Begonia semperflorens is an important ornamental plant worldwide, but its practical application is severely limited by low temperature sensitivity. However, the molecular regulatory mechanisms underlying low temperature-induced anthocyanin biosynthesis remain unclear. In this study, we assembled a high-quality chromosome-level B. semperflorens genome. Through genomic and MYB gene family analysis, we identified a key transcription factor BsTT2, which directly binds to the BsDFR promoter and enhances its activity, thereby driving anthocyanin accumulation in B. semperflorens. Furthermore, using BsTT2 as bait, we identified its interacting protein BsAlfin2. Under low temperature-induced reactive oxygen species (ROS) signaling, BsAlfin2 undergoes nuclear translocation and forms a complex with BsTT2, synergistically enhancing the activation of the BsDFR promoter and significantly improving anthocyanin production efficiency. Based on these results, we propose a previously uncharacterized BsAlfin2/BsTT2-BsDFR regulatory module, which reveals a molecular links low-temperature ROS signaling to anthocyanin biosynthesis in B. semperflorens. In summary, this study not only provides chromosome-level genomic resources for B. semperflorens research but also elucidates a key molecular module in low temperature-induced anthocyanin biosynthesis regulatory pathway, laying a theoretical and data foundation for future studies on leaf color improvement and stress resistance breeding in Begonia.
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.
Xinhui Wang, Han Wang, Hongyu Wei et al.· Science Advances· 0 citations