The Toxin Gene Protects from Gastrointestinal Stress.

is a major foodborne pathogen worldwide, responsible for seafood-associated poisoning. Among its toxin genes, is the most critical. To investigate the role of in under gastrointestinal conditions, we constructed deletion and complementation strains and compared their survival under acid (pH 3 and 4) and bile stress (2%). The results showed that expression was significantly upregulated under cold (4 °C) and bile stress (0.9%). Survival assays and PI staining revealed that the mutant strain (VP: △) was more sensitive to acid and bile stress than the wild-type (WT), and this sensitivity was rescued by complementation. These findings suggest that plays a protective role in enhancing tolerance to acid and bile stress. In the VP: △ strain, seven genes were significantly upregulated and six were downregulated as a result of deletion. These genes included (), (), (), and (ABC transporters), (), and (), among others. Additionally, LC-MS/MS analysis identified 12 differential metabolites between the WT and VP: △ strains, including phosphatidylserine (PS) (17:2 (9Z,12Z) /0:0 and 20:1 (11Z) /0:0), phosphatidylglycerol (PG) (17:0/0:0), flavin mononucleotide (FMN), and various nucleotides. The protective mechanism of may involve preserving cell membrane permeability through regulation of and ABC transporters and enhancing electron transfer efficiency via regulation of . The resulting reduction in ATP, DNA, and RNA synthesis-along with changes in membrane permeability and electron transfer due to decreased FMN-likely contributed to the reduced survival of the VP: △ strain. Meanwhile, the cells actively synthesized phospholipids to repair membrane damage, leading to increased levels of PS and PG. This study provides important insights into strategies for preventing and controlling food poisoning caused by .