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The IBI1 Receptor ofβ-Aminobutyric Acid Interacts with VOZ Transcription Factors to Regulate Abscisic Acid Signaling and Callose-Associated Defense

作     者:Roland E.Schwarzenbacher Grace Wardell Joost Stassen Emily Guest Peijun Zhang Estrella Luna Jurriaan Ton Roland E.Schwarzenbacher;Grace Wardell;Joost Stassen;Emily Guest;Peijun Zhang;Estrella Luna;Jurriaan Ton

作者机构:P3 Institute for Plant and Soil BiologyDepartment of Animal and Plant SciencesThe University of SheffieldSheffield S102TNUK School of BiosciencesUniversity of BirminghamBirmingham B152TTUK 

出 版 物:《Molecular Plant》 (分子植物(英文版))

年 卷 期:2020年第13卷第10期

页      面:1455-1469页

核心收录:

学科分类:0710[理学-生物学] 071001[理学-植物学] 07[理学] 0901[农学-作物学] 0902[农学-园艺学] 

基  金:the European Research Council(ERC,no.309944,“Prime-A-Plant”) J.T..a Research Leadership Award from the Leverhulme Trust(no.RL-2012-042) J.T..a BBSRC-IPA grant to J.T.(BB/P006698/1) J.T..and an ERC-PoC grant to J.T.(no.824985,“ChemPrime”) 

主  题:IBI1 priming abscisic acid β-aminobutyric acid callose E-MTAB-8720 

摘      要:Extemal and internal signals can prime the plant immune system for a faster and/or stronger response to pathogen attack.β-aminobutyric acid(BABA)is an endogenous stress metabolite that induces broad-spectrum disease resistance in *** perception in Arabidopsis is mediated by the aspartyl tRNA synthetase IBI1,which activates priming of multiple immune responses,including callose-associated cell wall defenses that are under control by abscisic acid(ABA).However,the immediate signaling components after BABA perception by IBI1,as well as the regulatory role of ABA therein,remain ***,we have studied the early signaling events controlling IBI1-dependent BABA-induced resistance(BABAIR),using untargeted transcriptome and protein interaction *** analysis revealed that IBI1-dependent expression of BABA-IR against the biotrophic oomycete Hyaloperonospora arabidopsidis is associated with suppression of ABA-inducible abiotic stress *** interaction studies identified the VOZ1 and VOZ2 transcription factors(TFs)as IBI1-interacting partners,which are transcrip-tionally induced by ABA but suppress pathogen-induced expression of ABA-dependent ***,we show that VOZ TFs require nuclear localization for their contribution to BABA-IR by mediating augmented expression of callose-associated ***,our study indicates that the IBI1-VOZ signaling module channels pathogen-induced ABA signaling toward cell wall defense while simultaneously suppressing abiotic stress-responsive genes.

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