GPAT3 facilitates AHPND-causing Vibrio parahaemolyticus pathogenesis by driving lipid droplets accumulation in shrimp

Acute hepatopancreatic necrosis disease (AHPND), caused by a specific strain of Vibrio parahaemolyticus (Vp_AHPND), disrupts host immune function by promoting the accumulation of lipid droplets (LDs). However, the underlying mechanisms and physiological consequences of LDs accumulation during Vp_AHPND infection in shrimp remain poorly characterized. In this study, we investigate the role of Penaeus vannamei glycerol-3-phosphate acyltransferase 3 (PvGPAT3), a key enzyme in triglyceride and LDs biosynthesis, during Vp_AHPND infection. Transcriptomic analysis and quantitative real-time PCR (qRT-PCR) revealed that PvGPAT3 expression is significantly upregulated following Vp_AHPND infection. Functional assays demonstrated that silencing PvGPAT3 via RNA interference (RNAi) improved shrimp survival and restricted bacterial proliferation, whereas its knockdown attenuated infection-induced LDs accumulation. Conversely, overexpression of PvGPAT3 in High Five cells significantly promoted LDs formation. Mechanistic studies further indicated that PvGPAT3-mediated LDs accumulation contributes to mitochondrial dysfunction and subsequent apoptosis. Collectively, these findings suggest that PvGPAT3 exacerbates Vp_AHPND pathogenesis by inducing mitochondrial dysfunction and apoptosis through the promotion of LDs accumulation.