Transcriptomic analysis reveals that hepatopancreatic necrosis disease in Eriocheir sinensis (Chinese mitten crabs) may be the result of autophagy and apoptosis

Massive economic losses have been caused by Hepatopancreas necrosis disease (HPND) to the Chinese mitten crab (Eriocheir sinensis) culture industry; however, the actual cause and pathological mechanisms is unknown. In this study, hepatopancreatic and intestinal cells of the diseased crabs showed distinctive pathological changes which were characteristic of autophagy and apoptosis, but no pathogens were observed. To understand the molecular pathogenesis, a transcriptomic analysis was conducted; approximately 21,523 (26,224) unigenes had COG (KEGG) annotations. The analysis of differentially expressed genes (DEGs) with fold changes > 2 and P < 0.05 between diseased crabs with mild symptoms (XHAF-1) and diseased crabs with severe symptoms (XHAF-2), and crabs without visible symptoms (XHAF-CK) in hepatopancreas showed that DEGs increased with the degree of hepatopancreatic necrosis. The DEGs of XHAF-1 vs XHAF-CK (XHAF-2 vs XHAF-CK) were enriched into 1191 (1366) gene ontology (GO) terms, including the positive regulation of phagocytosis, autophagic vacuole assembly and negative regulation of glial cell apoptotic processes. The DEGs of XHAF-1 vs XHAF-CK (XHAF-2 vs XHAF-CK) were enriched into 32 (45) KEGG pathways including autophagy and the p53 signaling pathway. Furthermore, the expression levels of genes related to autophagy and apoptosis were altered in diseased crabs, suggesting that HPND may be the result of autophagy and apoptosis. Moreover, expression of genes related to retinol metabolism disregulated, implying that the hepatopancreas of crabs with HPND turn from golden yellow/light yellow to almost white were associated with retinol metabolism dysregulation. These findings provide new clues in understanding of the etiology and pathogenesis of HPND.