Journal
MOLECULAR AND CELLULAR BIOLOGY
Volume 26, Issue 18, Pages 6832-6843Publisher
AMER SOC MICROBIOLOGY
DOI: 10.1128/MCB.01770-05
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Funding
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [R01DK058209, R01DK052356] Funding Source: NIH RePORTER
- NIDDK NIH HHS [DK 52356, R01 DK052356-15A1, R01 DK058209, R01 DK052356, R01 DK052356-10, DK 58209] Funding Source: Medline
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The human beta-globin genes are expressed in a developmental stage-specific manner in erythroid cells. Gene-proximal cis-regulatory DNA elements and interacting proteins restrict the expression of the genes to the embryonic, fetal, or adult stage of erythropoiesis. In addition, the relative order of the genes with respect to the locus control region contributes to the temporal regulation of the genes. We have previously shown that transcription factors TFII-I and USF interact with the beta-globin promoter in erythroid cells. Herein we demonstrate that reducing the activity of USF decreased beta-globin gene expression, while diminishing TFII-I activity increased beta-globin gene expression in erythroid cell lines. Furthermore, a reduction of USF activity resulted in a significant decrease in acetylated H3, RNA polymerase 11, and cofactor recruitment to the locus control region and to the adult beta-globin gene. The data suggest that TFII-I and USF regulate chromatin structure accessibility and recruitment of transcription complexes in the beta-globin gene locus and play important roles in restricting P-globin gene expression to the adult stage of erythropoiesis.
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