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PMID: 9414299 Published · ppublish English Journal Article Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, P.H.S.

Gamma-globin gene promoter elements required for interaction with globin enhancers.

Blood ·Vol. 91 ·No. 1 ·1998-01-01 ·Pages 309-18

Langdon SD, Kaufman RE

Abstract

Normal expression of the human beta-globin domain genes is dependent on at least three types of regulatory elements located within the beta-globin domain: the locus control region (LCR), globin enhancer elements (3'beta and 3'Agamma), and the individual globin gene promoter and upstream regions. It has been postulated that regulation occurs through physical interactions between factors bound to these elements, which are located at considerable distances from each other. To identify the elements required for promoter-enhancer interactions from a distance, we have investigated the expression of the wild-type, truncated, and mutated gamma-globin promoters linked to the 5'HS2 enhancer. We show that in K562 cells, 5'HS2 increases activity approximately 20-fold from both a wild-type and truncated (-135 --> +25) gamma promoter and that truncation or site-directed mutagenesis of the tandem CCAAT boxes eliminated the enhancement by 5'HS2. Mutation of the gamma-globin gene promoter GATA-1 binding sites did not decrease either promoter strength or enhancement of activity by 5'HS2. To determine if enhanced expression of gamma-globin gene promoters carrying mutations associated with hereditary persistence of fetal hemoglobin (HPFH) was due to greater interactions with enhancers, we linked these HPFH gamma-globin gene promoters to 5'HS2 and demonstrated a twofold to threefold higher expression than the corresponding wild-type promoter plus enhancer in MEL cells. Addition of the Agamma-globin gene 3' enhancer to a plasmid containing the gamma-globin gene promoter and 5'HS2 did not further enhance promoter strength. Furthermore, we have demonstrated that the previously identified core 5'HS2 enhancer (46-bp tandem AP-1/NF-E2 sites) increased expression only when located 5', but not 3', to the gamma-globin-luciferase reporter gene, suggesting that its enhancer effect is not by DNA looping. Our results suggest that CCAAT boxes, but not GATA or CACCC binding sites, are required for interaction between the gamma-globin promoter and the LCR/5'HS2 and that regulatory elements in addition to the core enhancer may be required for the enhancer to act from a distance.

MeSH Terms
Animals Binding Sites DNA-Binding Proteins/metabolism Enhancer Elements, Genetic/genetics Erythroid-Specific DNA-Binding Factors Fetal Hemoglobin/analysis GATA1 Transcription Factor Gene Expression Regulation Genes, Reporter Globins/genetics Humans Luciferases/biosynthesis Mice Mutagenesis, Site-Directed Promoter Regions, Genetic/genetics Recombinant Fusion Proteins/biosynthesis Regulatory Sequences, Nucleic Acid Transcription Factors/metabolism Transcription, Genetic Tumor Cells, Cultured
Chemicals
DNA-Binding Proteins Erythroid-Specific DNA-Binding Factors GATA1 Transcription Factor GATA1 protein, human Gata1 protein, mouse Recombinant Fusion Proteins Transcription Factors Globins Fetal Hemoglobin Luciferases
Authors & Affiliations
2 authors, click to expand affiliations / ORCID
Langdon S D
Departments of Medicine and Biochemistry, Duke University Medical Center, Durham, NC 27710, USA.
Kaufman R E
Article Info
Journal
Blood
Abbr.
Blood
ISSN
0006-4971
Published
1998-01-01
Pages
309-18
Language
English
Region
United States
NLM ID
7603509
Subset
IM
Grants
NHLBI NIH HHS · 5P60-HL-2839-1-13 · United States
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