSR)的功能,抑制P6的致病性,并赋予草莓植株对SVBV的抗性。此外,突变的FvRD21失去了与SVBV P6相互作用的能力,且不影响P6的积累和VSR功能。另外,对草莓植株进行脱落酸(ABA)预处理可促进FvRD21上调并抑制SVBV感染,且FvRD21过表达激活ABA途径。总之,FvRD21通过自噬途径降解SVBV P6来抑制SVBV感染。因此,本研究为草莓植株抵御SVBV感染的防御策略提供了新的报道。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0eee/12392972/0c67dfdc6aa6/PBI-23-3597-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0eee/12392972/955a26662aa0/PBI-23-3597-g005.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0eee/12392972/8e05b5d4a413/PBI-23-3597-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0eee/12392972/ad5bbe29cccd/PBI-23-3597-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0eee/12392972/a12aa3ac1c81/PBI-23-3597-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0eee/12392972/531619241733/PBI-23-3597-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0eee/12392972/9472e16e4a75/PBI-23-3597-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0eee/12392972/0c67dfdc6aa6/PBI-23-3597-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0eee/12392972/955a26662aa0/PBI-23-3597-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0eee/12392972/d24382a5a3cb/PBI-23-3597-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0eee/12392972/8e05b5d4a413/PBI-23-3597-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0eee/12392972/ad5bbe29cccd/PBI-23-3597-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0eee/12392972/a12aa3ac1c81/PBI-23-3597-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0eee/12392972/531619241733/PBI-23-3597-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0eee/12392972/9472e16e4a75/PBI-23-3597-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0eee/12392972/0c67dfdc6aa6/PBI-23-3597-g003.jpg

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