Transcriptome and eQTL analysis reveal the novel molecular mechanism underlying salt tolerance in the phytochrome B...

The phyB mutant exhibits robust salt tolerance via enhanced K⁺/Na⁺ homeostasis, proline accumulation, and membrane stability. Transcriptomics reveals PHYB coordinates a unique early-response network involving transcription factors, kinesins, and DNA metabolism. Integrated population eQTL analysis and transcriptional regulation prediction condense a core salt-tolerance module of four transcription factors, three kinesins, and six DNA metabolism genes. This study identifies actionable targets for genetic improvement of salt-tolerant varieties. Soil salinization poses a significant threat to global rice production, underscoring the urgent need to improve salt tolerance as a key strategy for ensuring food security. In this study, we report that the phytochrome B (phyB) mutant exhibits robust salt tolerance via enhanced K⁺/Na⁺ homeostasis, proline accumulation, and membrane stability. Transcriptomic profiling revealed that phyB modulates salt adaptation via transcription factor activity, DNA metabolism, and motor activity. Utilizing the salt-responsive expression quantitative trait loci (eQTL) data from global mini-core rice collection comprising 202 accessions, we systematically screened enriched Gene Ontology (GO) terms and predicted a set of core salt tolerance-related genes at genomic level in the phyB mutant. Transcriptional regulation analysis established a regulatory network in which four transcription factors potentially regulate three kinesin genes and six DNA metabolism-related genes. Luciferase (LUC) assays further confirmed that these transcription factors directly activate the promoters of downstream genes. Heterologous expression in yeast demonstrated that a representative transcription factor (Os10g0371100), a kinesin (Os05g0397900), and a DNA metabolism-related gene (Os01g0944900) significantly promoted yeast growth under salt stress conditions, indicating conserved functions. Collectively, these findings elucidate a novel molecular network through which PHYB deficiency enhances salt tolerance by integrating transcription factor activity, DNA metabolism, and motor activity, and provide a set of core candidate genes for the genetic improvement of salt tolerance in rice.