RNA-seq analysis reveals transcriptome changes in livers from Efcab4b knockout mice

Le résumé fourni par la source

EFCAB4B is an evolutionarily conserved protein that encodes for the Rab GTPase Rab46, and the CRAC channel modulator, CRACR2A. Previous genome wide association studies have demonstrated the association of EFCAB4B variants in the progression of non-alcoholic fatty liver disease (NAFLD). In this study we show that mice with global depletion of Efcab4b −/− have significantly larger livers than their wild-type (WT) counterparts. We performed RNA-sequencing (RNA-seq) analysis of liver tissues to investigate differential global gene expression among Efcab4b −/− and WT mice. Of the 69 differentially expressed genes (DEGs), analyses of biological processes found significant enrichment in liver and bile development, with 6 genes ( Pck1, Aacs, Onecut1, E2f8, Xbp1, and Hes1 ) involved in both processes. Specific consideration of possible roles of DEGs or their products in NAFLD progression to (NASH) and hepatocarcinoma (HCC), demonstrated DEGs in the livers of Efcab4b −/− mice had roles in molecular pathways including lipid metabolism, inflammation, ER stress and fibrosis. The results in this study provide additional insights into molecular mechanisms responsible for increasing susceptibility of liver injuries associated with EFCAB4B . • Efcab4b, a gene with variations associated with non-alcoholic fatty liver disease, is successfully knocked out in mice. • Efcab4b deletion in mice induces larger livers with inflammatory foci. • Efcab4b deletion evokes differential changes in liver gene expression. • Differentially expressed genes have roles in liver function and potential roles in pathological signaling pathways

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