{"database":"iProX","file_versions":[],"scores":null,"additional":{"omics_type":["Proteomics"],"submitter":["Bo Peng"],"species":["Edwardsiella Tarda Eib202"],"full_dataset_link":["http://www.iprox.org/page/project.html?id=IPX0016951000"],"submitter_email":["pengb26@mail.sysu.edu.cn"],"submitter_affiliation":["Sun Yat-sen University"],"sample_protocol":[""],"repository":["iProX"],"data_protocol":[""],"additional_accession":[]},"is_claimable":false,"name":"Phosphoenolpyruvate carboxykinase controls Edwardsiella tarda virulence via oxaloacetate","description":"Understanding the metabolic basis of bacterial virulence is essential for developing anti-infective strategies. Phosphoenolpyruvate carboxykinase (PEPCK), encoded by pckA, is a key enzyme at the metabolic junction between the pyruvate cycle and the TCA cycle, but its role in virulence regulation remains largely unexplored. In this study, we generated a pckA deletion mutant, ΔpckA, in Edwardsiella tarda and investigated its impact on virulence, metabolism, and vaccine potential. The ΔpckA mutant exhibited increased antibiotic sensitivity, faster growth, reduced autoaggregation, and significantly attenuated virulence in a tilapia infection model. Quantitative proteomics revealed global downregulation of type III and type VI secretion systems (T3SS and T6SS) and upregulation of flagellar proteins. Mechanistically, accumulation of oxaloacetate (OAA) in the mutant suppressed T3SS/T6SS expression without affecting flagellar motility. Importantly, ΔpckA induced a robust immune response in zebrafish and conferred strong protection against lethal challenge, with relative percent survival values of 64% and 81.82% in zebrafish and tilapia, respectively. Taken together, our findings identify PEPCK as a critical metabolic regulator of E. tarda virulence and highlight ΔpckA as a promising live attenuated vaccine candidate.","dates":{"publication":"Wed May 06 00:00:00 GMT+01:00 2026"},"accession":"PXD078087","cross_references":{"TAXONOMY":["498217"]}}