RESUMEN
Long noncoding RNAs (lncRNAs) are involved in many biological processes and have been extensively researched. Nonetheless, literature focusing on the roles of lncRNA in melanocytes is limited. Melanocytes are located in the basal layer of the epidermis and determine the color of an animal's skin and hair by producing melanin. The mechanisms of melanogenesis remain unclear. Here, melanocytes from Boer goat skins were successfully isolated and verified using morphological observation, dopamine staining, silver ammonia staining, and immunohistochemical staining in vitro. Phenotypic testing revealed that melanocytes isolated from goat skins with white and brown hairs showed significant differences in proliferation, migration, and melanogenesis (** P < 0.01). RNA sequencing was performed with the isolated melanocytes, and through bioinformatic analysis, several candidate lncRNAs and mRNAs involved in stage-specific melanogenesis were identified. Functional enrichment analysis indicated that miRNA precursors and cis-regulatory effects of lncRNAs were deeply dissected using the function prediction software. Multiple lncRNA-mRNA networks were presumed to be involved in melanocyte migration, proliferation, and melanogenesis based on the Kyoto Encyclopedia of Genes and Genomes (KEGG) annotation. This research provided novel bioinformatic insights into the roles of lncRNAs in mammalian pigmentation.
RESUMEN
Human embryonic stem cells (hESCs) depend on glycolysis for energy and substrates for biosynthesis. To understand the mechanisms governing the metabolism of hESCs, we investigated the transcriptional regulation of glucose transporter 1 (GLUT1, SLC2A1), a key glycolytic gene to maintain pluripotency. By combining the genome-wide data of binding sites of the core pluripotency factors (SOX2, OCT4, NANOG, denoted SON), chromosomal interaction and histone modification in hESCs, we identified a potential enhancer of the GLUT1 gene in hESCs, denoted GLUT1 enhancer (GE) element. GE interacts with the promoter of GLUT1, and the deletion of GE significantly reduces the expression of GLUT1, glucose uptake and glycolysis of hESCs, confirming that GE is an enhancer of GLUT1 in hESCs. In addition, the mutation of SON binding motifs within GE reduced the expression of GLUT1 as well as the interaction between GE and GLUT1 promoter, indicating that the binding of SON to GE is important for its activity. Therefore, SON promotes glucose uptake and glycolysis in hESCs by inducing GLUT1 expression through directly activating the enhancer of GLUT1.
