Abstract
High temperature adversely affects plant growth and development. The steroid phytohormones brassinosteroids (BRs) are recognized to play important roles in plant heat stress responses and thermotolerance, but the underlying mechanisms remain obscure. Here, we demonstrate that the glycogen synthase kinase 3 (GSK3)-like kinase BRASSINOSTEROID INSENSITIVE2 (BIN2), a negative component in the BR signaling pathway, interacts with the master heat-responsive transcription factors CLASS A1 HEAT SHOCK TRANSCRIPTION FACTORS (HsfA1s). Furthermore, BIN2 phosphorylates HsfA1d on T263 and S56 to suppress its nuclear localization and inhibit its DNA-binding ability, respectively. BR signaling promotes plant thermotolerance by releasing the BIN2 suppression of HsfA1d to facilitate its nuclear localization and DNA binding. Our study provides insights into the molecular mechanisms by which BRs promote plant thermotolerance by strongly regulating HsfA1d through BIN2 and suggests potential ways to improve crop yield under extreme high temperatures.