Аннотация:BRASSINAZOLE RESISTANT 1 (BZR1), the critical regulator of brassinosteroid (BR) response, participates in various BR-mediated developmental processes. However, the roles of BZR1 in stress tolerance are less clear. Here, we found that BZR1-like protein in tomato controls BR response and is involved in thermotolerance by regulating the FERONIA (FER) homologs. The CRISPR-bzr1 mutant showed reduced growth and was not responsive to 24-epibrassinolide (EBR) with regard to the promotion of plant growth. Mutation in BZR1 impaired the induction of RESPIRATORY BURST OXIDASE HOMOLOG1 (RBOH1), production of H2O2 in the apoplast and heat tolerance. Exogenous H2O2 recovered the heat tolerance of the tomato bzr1 mutant. Overexpression of BZR1 enhanced the production of apoplastic H2O2 and heat stress responses. However, silencing of RBOH1 abolished the BZR1-mediated heat tolerance. Further analysis showed that BZR1 bound to the promoters of FERONIA2 (FER2) and FER3 and induced their expression. Silencing of FER2/3 suppressed BZR1-dependent BR signaling for the induction of RBOH1 transcripts, accumulation of apoplastic H2O2 and heat tolerance. These results indicate that BZR1 regulates heat stress responses in tomato through RBOH1-dependent reactive oxygen species (ROS) signaling, which is at least partially mediated by FER2 and FER3.
