Novel JAZ co-operativity and unexpected JA dynamics underpin Arabidopsis defence responses to Pseudomonas syringae infection.

Novel JAZ co-operativity and unexpected JA dynamics underpin Arabidopsis defence responses to Pseudomonas syringae infection.
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DOI:
10.1111/nph.13683
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发表时间:
2016-02
期刊:
The New phytologist
影响因子:
--
通讯作者:
Grant M
Grant M
中科院分区:
其他
文献类型:
--
作者:
de Torres Zabala M;Zhai B;Jayaraman S;Eleftheriadou G;Winsbury R;Yang R;Truman W;Tang S;Smirnoff N;Grant M

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病原体靶向植物激素信号通路以促进疾病。植物部署水杨酸(SA)介导的防御对biotrophs。病原体通过激活茉莉酸信号传导来拮抗SA免疫,例如假单胞菌(Pseudomonaserichingae pv.)番茄DC 3000产生茉莉酸(JA)模拟物冠菌素(COR)。这项研究发现了SA,JA和COR之间的意外动力学以及DC 3000感染期间JAZ茉莉酸酯阻遏蛋白之间的合作。我们使用了一种基于系统的方法,包括靶向激素分析、高时间分辨率微阵列分析、反向遗传学和mRNA测序。出乎意料的是,叶片JA直到感染过程的后期才积累,并且在用COR缺陷型P. degeneriae或更具抗性的JA受体突变体coi 1攻击的叶片中更高。JAZ调节是复杂的,单独的COR不足以可持续地诱导JAZ。 JAZ有助于早期的基础和随后的次生植物防御反应。我们发现JAZ 5和JAZ 10通过复杂的转录重编程特异性地合作限制COR细胞毒性和病原体生长,该转录重编程不涉及基本的螺旋-环-螺旋转录因子MYC 2和先前显示限制病原体生长的相关MYC 3和MYC 4。mRNA-seq预测jaz 5/10突变体中SA信号传导受损以及细菌感染时JA相关组分的快速抑制。
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 JAZs. 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.