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一种甘蔗黑粉菌效应因子模拟宿主内源性激发肽抑制植物免疫。

A sugarcane smut fungus effector simulates the host endogenous elicitor peptide to suppress plant immunity.

机构信息

Key Laboratory of Sugarcane Biology and Genetic Breeding, Ministry of Agriculture, Key Laboratory of Ministry of Education for Genetics, Breeding and Multiple Utilization of Crops, Plant Immunity Center, College of Life Sciences, Fujian Agriculture and Forestry University, Fuzhou, 350002, China.

College of Agriculture, Yulin Normal University, Yulin, 537000, China.

出版信息

New Phytol. 2022 Jan;233(2):919-933. doi: 10.1111/nph.17835. Epub 2021 Nov 12.

DOI:10.1111/nph.17835
PMID:34716592
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9298926/
Abstract

The smut fungus Sporisorium scitamineum causes the most prevalent disease on sugarcane. The mechanism of its pathogenesis, especially the functions and host targets of its effector proteins, are unknown. In order to identify putative effectors involving in S. scitamineum infection, a weighted gene co-expression network analysis was conducted based on the transcriptome profiles of both smut fungus and sugarcane using a customized microarray. A smut effector gene, termed SsPele1, showed strong co-expression with sugarcane PLANT ELICITOR PEPTIDE RECEPTOR1 (ScPEPR1), which encodes a receptor like kinase for perception of plant elicitor peptide1 (ScPep1). The relationship between SsPele1 and ScPEPR1, and the biological function of SsPele1 were characterized in this study. The SsPele1 C-terminus contains a plant elicitor peptide-like motif, by which SsPele1 interacts strongly with ScPEPR1. Strikingly, the perception of ScPep1 on ScPEPR1 is competed by SsPele1 association, leading to the suppression of ScPEPR1-mediated immune responses. Moreover, the Ustilago maydis effector UmPele1, an ortholog of SsPele1, promotes fungal virulence using the same strategy. This study reveals a novel strategy by which a fungal effector can mimic the plant elicitor peptide to complete its perception and attenuate receptor-activated immunity.

摘要

盾孢霉引起甘蔗上最普遍的病害。其发病机制,尤其是其效应蛋白的功能和宿主靶标,尚不清楚。为了鉴定可能参与盾孢霉感染的效应子,本研究利用定制的微阵列,基于盾孢霉和甘蔗的转录组谱,进行了加权基因共表达网络分析。一个名为 SsPele1 的盾孢霉效应子基因与甘蔗 PLANT ELICITOR PEPTIDE RECEPTOR1(ScPEPR1)表现出强烈的共表达,ScPEPR1 编码了一种用于感知植物诱导肽 1(ScPep1)的受体样激酶。本研究对 SsPele1 和 ScPEPR1 之间的关系及其生物学功能进行了研究。SsPele1 的 C 端含有一个植物诱导肽样基序,通过该基序 SsPele1 与 ScPEPR1 强烈相互作用。引人注目的是,ScPep1 在 ScPEPR1 上的感知被 SsPele1 结合所竞争,导致 ScPEPR1 介导的免疫反应受到抑制。此外,玉米黑粉菌效应子 UmPele1 是 SsPele1 的同源物,也采用同样的策略促进真菌的毒力。本研究揭示了一种新的策略,即真菌效应子可以模拟植物诱导肽来完成其感知,并减弱受体激活的免疫。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/efd1/9298926/11b815cf1226/NPH-233-919-g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/efd1/9298926/c15872c40c32/NPH-233-919-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/efd1/9298926/11b815cf1226/NPH-233-919-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/efd1/9298926/fe8a6413b65b/NPH-233-919-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/efd1/9298926/dbfa2ebef7cc/NPH-233-919-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/efd1/9298926/39de279b419f/NPH-233-919-g004.jpg
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