Kim Jae Young, Park Young-Joon, Lee June-Hee, Kim Zee Hwan, Park Chung-Mo
Department of Chemistry, Seoul National University, Seoul 08826, Korea.
Plant Genomics and Breeding Institute, Seoul National University, Seoul 08826, Korea.
Plant Cell Physiol. 2021 Sep 24;62(4):708-720. doi: 10.1093/pcp/pcab028.
The gaseous phytohormone ethylene plays vital roles in diverse developmental and environmental adaptation processes, such as fruit ripening, seedling establishment, mechanical stress tolerance and submergence escape. It is also known that in the light, ethylene promotes hypocotyl growth by stimulating the expression of PHYTOCHROME INTERACTING FACTOR3 (PIF3) transcription factor, which triggers microtubule reorganization during hypocotyl cell elongation. In particular, ethylene has been implicated in plant responses to warm temperatures in recent years. However, it is currently unclear how ethylene signals are functionally associated with hypocotyl thermomorphogenesis at the molecular level. Here, we show that ETHYLENE-INSENSITIVE3 (EIN3)-mediated ethylene signals attenuate hypocotyl thermomorphogenesis by suppressing auxin response. At warm temperatures, when the activity of the PIF4 thermomorphogenesis promoter is prominently high, the ethylene-activated EIN3 transcription factor directly induces the transcription of ARABIDOPSIS PP2C CLADE D7 (APD7) gene encoding a protein phosphatase that inactivates the plasma membrane (PM) H+-ATPase proton pumps. In conjunction with the promotive role of the PM H+-ATPases in hypocotyl cell elongation, our observations strongly support that the EIN3-directed induction of APD7 gene is linked with the suppression of auxin-induced cell expansion, leading to the reduction in thermomorphogenic hypocotyl growth. Our data demonstrate that APD7 acts as a molecular hub that integrates ethylene and auxin signals into hypocotyl thermomorphogenesis. We propose that the ethylene-auxin signaling crosstalks via the EIN3-APD7 module facilitate the fine-tuning of hypocotyl thermomorphogenesis under natural environments, which often fluctuate in a complex manner.
气态植物激素乙烯在多种发育和环境适应过程中发挥着至关重要的作用，如果实成熟、幼苗建立、机械胁迫耐受性和淹水逃避。还已知在光照条件下，乙烯通过刺激光敏色素相互作用因子3（PIF3）转录因子的表达来促进下胚轴生长，该转录因子在胚轴细胞伸长过程中触发微管重组。特别是，近年来乙烯已被证明与植物对温暖温度的反应有关。然而，目前尚不清楚乙烯信号在分子水平上如何与下胚轴热形态建成功能相关。在这里，我们表明乙烯不敏感3（EIN3）介导的乙烯信号通过抑制生长素反应来减弱下胚轴热形态建成。在温暖温度下，当PIF4热形态建成促进子的活性显著较高时，乙烯激活的EIN3转录因子直接诱导编码一种使质膜（PM）H + -ATPase质子泵失活的蛋白磷酸酶的拟南芥PP2C家族D7（APD7）基因的转录。结合PM H + -ATPase在下胚轴细胞伸长中的促进作用，我们的观察结果有力地支持了EIN3对APD7基因的诱导与生长素诱导的细胞扩张的抑制有关，导致热形态建成的下胚轴生长减少。我们的数据表明，APD7作为一个分子枢纽，将乙烯和生长素信号整合到下胚轴热形态建成中。我们提出，通过EIN3 - APD7模块的乙烯 - 生长素信号串扰有助于在自然环境（通常以复杂方式波动）下对下胚轴热形态建成进行微调。
