Key Laboratory of Plant Molecular Physiology, CAS Center for Excellence in Molecular Plant Sciences, Institute of Botany, Chinese Academy of Sciences, Beijing, 100093, China.
University of Chinese Academy of Sciences, Beijing, 100049, China.
New Phytol. 2017 Jul;215(2):711-724. doi: 10.1111/nph.14585. Epub 2017 May 12.
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.
植物免疫反应的激活会在没有病原体的情况下拮抗生长和发育，而这种自身免疫表型通常会被环境温度的升高所抑制。然而，免疫反应和生长与环境温度敏感交叉的分子调控在很大程度上仍未被揭示。通过高温依赖性生长迟缓的表型，一个遗传筛选鉴定出拟南芥突变体 zed1-D。利用分子、细胞学和遗传学方法的组合，研究了 zed1-D 中温度敏感生长和免疫反应背后的分子基础。HOPZ-ETI-DEFICIENT 1（ZED1）中的显性突变是 zed1-D 中高温依赖性自身免疫和生长迟缓的原因。zed1-D 的自身免疫表型依赖于 HOPZ-ACTIVATED RESISTANCE 1（ZAR1）。高温诱导 ZED1 和一些 ZED1 相关激酶（ZRKs）的表达，并在没有病原体的情况下通过调节 SUPPRESSOR OF NPR1-1 CONSTITUTIVE 1（SNC1）的转录，共同抑制免疫反应。我们的数据揭示了 ZRKs 在没有病原体的情况下，对环境温度敏感免疫反应的先前未被识别的作用，从而揭示了植物中免疫反应和生长与温度介导交叉的可能分子机制。
