Abstract:
: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.
journal_name
Protein Celljournal_title
Protein & cellauthors
Yu L,Ji KY,Zhang J,Xu Y,Ying Y,Mai T,Xu S,Zhang QB,Yao KT,Xu Ydoi
10.1007/s13238-019-0637-9subject
Has Abstractpub_date
2019-09-01 00:00:00pages
668-680issue
9eissn
1674-800Xissn
1674-8018pii
10.1007/s13238-019-0637-9journal_volume
10pub_type
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