DET1 modulates ATAF1-repressed thermosensory elongation through ubiquitination in Arabidopsis.

The Arabidopsis transcription factor ATAF1 negatively regulates thermomorphogenesis by inhibiting the expression of key genes involved in thermoresponsive elongation. DET1-mediated ubiquitination promotes ATAF1 degradation. In response to warmer, non-stressful average temperatures, plants have evolved an adaptive morphologic response called thermomorphogenesis to increase their fitness. This adaptive morphologic development is regulated by transcription factors (TFs) that control the expression of heat-induced genes that gate thermoresponsive growth. No apical meristem (NAM), Arabidopsis thaliana-activating factor 1/2 (ATAF1/2), and cup-shaped cotyledon 2 (CUC2) (collectively known as NAC) TFs regulate morphogenesis and respond to temperature stress, but whether they regulate thermomorphogenesis remains largely unknown. Here, we identified ATAF1 as a negative regulator of thermomorphogenesis and revealed that the E3-ligase component de-etiolated 1 (DET1) mediated ATAF1 ubiquitination and degradation. Our results revealed that ATAF1 negatively regulates warm temperature-induced hypocotyl elongation and inhibits the expression of thermoresponsive genes. Moreover, ATAF1 directly targeted and repressed the expression of YUCCA 8 (YUC8) and phytochrome interacting factor 4 (PIF4), two key regulators involved in elongation. At the post-translational level, elevated ambient temperatures negatively modulated the stability of ATAF1 by inducing the DET1-mediated ubiquitination pathway. Our results demonstrated the presence of a DET1-ATAF1-PIF4/YUC8 control module for thermomorphogenesis in plants, which may increase fitness by fine-tuning thermoresponsive gene expression under warm temperatures.