Peribacillus simplex P10 Enhances Salt Tolerance in Asparagus by Modulating Amino Acid and Phenylpropanoid Metabolism

While Peribacillus simplex has been reported to alleviate abiotic stress-induced damage in diverse plant species, its precise functional mechanism in mediating salt tolerance in asparagus remains unclear. The present study sought to uncover the molecular regulatory mechanisms through which strain P10 enhances the salt adaptability of asparagus seedlings. We investigated physiological responses, as well as transcriptomic and metabolomic alterations, in P10-inoculated asparagus seedlings grown under saline conditions. The results demonstrated that P10 inoculation alleviated salt-induced physiological damage by enhancing antioxidant enzyme activities and promoting the accumulation of osmotic regulatory substances. Comparative transcriptomic and metabolomic analyses identified 1659 differentially expressed genes (DEGs) and 128 differentially accumulated metabolites (DAMs) between P10-inoculated and non-inoculated seedlings under salt stress. These DEGs were primarily associated with multiple biological pathways, including phenylpropanoid biosynthesis, nitrogen metabolism, and flavonoid biosynthesis pathways (flavone, flavonol, and total flavonoid synthesis). Metabolomic profiling indicated that organic acids constituted the most abundant class of DAMs, followed by amino acids and their derivatives, and flavonoids. Integrated transcriptomic and metabolomic analyses suggested that P10 optimized the amino acid metabolic network under salt stress by upregulating genes involved in nitrogen assimilation, glutathione biosynthesis, and polyamine biosynthesis, thereby promoting amino acid accumulation and enhancing glutathione and polyamine levels. In addition, P10 markedly stimulated flavone and flavonol biosynthesis while maintaining elevated anthocyanin levels. Overall, P10 mitigated salt stress injury in asparagus by regulating amino acid metabolism to improve osmotic balance and growth stability, while simultaneously redirecting phenylpropanoid flux toward flavone and flavonol biosynthetic pathways to fine-tune stress responses.