ABI5-mediated ABA signaling enhances aliphatic glucosinolates biosynthesis by transcriptionally suppressing BR signaling factors in Arabidopsis

Brassinosteroids (BRs) are key regulators of plant growth and have been implicated in suppressing glucosinolates (GSLs) biosynthesis in Brassicaceae species, including Arabidopsis thaliana. However, the molecular mechanism linking BR signaling to transcriptional control of the aliphatic GSL pathway remains unclear. Here, we provide genetic and molecular evidence that the BR-responsive transcription factor BZR1 negatively regulates aliphatic GSL biosynthesis through interaction with TOPLESS (TPL) family corepressors and the histone deacetylase HISTONE DEACETYLASE 19 (HDA19). The gain-of-function mutant bzr1-1D exhibited reduced accumulation of aliphatic glucosinolates (GSLs), whereas disruption of TPL family genes (tpl, tpr1, tpr4) or HDA19 resulted in elevated GSL levels, supporting a repressive role for the BZR1-associated complex in the regulation of GSL biosynthetic gene expression. Furthermore, we uncover a functional connection between ABA and BR signaling in this process. The ABA-responsive transcription factor ABI5 reduces the expression of UBP12 and UBP13, which encode deubiquitinases known to influence BZR1 stability. Genetic and transcriptional analyses indicate that ABI5-mediated attenuation of the UBP12/13-BZR1 pathway contributes to enhanced aliphatic GSL accumulation under ABA treatment. Collectively, our findings delineate a regulatory framework linking ABA and BR signaling pathways and suggest that modulation of the UBP12/13-BZR1 module by ABI5 integrates growth and defense responses by fine-tuning aliphatic GSLs biosynthesis in Arabidopsis. One sentence summaryan ABA signaling factor, ABI5 acts to suppress expression of brassinosteroids (BR) hormone signaling genes like UBP12, UBP13, and BZR1 to promote biosynthesis of defensive secondary metabolites, glucosinolates (GSLs) in Arabidopsis.