Novel JAZ co‐operativity and unexpected JA dynamics underpin Arabidopsis defence responses to Pseudomonas syringae infection. Issue 3 (2nd October 2015)

• Record Type: Journal Article
• Authors: de Torres Zabala, Marta; Zhai, Bing; Jayaraman, Siddharth; Eleftheriadou, Garoufalia; Winsbury, Rebecca; Yang, Ron; Truman, William; Tang, Saijung; Smirnoff, Nicholas; Grant, Murray
• Is Part Of: New phytologist. Volume 209:Issue 3(2016)
• Page Start: 1120
• Page End: 1134
• Publication Date: 2015-10-02
• Subjects: Arabidopsis thaliana -- hormone -- jasmonic acid (JA) -- JAZ -- Pseudomonas syringae; Botany -- Periodicals; 580
• DOI: 10.1111/nph.13683
• Languages: English
• ISSNs: 0028-646X

Abstract

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 DC3000 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 DC3000 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. JAZs contribute to early basal and subsequent secondary plant defence responses. We showed that JAZ5 and JAZ10 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 MYC2 and related MYC3 and MYC4 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.