Chromatin accessibility and histone landscapes define immune signal-specific transcriptional reprogramming in Arabidopsis

ABSTRACT Plant immunity relies on dynamic reprogramming of the transcriptome, but the underlying regulatory mechanisms that modulate chromatin accessibility and thus transcriptional activity remain poorly defined. In this study, we explore how salicylic acid (SA) and the pathogen-associated molecular pattern (PAMP) peptide flg22 reprogram immune gene expression through epigenetic modifications in Arabidopsis thaliana . We integrated RNA-seq, ChIP-seq, and ATAC-seq data to show that exogenous SA and flg22 induce distinct, widespread patterns of chromatin remodeling and differential gene expression. SA predominantly promotes a coordinated increase in H3K4me3 and H3 acetylation (H3Ac), two histone marks that are strongly associated with enhanced chromatin accessibility, at defense-related loci. By contrast, flg22 mainly activates defense gene expression via H3Ac, with minimal changes in H3K4me3 levels, suggesting distinct epigenetic strategies. Greater chromatin accessibility was closely linked to the activation of immune-responsive genes and correlated positively with H3K4me3 and H3Ac levels. Network analysis highlighted central roles for NPR1 , ICS1 , PR1 , and proteasome-related genes in SA-triggered immunity. Collectively, our results reveal that SA and flg22 modulate immune gene expression through shared and unique chromatin-based pathways, offering insight into the epigenetic regulation of plant defense.