Sex-biased expression differences unique to adult liver were enriched for growth hormone-responsiveness.
We found, in a gene set enrichment analysis, that the genes with the most significant negative correlations with miRNAs in liver were enriched for cell adhesion molecules.
Consistent with our findings, they saw that CpGs hypomethylated in fetal liver were enriched among genes encoding components of steroid and lipid metabolic pathways.
To test if growth hormone responsiveness underlies the differences in dimorphic expression between fetal and adult liver, we asked if the dimorphic genes present in adult, but not fetal liver were enriched for previously identified growth hormone responsive transcripts [ 35].
The functions of differentially expressed genes in liver are enriched in metabolic process, catalytic activity and oxidoreductase activity.
It is well known that liver is enriched in NK cells, and the chronic inflammation (especially virus infection-induced inflammation) may be involved in the pathogenesis of hepatocellular carcinoma.
Contrary to this, buffalo liver was enriched with Smoc-1 transcripts as well as protein whereas other tissues contained fewer or no transcript/protein substantiating species and tissue specificity of this gene.
For instance, Rnap2 binding sites are enriched for genes related to fatty acid metabolism in liver and muscle cell development in the muscle, while genes near Rxrα binding sites in liver are enriched for lipid and cholesterol metabolic processes, and Rxrα binding in skeletal muscles enriches for genes involved in actin filament-based processes and actin cytoskeleton organization.
Similarly, differentially expressed genes in human liver are enriched for metabolic function (Blekhman et al., 2008), suggesting a potential molecular basis for arguments implicating dietary shifts in the emergence of modern humans (Kaplan et al., 2000; Ungar and Teaford, 2002; Wrangham, 2009).
We also identified 1,000 genes specific to fetal liver, which were enriched for GATA1, STAT5A, STAT5B and YY1 binding sites.
