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一个完整的丝裂原活化蛋白激酶级联反应控制着(某种生物的)附着胞形成和毒力。

A complete MAP kinase cascade controls hyphopodium formation and virulence of .

作者信息

Ye Ziqin, Qin Jun, Wang Yu, Zhang Jinghan, Wu Xiaoyun, Li Xiangguo, Sun Lifan, Zhang Jie

机构信息

State Key Laboratory of Plant Genomics, Institute of Microbiology, Chinese Academy of Sciences, Beijing, 100101 China.

CAS Center for Excellence in Biotic Interactions, University of Chinese Academy of Sciences, Beijing, 100049 China.

出版信息

aBIOTECH. 2023 May 2;4(2):97-107. doi: 10.1007/s42994-023-00102-y. eCollection 2023 Jun.

Abstract

UNLABELLED

Phytopathogens develop specialized infection-related structures to penetrate plant cells during infection. Different from phytopathogens that form appressoria or haustoria, the soil-borne root-infecting fungal pathogen forms hyphopodia during infection, which further differentiate into penetration pegs to promote infection. The molecular mechanisms underlying the regulation of hyphopodium formation in remain poorly characterized. Mitogen-activated protein kinases (MAPKs) are highly conserved cytoplasmic kinases that regulate diverse biological processes in eukaryotes. Here we found that deletion of , out of the five MAPKs encoded by , significantly impaired hyphopodium formation, in vitro penetration, and pathogenicity in cotton plants. Constitutive activation of MAPK kinase (MAPKK) VdSte7 and MAPK kinase kinase (MAPKKK) VdSte11 specifically activate VdKss1. Deletion of or resulted in a phenotype similar to that of the mutant with deletion. Thus, this study demonstrates that VdSte11-VdSte7-VdKss1 is a core MAPK cascade that regulates hyphopodium formation and pathogenicity in .

SUPPLEMENTARY INFORMATION

The online version contains supplementary material available at 10.1007/s42994-023-00102-y.

摘要

未标记

植物病原体在感染过程中会形成专门的与感染相关的结构来穿透植物细胞。与形成附着胞或吸器的植物病原体不同,土壤传播的根部感染真菌病原体在感染过程中形成附着胞状的短菌丝,其进一步分化为侵入钉以促进感染。在[具体真菌名称未给出]中调控附着胞状短菌丝形成的分子机制仍不清楚。丝裂原活化蛋白激酶(MAPKs)是高度保守的细胞质激酶,可调节真核生物中的多种生物学过程。在这里,我们发现,在[具体真菌名称未给出]编码的五个MAPK中,缺失其中一个会显著损害[具体真菌名称未给出]的附着胞状短菌丝形成、体外穿透以及在棉花植株中的致病性。MAPK激酶(MAPKK)VdSte7和MAPK激酶激酶(MAPKKK)VdSte11的组成型激活特异性激活VdKss1。缺失VdSte7或VdSte11会导致与缺失VdKss1的突变体相似的表型。因此,本研究表明VdSte11-VdSte7-VdKss1是一个核心MAPK级联,可调节[具体真菌名称未给出]中的附着胞状短菌丝形成和致病性。

补充信息

在线版本包含可在10.1007/s42994-023-00102-y获取的补充材料。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d3b5/10423180/a6691007e347/42994_2023_102_Fig1_HTML.jpg

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