Multi-omics reveal the mechanism of Plantaricin BM-1 in controlling yoghurt post-acidification by affecting the membrane and metabolism of Lactobacillus delbrueckii subsp. bulgaricus.

Abstract

The post-acidification of fermented milk is primarily caused by the sustained acid production of Lactobacillus delbrueckii subsp. bulgaricus during storage at ambient temperature, which significantly compromises product quality. Results from growth curves, acid production assays, and multiple microscopy techniques (laser scanning confocal microscopy, scanning electron microscopy, and transmission electron microscopy) collectively demonstrate that 256 AU/mL plantaricin BM-1 alters the morphology and cell membrane permeability of L. bulgaricus YR, reducing its acid production capacity while preserving its viability. Transcriptomic analysis revealed that this treatment significantly upregulated fatty acid metabolism and the gene LDB_RS05285, and downregulated atpE in L. bulgaricus YR. Metabolomics further revealed significant alterations in membrane-associated fatty acids and sterol lipids, corroborating BM-1's influence on cell membrane structure. Integrating observational, transcriptomic, and metabolomic data, it is concluded that 256 AU/mL plantaricin regulates post-fermentation acidification by modulating membrane permeability and structure, thereby controlling the expression of marker genes LDB_RS05285 and atpE. Storage experiments demonstrate that BM-1 addition maintains yoghurt pH ≥ 3.9 for 21 days at ambient temperature, effectively retarding post-acidification.