Heat Shock-Induced Accumulation of the Glycogen Synthase Kinase 3-Like Kinase BRASSINOSTEROID INSENSITIVE 2 Promotes Early Flowering but Reduces Thermotolerance in .

Brassinosteroids (BRs) are essential plant growth- and development-regulating phytohormones. When applied exogenously, BRs ameliorate heat shock (HS)-induced cell damage and enhance plant thermotolerance; however, the molecular mechanism by which BRs regulate plant thermotolerance is unknown. In this study, by analyzing the thermotolerance of a series of BR signaling mutants and plants that overexpressed different BR signaling components, we obtained comprehensive data showing that BRASSINOSTEROID INSENSITIVE 2 (BIN2) plays a major role in mediating the crosstalk between BR signaling and plant HS responses. By RNA-Seq, 608 HS- and BIN2-regulated genes were identified. An analysis of the 1-kb promoter sequences of these genes showed enrichment of an abscisic acid (ABA) INSENSITIVE 5 (ABI5)-binding -element. Physiological studies showed that thermotolerance was reduced in mutant and plants but increased in the mutant, and that the mutation could recover the thermotolerance of plants to a wild-type level, suggesting that ABI5 functions downstream of BIN2 in regulating plant thermotolerance. Further, HS treatment increased the cellular abundance of BIN2. Both mutant and plants showed early flowering, while the loss-of-function mutant flowered late. Given these findings, we propose that under HS conditions plants increase BIN2 activity to promote early flowering and ensure species survival; however, this reduces the thermotolerance and survivability of individual plants partially by activating ABI5.