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作 者:Jianlong Zhao Kaiwei Huang Rui Liu Yuqing Lai Pierre Abad Bruno Favery Heng Jian Jian Ling Yan Li Yuhong Yang Bingyan Xie Michael Quentin Zhenchuan Mao
机构地区:[1]State Key Laboratory of Vegetable Biobreeding,Institute of Vegetables and Flowers,Chinese Academy of Agricultural Sciences,Beijing 100081,China [2]INRAE,Universite´Cote d’Azur,CNRS,ISA,06903 Sophia Antipolis,France [3]Department of Plant Pathology and Key Laboratory of Pest Monitoring and Green Management of the Ministry of Agriculture,China Agricultural University,Beijing 100193,China
出 处:《Plant Communications》2024年第2期151-168,共18页植物通讯(英文)
基 金:supported by the Youth Innovation Program of the Chinese Academy of Agricultural Sciences (grant no.Y2022QC06);the National Natural Science Foundation of China (grant nos.32001878,32172366);the Natural Science Foundation of Beijing (grant no.6222054);the China Agricultural Research System (CARS-23);the French Government (National Research Agency,ANR)through"Investments for the Future"LabEx SIGNALIFE (#ANR-11-LABX-0028-01),IDEX UCAJedi (#ANR-15-IDEX-0).
摘 要:Root-knot nematodes(RKNs)cause huge agricultural losses every year.They secrete a repertoire of effectors to facilitate parasitism through the induction of plant-derived giant feeding cells,which serve as their sole source of nutrients.However,the mode of action of these effectors and their targeted host pro-teins remain largely unknown.In this study,we investigated the role of the effector Mi2G02 in Meloidogyne incognita parasitism.Host-derived Mi2G02 RNA interference in Arabidopsis thaliana affected giant cell development,whereas ectopic expression of Mi2G02 promoted root growth and increased plant sus-ceptibility to M.incognita.We used various combinations of approaches to study the specific interactions between Mi2G02 and A.thaliana GT-3a,a trihelix transcription factor.GT-3a knockout in A.thaliana affected feeding-site development,resulting in production of fewer egg masses,whereas GT-3a overex-pression in A.thaliana increased susceptibility to M.incognita and also root growth.Moreover,we demon-strated that Mi2G02 plays a role in maintaining GT-3a protein stabilization by inhibiting the 26S proteasome-dependent pathway,leading to suppression of TOZ and RAD23C expression and thus promoting nematode parasitism.This work enhances our understanding of how a pathogen effector manipulates the role and regulation of a transcription factor by interfering with a proteolysis pathway to reprogram gene expression for development of nematode feeding cells.
关 键 词:Meloidogyne incognita EFFECTOR giant cell Mi2G02 transcription factor interaction
分 类 号:S432.45[农业科学—植物病理学]
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