葡萄原原虫效应子 PvCRN20 可抑制 VvDEG5 进入叶绿体，从而抑制葡萄树的免疫。

IF 8.3 1区生物学 Q1 PLANT SCIENCES

New Phytologist Pub Date : 2024-08-01 DOI:10.1111/nph.20002

Qingqing Fu, Tingting Chen, Yunlei Wang, Huixuan Zhou, Kangzhuang Zhang, Runlong Zheng, Yanan Zhang, Ruiqi Liu, Xiao Yin, Guotian Liu, Yan Xu

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引用次数: 0

摘要

叶绿体在植物抵御病原体的过程中起着至关重要的作用，因此成为抑制宿主免疫的病原体效应物的主要靶标。本研究描述了 Plasmopara viticola CRN 样效应物 PvCRN20 的特征，它与细胞质中的 DEG5 相互作用，但与其相互作用的蛋白 DEG8 却不相互作用，后者位于叶绿体中。通过在烟草叶片中瞬时过表达，我们发现 PvCRN20 可抑制 INF1 和 Bax 触发的细胞死亡。PvCRN20 的连续表达能抑制活性氧（ROS）的积累并促进病原体的定植。PvCRN20 可减少 DEG5 进入叶绿体，从而破坏叶绿体中 DEG5 和 DEG8 的相互作用。过表达 VvDEG5 和 VvDEG8 会诱导 ROS 积累，增强葡萄对葡萄孢的抗性，而敲除 VvDEG8 则会抑制 ROS 的产生，促进葡萄孢的定殖。同样，在烟草中异位表达 VvDEG5 和 VvDEG8 会促进叶绿体源性 ROS 的积累，而共同表达 PvCRN20 则会抵消 VvDEG5 的这种促进作用。因此，DEG5 对 PvCRN20 的毒力功能至关重要。虽然 PvCRN20 位于细胞核和细胞质中，但只有细胞质中的 PvCRN20 能抑制植物免疫并促进病原体感染。我们的研究结果表明，PvCRN20 通过抑制叶绿体导入 DEG5 来抑制植物的防御能力，从而减少宿主 ROS 的积累，促进病原体的定殖。

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Plasmopara viticola effector PvCRN20 represses the import of VvDEG5 into chloroplasts to suppress immunity in grapevine

Chloroplasts play a crucial role in plant defense against pathogens, making them primary targets for pathogen effectors that suppress host immunity. This study characterizes the Plasmopara viticola CRN-like effector, PvCRN20, which interacts with DEG5 in the cytoplasm but not with its interacting protein, DEG8, which is located in the chloroplast.
By transiently overexpressing in tobacco leaves, we show that PvCRN20 could inhibit INF1- and Bax-triggered cell death. Constitutive expression of PvCRN20 suppresses the accumulation of reactive oxygen species (ROS) and promotes pathogen colonization. PvCRN20 reduces DEG5 entry into chloroplasts, thereby disrupting DEG5 and DEG8 interactions in chloroplasts.
Overexpression of VvDEG5 and VvDEG8 induces ROS accumulation and enhances grapevine resistance to P. viticola, whereas knockout of VvDEG8 represses ROS production and promotes P. viticola colonization. Consistently, ectopic expression of VvDEG5 and VvDEG8 in tobacco promotes chloroplast-derived ROS accumulation, whereas co-expression of PvCRN20 counteracted this promotion by VvDEG5. Therefore, DEG5 is essential for the virulence function of PvCRN20. Although PvCRN20 is located in both the nucleus and cytoplasm, only cytoplasmic PvCRN20 suppresses plant immunity and promotes pathogen infection.
Our results reveal that PvCRN20 dampens plant defenses by repressing the chloroplast import of DEG5, thus reducing host ROS accumulation and facilitating pathogen colonization.

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来源期刊

New Phytologist 生物-植物科学

自引率

5.30%

发文量

728

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