Abstract

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 ( Pv GPAT3), 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 Pv GPAT3 via RNA interference (RNAi) improved shrimp survival and restricted bacterial proliferation, whereas its knockdown attenuated infection-induced LDs accumulation. Conversely, overexpression of Pv GPAT3 in High Five cells significantly promoted LDs formation. Mechanistic studies further indicated that Pv GPAT3-mediated LDs accumulation contributes to mitochondrial dysfunction and subsequent apoptosis. Collectively, these findings suggest that Pv GPAT3 exacerbates Vp AHPND pathogenesis by inducing mitochondrial dysfunction and apoptosis through the promotion of LDs accumulation.