Microcystin-LR-induced changes of hepatopancreatic transcriptome, intestinal microbiota, and histopathology of
Yu Zhang1, Zheyu Li1, Sergey Kholodkevich2
1State Key Lab of Urban Water Resource and Environment, School of Environment, Harbin Institute of Technology, Harbin 150090, China.
Abstract:
As a hepatotoxin, microcystin-LR (MC-LR) poses a great threat to aquatic organisms. In this research, the hepatopancreatic transcriptome, intestinal microbiota, and histopathology of Procambarus clarkii (P. clarkii) in response to acute MC-LR exposure were studied. RNA-seq analysis of hepatopancreas identified 372 and 781 differentially expressed genes (DEGs) after treatment with 10 and 40 μg/L MC-LR, respectively. Among the DEGs, 23 genes were immune-related and 21 genes were redox-related. GO functional enrichment analysis revealed that MC-LR could impact nuclear-transcribed mRNA catabolic process, cobalamin- and heme-related processes, and sirohydrochlorin cobaltochelatase activity of P. clarkii. In addition, the only significantly enriched KEGG pathway induced by MC-LR was galactose metabolism pathway. Meanwhile, sequencing of the bacterial 16S rRNA gene demonstrated that MC-LR decreased bacterial richness and diversity, and altered the intestinal microbiota composition. At the phylum level, after 96 h, the abundance of Verrucomicrobia decreased after treatment with 10 and 40 μg/L MC-LR, while Firmicutes increased in the 40 μg/L MC-LR-treated group. At the genus level, the abundances of 15 genera were significantly altered after exposure to MC-LR. Our research demonstrated that MC-LR exposure caused histological alterations such as structural damage of hepatopancreas and intestines. This research provides an insight into the mechanisms associated with MC-LR toxicity in aquatic crustaceans.
