Abscisic acid-regulated stability of CmABF1 and CmBRM modulates salt tolerance in chrysanthemum via epigenetic regulation of <i>CmHSFA4</i>.

Abstract

Soil salinization poses a major threat to global agricultural productivity and plant biodiversity. The phytohormone abscisic acid (ABA) is central to plant adaptation to abiotic stress; however, the mechanisms by which ABA coordinates posttranslational modifications of signaling proteins with epigenetic regulation remain poorly understood. Here, we show that salt stress-induced ABA accumulation up-regulates <i>Heat Shock Factor 4</i> (<i>CmHSFA4</i>), a gene that is known to enhance chrysanthemum salt tolerance. The ABA responsive transcription factor ABRE binding factor 1 (CmABF1) binds to the <i>CmHSFA4</i> promoter to activate its expression and also recruits the chromatin remodeler BRAHMA (CmBRM) to repress transcription by limiting H3 lysine-4 trimethylation (H3K4me3) deposition. We further demonstrate that the ABA-activated sucrose non-fermenting-1-related protein kinase 2.2 (CmSnRK2.2) phosphorylates and stabilizes CmABF1, while concurrently phosphorylating and promoting CmBRM degradation under salt stress. This dual regulation enhances H3K4me3 enrichment at the <i>CmHSFA4</i> promoter, thereby inducing its transcription and conferring salt tolerance. Together, our findings reveal an ABA-SnRK2.2-ABF1/BRM signaling module that integrates phosphorylation-dependent protein stabilization and degradation with histone methylation dynamics to fine-tune salt stress-responsive gene expression in chrysanthemum.