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一个 MKP-MAPK 蛋白磷酸化级联反应控制着植物的血管免疫。

An MKP-MAPK protein phosphorylation cascade controls vascular immunity in plants.

机构信息

School of Life Science and Technology, ShanghaiTech University, Shanghai 201210, China.

National Key Laboratory of Plant Molecular Genetics, CAS Centre for Excellence in Molecular Plant Sciences, Shanghai Institute of Plant Physiology and Ecology, Chinese Academy of Sciences, Shanghai 200032, China.

出版信息

Sci Adv. 2022 Mar 11;8(10):eabg8723. doi: 10.1126/sciadv.abg8723. Epub 2022 Mar 9.

DOI:10.1126/sciadv.abg8723
PMID:35263144
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8906744/
Abstract

Global crop production is greatly reduced by vascular diseases. These diseases include bacterial blight of rice and crucifer black rot caused by pv. () and pv. (). The molecular mechanisms that activate vascular defense against such pathogens remains underexplored. Here, we show that an MAPK phosphatase 1 (MKP1) mutant has increased host susceptibility to the adapted pathogen and is compromised in nonhost resistance to the rice pathogen . MKP1 regulates MAPK-mediated phosphorylation of the transcription factor MYB4 that negatively regulates vascular lignification through inhibiting lignin biosynthesis. Induction of lignin biosynthesis is, therefore, an important part of vascular-specific immunity. The role of MKP-MAPK-MYB signaling in lignin biosynthesis and vascular resistance to is conserved in rice, indicating that these factors form a tissue-specific defense regulatory network. Our study likely reveals a major vascular immune mechanism that underlies tissue-specific disease resistance against bacterial pathogens in plants.

摘要

全球作物生产受到血管疾病的严重影响。这些疾病包括由 pv. () 和 pv. () 引起的水稻细菌性条斑病和十字花科黑腐病。激活血管防御此类病原体的分子机制仍未得到充分探索。在这里,我们表明一个 MAPK 磷酸酶 1 (MKP1) 突变体增加了宿主对适应性病原体的易感性,并且在非宿主对水稻病原体的抗性中受损。MKP1 调节 MAPK 介导的转录因子 MYB4 的磷酸化,MYB4 通过抑制木质素生物合成来负调控血管木质化。因此,木质素生物合成的诱导是血管特异性免疫的重要组成部分。MKP-MAPK-MYB 信号在木质素生物合成和对 的血管抗性中的作用在水稻中是保守的,表明这些因素形成了组织特异性防御调控网络。我们的研究可能揭示了一个主要的血管免疫机制,该机制是植物中针对细菌性病原体的组织特异性疾病抗性的基础。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/de41/8906744/cbd36da6972c/sciadv.abg8723-f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/de41/8906744/1aadfa40e649/sciadv.abg8723-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/de41/8906744/5a58808b86cb/sciadv.abg8723-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/de41/8906744/0a1370269322/sciadv.abg8723-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/de41/8906744/c10c859e0c23/sciadv.abg8723-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/de41/8906744/71dcce8d0ed2/sciadv.abg8723-f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/de41/8906744/cbd36da6972c/sciadv.abg8723-f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/de41/8906744/1aadfa40e649/sciadv.abg8723-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/de41/8906744/5a58808b86cb/sciadv.abg8723-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/de41/8906744/0a1370269322/sciadv.abg8723-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/de41/8906744/c10c859e0c23/sciadv.abg8723-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/de41/8906744/71dcce8d0ed2/sciadv.abg8723-f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/de41/8906744/cbd36da6972c/sciadv.abg8723-f6.jpg

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