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Transcription factor ANAC032 modulates JA/SA signalling in response to Pseudomonas syringae infection
Author(s) -
Allu Annapurna Devi,
Brotman Yariv,
Xue GangPing,
Balazadeh Salma
Publication year - 2016
Publication title -
embo reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.584
H-Index - 184
eISSN - 1469-3178
pISSN - 1469-221X
DOI - 10.15252/embr.201642197
Subject(s) - pseudomonas syringae , coronatine , jasmonic acid , biology , transcription factor , wrky protein domain , regulator , microbiology and biotechnology , arabidopsis , effector , sigma factor , transcriptional regulation , promoter , arabidopsis thaliana , genetics , gene , gene expression , mutant
Responses to pathogens, including host transcriptional reprogramming, require partially antagonistic signalling pathways dependent on the phytohormones salicylic (SA) and jasmonic (JA) acids. However, upstream factors modulating the interplay of these pathways are not well characterized. Here, we identify the transcription factor ANAC032 from Arabidopsis thaliana as one such regulator in response to the bacterial pathogen Pseudomonas syringae pv. tomato DC3000 ( Pst ). ANAC032 directly represses MYC2 activation upon Pst attack, resulting in blockage of coronatine‐mediated stomatal reopening which restricts entry of bacteria into plant tissue. Furthermore, ANAC032 activates SA signalling by repressing NIMIN1 , a key negative regulator of SA‐dependent defence. Finally, ANAC032 reduces expression of JA‐responsive genes, including PDF1.2A . Thus, ANAC032 enhances resistance to Pst by generating an orchestrated transcriptional output towards key SA‐ and JA‐signalling genes coordinated through direct binding of ANAC032 to the MYC2 , NIMIN1 and PDF1.2A promoters.