Plants need to coordinate growth and stress responses to survive adverse environmental conditions. Recent evidence showed that plant steroid hormones, brassinosteroid (BRs), are involved in coordination of plant growth and various stress responses (Nolan et al., 2020 Plant Cell). BRs function through plasma membrane-localized receptors, negative regulator BIN2 kinase and other signaling components to control the activities of BES1/BZR1 family transcription factors, which regulate the expression of thousands of genes for plant growth and stress responses. We have previously reported that under drought and other stress conditions, BES1 is ubiquitinated by SINAT2 E3 ubiqutin ligase and targeted to selective autophagy for degradation via ubiquitin receptor DSK2 (Nolan et al., 2017. Developmental Cell; and Yang et al., 2017. Developmental Cell). We have further identified a F-box E3 ubiquitin ligase, BAF1, that interacts with BES1 and targets BES1 for degradation through autophagy. The loss-of-function mutant of BAF1 gene (baf1) displayed increased plant growth under BR biosynthesis inhibitor Brassinazole (BRZ). BES1 protein is more stable in baf1 mutant than wild-type plants. Consistent with the hypothesis that BAF1 targets BES1 degradation under stresses, baf1 mutants are more sensitive to sucrose starvation and less sensitive to stress hormone abscisic acid (ABA). We further found that BIN2 interacts with, phosphorylates and stabilizes BAF1, providing another mechanism by which BIN2 inhibits BES1 function. Finally, we discovered that expression of BAF1 increased BES1 autophagy but not general autophagy, suggesting that BAF1 ubiquitinates BES1 and selectively targets it to autophagy. Taken together, our results demonstrated that different E3 ubiquitin ligase function under different conditions to target BES1 to autophagy for degradation, thus precisely adjusting plant growth under changing environments. This work is supported by National Institute of Health (NIH 1R01GM120316-01A1) and the Plant Sciences Institute at Iowa State University.
Coauthors: Ping Wang – Iowa State University;Trevor Nolan – Iowa State University;Hongqing Guo – Iowa State University;Diane Bassham – Iowa State University;Justin Walley – Iowa State University