Piecyk, R. S. | bioRxiv Science

bioRxiv2026

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

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 1,2. In this study, we reveal that the steroid hormones brassinosteroids (BRs) contribute to this control in Arabidopsis thaliana 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 SUPPRESSOR OF NPR1-1 CONSTITUTIVE 1 (SNC1). These CES-induced methylation changes correlate with altered splicing of SNC1 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. Significance statementSteroid hormones are powerful regulators of growth but also act as potent suppressors of immunity, with well-established clinical applications, for example in treating autoimmune diseases in humans. In plants, the steroid hormones brassinosteroids (BRs) exert similar effects. Here, we uncover that BR-mediated immune suppression involves DNA methylation changes and alternative splicing of a subset of immune receptor genes, that govern resistance responses mediated by the plant hormone salicylic acid. We provide evidence for a function of specific bHLH transcription factors in this process that link BR signaling to chromatin remodelling and RNA processing. Thereby our study reveals a novel mode of steroid hormone activity in immune repression, which involves epigenetic and posttranscriptional adjustment of immune receptor function.

plant biology↗

bioRxiv2022

Parental pericentromeric methylation status drives methylome remodelling and heterosis in epigenetic hybrids

Heterosis is the superior phenotypic performance of F1 hybrids relative to their parents. Although this phenomenon is extensively exploited commercially, its molecular causes remain elusive. A central challenge is to understand how specific features of parental (epi)genomes contribute to the widespread functional remodelling that occurs in hybrids. Using Arabidopsis, we show that differentially methylated regions (DMRs) in parental pericentromeres act as major re-organizers of hybrid methylomes and transcriptomes, even in the absence of genetic variation. We demonstrate that these parental DMRs facilitate methylation changes in the hybrids not only in cis, but also in trans at thousands of target regions throughout the genome. Many of these trans-induced changes facilitate the expression of nearby genes, and are significantly associated with phenotypic heterosis. Our study establishes the epigenetic status of parental pericentromeres as an important predictor of heterosis and elucidates its pleiotropic potential in the functional remodelling of hybrid genomes.

genomics↗