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一种含有真菌 CFEM 的效应子靶向 NPR1 调节剂 NIMIN2 以抑制植物免疫。

A fungal CFEM-containing effector targets NPR1 regulator NIMIN2 to suppress plant immunity.

机构信息

State Key Laboratory of Crop Stress Biology in Arid Areas, Key Laboratory of Protection Resources and Pest Management of Ministry of Education, Key Laboratory of Integrated Pest Management on the Loess Plateau of Minishtry of Agriculture and Rural Affairs, and College of Plant Protection, Northwest A&F University, Yangling, China.

出版信息

Plant Biotechnol J. 2024 Jan;22(1):82-97. doi: 10.1111/pbi.14166. Epub 2023 Aug 19.

DOI:10.1111/pbi.14166
PMID:37596985
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10754009/
Abstract

Colletotrichum fructicola causes a broad range of plant diseases worldwide and secretes many candidate proteinous effectors during infection, but it remains largely unknown regarding their effects in conquering plant immunity. Here, we characterized a novel effector CfEC12 that is required for the virulence of C. fructicola. CfEC12 contains a CFEM domain and is highly expressed during the early stage of host infection. Overexpression of CfEC12 suppressed BAX-triggered cell death, callose deposition and ROS burst in Nicotiana benthamiana. CfEC12 interacted with apple MdNIMIN2, a NIM1-interacting (NIMIN) protein that putatively modulates NPR1 activity in response to SA signal. Transient expression and transgenic analyses showed that MdNIMIN2 was required for apple resistance to C. fructicola infection and rescued the defence reduction in NbNIMIN2-silenced N. benthamiana, supporting a positive role in plant immunity. CfEC12 and MdNPR1 interacted with a common region of MdNIMIN2, indicating that CfEC12 suppresses the interaction between MdNIMIN2 and MdNPR1 by competitive target binding. In sum, we identified a fungal effector that targets the plant salicylic acid defence pathway to promote fungal infection.

摘要

胶孢炭疽菌可引起全球范围内的多种植物病害，并在侵染过程中分泌许多候选蛋白效应子，但这些效应子在克服植物免疫方面的作用在很大程度上仍不清楚。在这里，我们对一种新型效应子 CfEC12 进行了特征描述，该效应子是胶孢炭疽菌毒力所必需的。CfEC12 含有一个 CFEM 结构域，在宿主侵染的早期高度表达。过表达 CfEC12 可抑制 BAX 诱导的细胞死亡、胼胝质沉积和 ROS 爆发。CfEC12 与苹果 MdNIMIN2 相互作用，MdNIMIN2 是一种与 NIM1 相互作用的（NIMIN）蛋白，可能在响应 SA 信号时调节 NPR1 活性。瞬时表达和转基因分析表明，MdNIMIN2 是苹果对胶孢炭疽菌感染产生抗性所必需的，并且挽救了在 NbNIMIN2 沉默的 N. benthamiana 中防御的降低，支持其在植物免疫中的积极作用。CfEC12 和 MdNPR1 与 MdNIMIN2 的一个共同区域相互作用，表明 CfEC12 通过竞争性靶标结合抑制 MdNIMIN2 和 MdNPR1 之间的相互作用。总之，我们鉴定了一种靶向植物水杨酸防御途径的真菌效应子，以促进真菌侵染。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7d25/11373912/9b2bac778e3f/PBI-22-82-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7d25/11373912/3fffb09545bb/PBI-22-82-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7d25/11373912/7d995cd46d91/PBI-22-82-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7d25/11373912/39c37c4fce06/PBI-22-82-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7d25/11373912/08851342d4a9/PBI-22-82-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7d25/11373912/9e96c0578fa2/PBI-22-82-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7d25/11373912/382b698a0dfa/PBI-22-82-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7d25/11373912/9b2bac778e3f/PBI-22-82-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7d25/11373912/3fffb09545bb/PBI-22-82-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7d25/11373912/7d995cd46d91/PBI-22-82-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7d25/11373912/39c37c4fce06/PBI-22-82-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7d25/11373912/08851342d4a9/PBI-22-82-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7d25/11373912/9e96c0578fa2/PBI-22-82-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7d25/11373912/382b698a0dfa/PBI-22-82-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7d25/11373912/9b2bac778e3f/PBI-22-82-g002.jpg

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