Abstract
SCARB1 is an important gene for carotenoid functioning and maintaining body color. In this study, we examined wild red (SCARB1+/+), mutant red (SCARB1−/+), and mutant white (SCARB1−/−) fish to investigate changes in gene expression and metabolic processes using skin transcriptomics and blood metabolomics in Oujiang color common carp, Cyprinus carpio var. color. According to our findings, 85 and 30 genes for lipid transport and metabolism and 12 and 4 genes for retinol metabolism were significantly differentially expressed (DE) respectively between the comparison of pairs SCARB1−/− vs SCARB1+/+ and SCARB1−/− vs SCARB1−/+. Besides, 6 metabolites for lipid transport and metabolism and 1 metabolite for retinol metabolism were significantly DE in SCARB1−/− vs SCARB1+/+ pair comparison. Analysis of data from multiple omics systems revealed significant changes in metabolic pathways, including statin, lipid, and carotenoid pathways. Notably, downregulation in gene expression and blood metabolite levels was observed in the glycerophospholipid and retinol metabolic pathways in SCARB1−/− fish as a result of the SCARB1 gene knock out. Down-regulated genes such as dgkA, CYP27C1, and the l-serine, and 4-Oxoretinol metabolites of the glycerophospholipid and retinol metabolic pathway are likely to regulate the pigmentation mechanism and carotenoid production in the skin cells of SCARB1−/− fish. Our investigation into the effects of SCARB1 gene knock out has yielded valuable insights into carotenoid functioning and integrated networks. This information contributes to further research on the molecular mechanisms underlying carotenoid functioning and its correlation with genes related to the SCARB1 gene.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.