Brassinosteroid-regulated transcription factors confer epigenetic changes that repress plant immunity.

Abstract

When organisms encounter pathogens, they rapidly activate complex defense programs to ensure survival. While these immune responses are vital, they often also incur trade-offs, such as reduced growth and development and must therefore be tightly controlled. In this study, we reveal that the steroid hormones brassinosteroids (BRs) contribute to this control in <i>Arabidopsis thaliana</i> by repressing immunity-related genes. We provide evidence that the BR-regulated basic helix-loop-helix (bHLH) transcription factor CESTA (CES), along with its homologs BR ENHANCED EXPRESSION (BEE)1-3, mediate DNA methylation changes at transposable element (TE)-rich loci containing nucleotide-binding leucine-rich-repeat (NLR)-type receptor genes, including <i>SUPPRESSOR OF NPR1-1 CONSTITUTIVE 1</i> (<i>SNC1</i>). These CES-induced methylation changes correlate with altered splicing of <i>SNC1</i> pre-mRNA, a process that requires the BR receptor BRASSINOSTEROID INSENSITIVE 1 (BRI1). In support, we show that CES associates with components of the chromatin remodeling and splicing machinery. Together, our findings reveal a previously unrecognized BR-induced mechanism that modulates the epigenetic and post transcriptional regulation of immune genes, enabling plants to prioritize growth over defense.