Arabidopsis ZED1-related kinases mediate the temperature-sensitive intersection of immune response and growth homeostasis
Arabidopsis ZED1-related kinases mediate the temperature-sensitive intersection of immune response and growth homeostasis
复制标题
拟南芥 ZED1 相关激酶介导免疫反应和生长稳态的温度敏感交叉。
DOI：
10.1111/nph.14585
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发表时间：
2017-07-01
期刊：
影响因子：
9.4
通讯作者：
Hu, Yuxin
中科院分区：
文献类型：
--
作者：
Wang, Zhicai;Cui, Dayong;Hu, Yuxin
在没有病原体的情况下，植物免疫反应的激活会拮抗生长和发育，而这种自身免疫表型通常被环境温度的升高所抑制。然而，对环境温度敏感的免疫反应和生长的分子调控在很大程度上是难以捉摸的。基因筛选鉴定了拟南芥突变体zed1-D，其高温依赖性生长迟缓。采用分子、细胞学和遗传学相结合的方法来研究zed1-D温度敏感生长和免疫反应背后的分子基础。hopz - ei - deficient 1 （ZED1）的显性突变导致ZED1 - d的高温依赖性自身免疫和生长迟缓。zed1-D的自身免疫表型依赖于hopz活化的抗性1 （ZAR1）。在没有病原体的情况下，温度升高诱导ZED1和一些ZED1相关激酶（ZRKs）协同作用，通过调节NPR1-1 - CONSTITUTIVE 1 (SNC1) SUPPRESSOR的转录抑制免疫应答。我们的数据揭示了在没有病原体的情况下，ZRKs在环境温度敏感免疫反应中的作用，从而揭示了温度介导的免疫反应和植物生长交叉的可能分子机制。
Activation of the immune response in plants antagonizes growth and development in the absence of pathogens, and such an autoimmune phenotype is often suppressed by the elevation of ambient temperature. However, molecular regulation of the ambient temperature-sensitive intersection of immune response and growth is largely elusive.A genetic screen identified an Arabidopsis mutant, zed1-D, by its high temperature-dependent growth retardation. A combination of molecular, cytological and genetic approaches was used to investigate the molecular basis behind the temperature-sensitive growth and immune response in zed1-D.A dominant mutation in HOPZ-ETI-DEFICIENT 1 (ZED1) is responsible for a high temperature- dependent autoimmunity and growth retardation in zed1-D. The autoimmune phenotype in zed1-D is dependent on the HOPZ-ACTIVATED RESISTANCE 1 (ZAR1). ZED1 and some ZED1-related kinases (ZRKs) are induced by elevated temperature and function cooperatively to suppress the immune response by modulating the transcription of SUPPRESSOR OF NPR1-1 CONSTITUTIVE 1 (SNC1) in the absence of pathogens.Our data reveal a previously unidentified role of ZRKs in the ambient temperature-sensitive immune response in the absence of pathogens, and thus reveals a possible molecular mechanism underlying the temperature-mediated intersection of immune response and growth in plants.