GCN5 restricts PRX-dependent lignin deposition during salt stress in Arabidopsis

Abstract

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 under NaCl stress 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 under salt stress 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 upstream transcription factors (TFs), including GATA21 and MYBS2, 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.