IBR5 Modulates Temperature-Dependent, R Protein CHS3-Mediated Defense Responses in Arabidopsis.
IBR5 Modulates Temperature-Dependent, R Protein CHS3-Mediated Defense Responses in Arabidopsis.
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DOI：
10.1371/journal.pgen.1005584
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发表时间：
2015-10
期刊：
影响因子：
4.5
通讯作者：
Yang S
中科院分区：
文献类型：
--
作者：
Liu J;Yang H;Bao F;Ao K;Zhang X;Zhang Y;Yang S
植物对低温的反应与防御反应密切相关。我们先前表征了由Toll和白细胞介素1受体-核苷酸结合-富含亮氨酸重复序列（TIR-NB-LRR）-型抗性（R）蛋白的激活引起的冷冻敏感突变体chs 3 -1，所述抗性（R）蛋白具有C-末端LIM（Lin-11、Isl-1和Mec-3结构域）结构域。在这里，我们报告的chs 3，ibr 5 -7（吲哚-3-丁酸反应5），这在很大程度上抑制寒冷激活的防御反应的抑制剂的鉴定。IBR 5编码一种推定的双特异性蛋白磷酸酶。CHS 3蛋白在低温下的积累受到IBR 5突变的抑制。此外，chs 3赋予的防御表型协同抑制的突变HSP 90和IBR 5。进一步的分析表明，具有保持酶活性的IBR 5与CHS 3，HSP 90和SGT 1b（skp 1的G2等位基因的抑制因子）物理结合，形成保护CHS 3的复合物。除了IBR 5在调节CHS 3中的积极作用外，IBR 5还参与由R基因介导的防御反应，包括SNC 1（Suppressor of npr 1 -1，Constitutive 1）、RPS 4（Resistance to P. degringae 4）和RPM 1（Resistance to Pseudomonas degringae pv. maculicola 1）。因此，本研究的结果揭示了IBR 5在调节多种R蛋白介导的防御反应中的作用。抗性基因在识别病原菌和引发植物防御反应中起着重要作用。CHS 3编码一种TIR-NB-LRR型R蛋白，其C-末端具有LIM结构域。CHS 3的一个点突变激活了低温胁迫下的防御反应。在这里，我们确定和特点ibr 5 -7，一个突变体，抑制寒冷诱导的防御反应的chs 3 -1。我们观察到chs 3 -1突变体中增强的防御反应和细胞死亡协同依赖于IBR 5和HSP 90。IBR 5与CHS 3物理相互作用，与SGT 1b/HSP 90形成复合物。此外，IBR 5还参与SNC 1、RPS 4和RPM 1介导的R基因抗性。因此，IBR 5在调节多种R蛋白介导的防御反应中起关键作用。
Plant responses to low temperature are tightly associated with defense responses. We previously characterized the chilling-sensitive mutant chs3-1 resulting from the activation of the Toll and interleukin 1 receptor-nucleotide binding-leucine-rich repeat (TIR-NB-LRR)-type resistance (R) protein harboring a C-terminal LIM (Lin-11, Isl-1 and Mec-3 domains) domain. Here we report the identification of a suppressor of chs3, ibr5-7 (indole-3-butyric acid response 5), which largely suppresses chilling-activated defense responses. IBR5 encodes a putative dual-specificity protein phosphatase. The accumulation of CHS3 protein at chilling temperatures is inhibited by the IBR5 mutation. Moreover, chs3-conferred defense phenotypes were synergistically suppressed by mutations in HSP90 and IBR5. Further analysis showed that IBR5, with holdase activity, physically associates with CHS3, HSP90 and SGT1b (Suppressor of the G2 allele of skp1) to form a complex that protects CHS3. In addition to the positive role of IBR5 in regulating CHS3, IBR5 is also involved in defense responses mediated by R genes, including SNC1 (Suppressor of npr1-1, Constitutive 1), RPS4 (Resistance to P. syringae 4) and RPM1 (Resistance to Pseudomonas syringae pv. maculicola 1). Thus, the results of the present study reveal a role for IBR5 in the regulation of multiple R protein-mediated defense responses. Resistance (R) genes play central roles in recognizing pathogens and triggering plant defense responses. CHS3 encodes a TIR-NB-LRR-type R protein harboring a C-terminal LIM domain. A point mutation in CHS3 activates the defense response under chilling stress. Here we identified and characterized ibr5-7, a mutant that suppresses the chilling-induced defense responses of chs3-1. We observed that the enhanced defense responses and cell death in the chs3-1 mutant are synergistically dependent on IBR5 and HSP90. IBR5 physically interacts with CHS3, forming a complex with SGT1b/ HSP90. Moreover, IBR5 is also involved in the R-gene resistance mediated by SNC1, RPS4 and RPM1. Thus, IBR5 plays key roles in regulating defense responses mediated by multiple R proteins.