Erythroid differentiation of mouse erythroleukemia cells results in reorganization of protein-DNA complexes in the mouse beta maj globin promoter but not its distal enhancer.
Dimethyl sulfoxide (DMSO) induction of mouse erythroleukemia (MEL) cells represents a well-defined in vitro system of terminal erythroid differentiation. We have studied the molecular mechanisms of transcriptional activation of the mouse beta maj globin gene during MEL cell differentiation by analyzing nuclear factor-DNA interactions in vivo at the gene's upstream promoter and a distal enhancer, 5'HS-2. Genomic footprinting data indicate that three motifs, CAC, NF-E2/AP1, and GATA-1, of the 5'HS-2 enhancer are bound with nuclear factors in MEL cells both prior to and after DMSO induction. No obvious conformational change of these nuclear factor-DNA complexes could be detected upon terminal differentiation of MEL cells. On the other hand, DMSO induction of MEL cells leads to the formation of specific nuclear factor-DNA complexes at several transcriptional regulatory elements of the mouse beta maj globin upstream promoter. Our genomic footprinting data have interesting implications with respect to the molecular mechanisms of transcriptional regulation and chromatin change of the mouse beta maj globin gene during erythroid differentiation.[1]References
- Erythroid differentiation of mouse erythroleukemia cells results in reorganization of protein-DNA complexes in the mouse beta maj globin promoter but not its distal enhancer. Reddy, P.M., Shen, C.K. Mol. Cell. Biol. (1993) [Pubmed]
Annotations and hyperlinks in this abstract are from individual authors of WikiGenes or automatically generated by the WikiGenes Data Mining Engine. The abstract is from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.About WikiGenesOpen Access LicencePrivacy PolicyTerms of Useapsburg
