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This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Gumucio, D. L. Articles by Collins, F. S. Search for Related Content PubMed PubMed Citation Articles by Gumucio, D. L. Articles by Collins, F. S. Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  The -175T----C mutation increases promoter strength in erythroid cells: correlation with evolutionary conservation of binding sites for two trans-acting factors DL Gumucio, WK Lockwood, JL Weber, AM Saulino, K Delgrosso, S Surrey, E Schwartz, M Goodman and FS Collins Department of Internal Medicine, University of Michigan, Ann Arbor 48109-0650. A point mutation at position -175 has been detected in Agamma as well as Ggamma globin genes in individuals with hereditary persistence of fetal hemoglobin (HPFH). To prove that this single point mutation results in increased promoter strength, we transfected erythroid and nonerythroid cell lines with constructs containing normal and mutant promoters linked to the bacterial chloramphenicol acetyl transferase (CAT) gene. Differences in transfection efficiency were controlled by cotransfection of pRSVgpt. In K562 erythroleukemia cells, the -175 HPFH promoter directed three- to fourfold more CAT activity than its wild type counterpart. However, in HeLa cells the two promoters were similar in strength. The -195 to -165 region of the gamma-globin promoter contains binding sites for two proteins: a ubiquitously distributed octamer binding protein, OBP, and the erythroid-specific protein, GF-1. We find that while the GF-1 binding site is highly conserved among related primate gamma-globin genes, the octamer binding site is not. The evolutionary conservation of GF-1 as well as its erythroid-specific distribution suggest that this protein is important in gamma-globin gene expression. A role for OBP in the regulation of gamma-globin, if any, must have arisen recently in primate evolution. Volume 75, Issue 3, pp. 756-761, 02/01/1990 Copyright © 1990 by The American Society of Hematology CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: S. D. Langdon and R. E. Kaufman Gamma-Globin Gene Promoter Elements Required for Interaction With Globin Enhancers Blood, January 1, 1998; 91(1): 309 - 318. [Abstract] [Full Text] [PDF]

	Copyright © 1990 by American Society of Hematology         Online ISSN: 1528-0020