Brassinosteroid-mediated shoot branching in tomato requires SRT1-dependent histone deacetylation

Shoot branching is a crucial agronomic trait influencing crop yield. Multiple transcription factors orchestrate a sophisticated regulatory network to control shoot branching in response to internal and external cues. However, the role of epigenetic modification in shoot branching is less clear. Here, we found that SIRTUIN1 (SlSRT1), a histone deacetylase, promotes shoot branching by regulating transcription in lateral buds in response to brassinosteroid signaling in tomato (Solanum lycopersicum). SlSRT1 interacted with BRASSINAZOLE-RESISTANT 1 (SlBZR1), a critical component of brassinosteroid signaling, to repress the transcription of RELATED TO ABI3/VP1 1 (SlRAV1) and BRANCHED1 (SlBRC1) by decreasing H3K9 acetylation. SlBRC1 and SlRAV1 both inhibited shoot branching in tomato. Intriguingly, the genetic analysis, spatiotemporal expression of SlBRC1 and SlRAV1, and the transcriptomes in the buds of slbrc1 and slrav1 mutants indicated that SlBRC1 and SlRAV1 function by partially independent mechanisms. Our results demonstrate that SlSRT1-dependent histone deacetylation is essential for brassinosteroid regulation of shoot branching.