GCN5 negatively regulates class III peroxidases PRX71 and PRX33 to promote lignin deposition in Arabidopsis

Histone acetylation shapes transcriptional programs during environmental stress. The Arabidopsis histone acetyltransferase GCN5 (HAG1), a catalytic subunit of the SAGA complex, has been implicated in salt stress responses and cell wall integrity. Here, we show that loss of GCN5 enhances reactive oxygen species (ROS) accumulation and is accompanied by altered expression of class III peroxidase genes, with strong salt-induced upregulation of PRX71 and elevated basal PRX33 transcript abundance. Consistent with a role for these peroxidases in stress-associated cell wall remodeling, overexpression of PRX71 or PRX33 in the wild type is sufficient to promote ectopic lignin deposition in roots. Conversely, prx71 and prx33 mutants show improved growth on salt and on the cellulose biosynthesis inhibitor isoxaben, and they lack the pronounced ectopic root lignification observed in gcn5 under salt stress. Chromatin immunoprecipitation followed by qPCR (ChIP-qPCR) reveals reduced H3K9 acetylation at PRX71 and PRX33 promoter regions in gcn5 compared with the wild type, and reduced transcript abundance of candidate transcription factors (TFs), including MYBS2 and GATA21, accompanied by reduced H3K9ac at their loci. Together, our results support a model in which GCN5 constrains PRX71/PRX33-mediated lignification during stress, likely through an indirect regulatory route that integrates chromatin state and transcription factor activity to limit stress-associated lignification while maintaining root growth under salt stress.