TCP transcription factors interact with ZED1-related kinases as components of the temperature-regulated immunity
TCP transcription factors interact with ZED1-related kinases as components of the temperature-regulated immunity
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TCP 转录因子与 ZED1 相关激酶相互作用，作为温度调节免疫的组成部分
DOI：
10.1111/pce.13515
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发表时间：
2019
期刊：
影响因子：
--
通讯作者：
Yuxin Hu
中科院分区：
文献类型：
--
作者：
Zhicai Wang;Dayong Cui;Cheng Liu;Jingbo Zhao;Jing Liu;Na Liu;Dingzhong Tang;Yuxin Hu
环境温度的升高通常会抑制植物的免疫，但环境温度对植物免疫的分子调控在很大程度上是未知的。我们之前报道了拟南芥hopz - ei - deficient 1 （ZED1）相关激酶（ZRKs）通过抑制NPR1-1， CONSTITUTIVE 1 （SNC1）的转录介导温度敏感免疫。在这里，我们进一步证明了核定位的ZED1和ZRKs促进了与TEOSINTE BRANCHED1， CYCLOIDEA和增殖细胞因子（TCP）转录因子相关的这种抑制作用。我们发现一些TCP成员可以与ZRKs发生物理相互作用，并被高温诱导。tcp的破坏导致轻度自身免疫表型，而TCP15的过表达可以抑制SNC1 -2中过表达SNC1激活的自身免疫。这些发现表明，TCP转录因子与核ZRK作为温度调节免疫的组成部分相关，揭示了植物环境温度调节免疫的可能分子机制。
The elevation of ambient temperature generally inhibits plant immunity, but the molecular regulations of immunity by ambient temperature in plants are largely elusive. We previously reported that the Arabidopsis HOPZ-ETI-DEFICIENT 1 (ZED1)-related kinases (ZRKs) mediate the temperature-sensitive immunity by inhibiting the transcription of SUPPRESSOR OF NPR1-1, CONSTITUTIVE 1 (SNC1). Here, we further demonstrate that the nucleus-localized ZED1 and ZRKs facilitate such inhibitory role in associating with the TEOSINTE BRANCHED1, CYCLOIDEA AND PROLIFERATING CELL FACTOR (TCP) transcription factors. We show that some of TCP members could physically interact with ZRKs and are induced by elevated temperature. Disruption of TCPs leads to a mild autoimmune phenotype, while overexpression of the TCP15 could suppress the autoimmunity activated by the overexpressed SNC1 in the snc1-2. These findings demonstrate that the TCP transcription factors associate with nuclear ZRK as components of the temperature-regulated immunity, which discloses a possible molecular mechanism underlying the regulation of immunity by ambient temperature in plants.