Aug 2026· Science Advances· Vol 12· 0 citations· 67 references
Medicine
TL;DR
It is shown that salt stress–induced ABA accumulation up-regulates Heat Shock Factor 4 (CmHSFA4), a gene that is known to enhance chrysanthemum salt tolerance, and 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 is revealed.
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 Heat Shock Factor 4 (CmHSFA4), a gene that is known to enhance chrysanthemum salt tolerance. The ABA responsive transcription factor ABRE binding factor 1 (CmABF1) binds to the CmHSFA4 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 CmHSFA4 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.
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