ORE1 stabilizes PIF4 protein through a UBP12-dependent regulatory module in thermomorphogenesis

Understanding how plants integrate developmental programs with temperature-responsive growth remains a central challenge in thermal biology. Here, we uncover a previously unrecognized mechanism by which a canonical senescence regulator directly governs thermomorphogenesis in Arabidopsis. We show that ORESARA1 (ORE1), best known for orchestrating leaf senescence, plays an indispensable role in warm temperature-induced elongation growth. Mutant plants of ore1 display significantly reduced hypocotyl and petiole elongation and attenuated induction of the thermoresponsive genes IAA19 and YUC8. ORE1 acts upstream of PHYTOCHROME INTERACTING FACTOR 4 (PIF4), the central transcriptional hub for thermomorphogenesis, not by altering its transcript abundance but by stabilizing PIF4 protein specifically under warmth. ORE1 physically interacts with PIF4 in the nucleus and enhances its deubiquitination. We further identify the deubiquitinase UBP12 as a critical component of this pathway: UBP12 is required for PIF4 accumulation and thermomorphogenic growth, yet PIF4 does not bind UBP12 directly. Instead, our biochemical and genetic analyses support a model in which ORE1 functions as a scaffold, to recruit PIF4 to an ORE1-UBP12 complex that positions UBP12 for PIF4 deubiquitination. This UBP12-ORE1-PIF4 module defines a new mechanistic paradigm whereby a senescence regulator controls thermomorphogenesis by orchestrating deubiquitinase-mediated tuning of PIF4 proteostasis.