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A candidate RxLR effector from Plasmopara viticola can elicit immune responses in Nicotiana benthamiana

文献类型： 外文期刊

作者： Xiang, Jiang 2 ; Li, Xinlong 1 ; Yin, Ling 3 ; Liu, Yunxiao 1 ; Zhang, Yali 1 ; Qu, Junjie 3 ; Lu, Jiang 1 ;

作者机构： 1.China Agr Univ, Coll Food Sci & Nutr Engn, Viticulture & Enol Program, Beijing, Peoples R China

2.Shanghai Jiao Tong Univ, Sch Agr & Biol, Ctr Viticulture & Enol, Shanghai 200240, Peoples R China

3.Guangxi Acad Agr Sci, Guangxi Crop Genet Improvement & Biotechnol Lab, Nanning, Peoples R China

关键词： Plasmopara viticola;grapevine;RxLR effector;Nicotiana benthamiana cell death;immune responses

期刊名称：BMC PLANT BIOLOGY （ 影响因子：4.215； 五年影响因子：4.96 ）

ISSN： 1471-2229

年卷期： 2017 年 17 卷

页码：

收录情况： SCI

摘要： Background: Diverse plant pathogens deliver effectors into plant cells to alter host processes. Oomycete pathogen encodes a large number of putative RxLR effectors which are likely to play a role in manipulating plant defense responses. The secretome of Plasmopara viticola (downy mildew of grapevine) contains at least 162 candidate RxLR effectors discovered in our recent studies, but their roles in infection and pathogenicity remain to be determined. Here, we characterize in depth one of the putative RxLR effectors, PvRxLR16, which has been reported to induce cell death in Nicotiana benthamiana in our previous study. Results: The nuclear localization, W/Y/L motifs, and a putative N-glycosylation site in C-terminal of PvRxLR16 were essential for cell death-inducing activity. Suppressor of G-two allele of Skp1 (SGT1), heat shock protein 90 (HSP90) and required for Mla12 resistance (RAR1), but not somatic embryogenesis receptor-like kinase (SERK3), were required for the cell death response triggered by PvRxLR16 in N. benthamiana. Some mitogen-activated protein kinases and transcription factors were also involved in the perception of PvRxLR16 by N. benthamiana. PvRxLR16 could also significantly enhance plant resistance to Phytophthora capsici and the nuclear localization was required for this ability. However, some other PvRxLR effectors could suppress defense responses and disease resistance induced by PvRxLR16, suggesting that it may not trigger host cell death or immune responses during physiological infection under natural conditions. Conclusion: These data demonstrate that PvRxLR16 may be recognized by endogenous proteins in nucleus to trigger immune responses in N. benthamiana, which in turn can be suppressed by other PvRxLR effectors.

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