Premium
Novel JAZ co‐operativity and unexpected JA dynamics underpin A rabidopsis defence responses to P seudomonas syringae infection
Author(s) -
Torres Zabala Marta,
Zhai Bing,
Jayaraman Siddharth,
Eleftheriadou Garoufalia,
Winsbury Rebecca,
Yang Ron,
Truman William,
Tang Saijung,
Smirnoff Nicholas,
Grant Murray
Publication year - 2016
Publication title -
new phytologist
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.742
H-Index - 244
eISSN - 1469-8137
pISSN - 0028-646X
DOI - 10.1111/nph.13683
Subject(s) - jasmonate , pseudomonas syringae , jasmonic acid , coronatine , biology , repressor , microbiology and biotechnology , mutant , transcription factor , arabidopsis , genetics , salicylic acid , pathogen , gene
Summary Pathogens target phytohormone signalling pathways to promote disease. Plants deploy salicylic acid ( SA )‐mediated defences against biotrophs. Pathogens antagonize SA immunity by activating jasmonate signalling, for example Pseudomonas syringae pv. tomato DC 3000 produces coronatine ( COR ), a jasmonic acid ( JA ) mimic. This study found unexpected dynamics between SA , JA and COR and co‐operation between JAZ jasmonate repressor proteins during DC 3000 infection. We used a systems‐based approach involving targeted hormone profiling, high‐temporal‐resolution micro‐array analysis, reverse genetics and mRNA ‐seq. Unexpectedly, foliar JA did not accumulate until late in the infection process and was higher in leaves challenged with COR ‐deficient P. syringae or in the more resistant JA receptor mutant coi1 . JAZ regulation was complex and COR alone was insufficient to sustainably induce JAZ s. JAZ s contribute to early basal and subsequent secondary plant defence responses. We showed that JAZ 5 and JAZ 10 specifically co‐operate to restrict COR cytotoxicity and pathogen growth through a complex transcriptional reprogramming that does not involve the basic helix‐loop‐helix transcription factors MYC 2 and related MYC 3 and MYC 4 previously shown to restrict pathogen growth. mRNA ‐seq predicts compromised SA signalling in a jaz5/10 mutant and rapid suppression of JA ‐related components on bacterial infection.