Changes in gluconeogenesis pathways and key genes associated with mass mortality in the clam Meretrix petechialis upon Vibrio infection

Abstract Mass mortality events frequently occur in marine bivalves growing in natural habitats and artificial culture environments due to pathogen infection. The clam Meretrix petechialis is an important commercial bivalve species, and the clam culture industry has suffered frequent mass mortality events during summer. However, the pathogenesis of the host is still poorly understood. In this study, M. petechialis was challenged with Vibrio parahaemolyticus, and the clams were sampled at different infection phases and physiological statuses. The transcriptome analysis of the clam hepatopancreas in the onset phase of Vibrio challenge showed the significant enrichment of multiple metabolism-related signaling pathways, including peroxisome proliferator-activated receptors (PPARs), adenosine 5′-monophosphate activated protein kinase (AMPK), phosphatidylinositol 3′-kinase (PI3K)-Akt signaling pathways and glycolysis/gluconeogenesis, which revealed the involvement of metabolism-related signaling pathways in host immune defense. Weighted correlation network analysis (WGCNA) revealed that key enzymes involved in gluconeogenesis were enriched in this phase, suggesting that gluconeogenesis may be associated with infection-induced mortality in clams. Examinations of the glucose content, phosphoenolpyruvate carboxykinase (PEPCK) activity and the expression of key genes involved in gluconeogenesis showed that gluconeogenesis was repressed during Vibrio infection. An analysis of the expression of eight key genes in the PI3K-Akt signaling pathway between moribund and surviving individuals implied that gluconeogenesis was related to clam mass mortality. The results might help us to understand the molecular mechanism of death outbreak events and provide potential markers to detect the physiological status of this clam species.