NDLI: Flanking HS-62.5 and 3′ HS1, and regions upstream of the LCR, are not required for β-globin transcription

Content Provider	PubMed Central
Author	Bender, M. A. Byron, Rachel Tobias, Ragoczy Telling, Agnes Bulger, Michael Mark, Groudine
Copyright Year	2006
Abstract	The locus control region (LCR) was thought to be necessary and sufficient for establishing and maintaining an open β-globin locus chromatin domain in the repressive environment of the developing erythrocyte. However, deletion of the LCR from the endogenous locus had no significant effect on chromatin structure and did not silence transcription. Thus, the cis-regulatory elements that confer the open domain remain unidentified. The conserved DNaseI hypersensitivity sites (HSs) HS-62.5 and 3′HS1 that flank the locus, and the region upstream of the LCR have been implicated in globin gene regulation. The flanking HSs bind CCCTC binding factor (CTCF) and are thought to interact with the LCR to form a “chromatin hub” involved in β-globin gene activation. Hispanic thalassemia, a deletion of the LCR and 27 kb upstream, leads to heterochromatinization and silencing of the locus. Thus, the region upstream of the LCR deleted in Hispanic thalassemia (upstream Hispanic region [UHR]) may be required for expression. To determine the importance of the UHR and flanking HSs for β-globin expression, we generated and analyzed mice with targeted deletions of these elements. We demonstrate deletion of these regions alone, and in combination, do not affect transcription, bringing into question current models for the regulation of the β-globin locus.
Related Links	http://dx.doi.org/10.1182/blood-2006-04-014431
Ending Page	1401
Page Count	7
Starting Page	1395
File Format	PDF
ISSN	00064971
e-ISSN	15280020
Journal	Blood
Issue Number	4
Volume Number	108
Language	English
Publisher	The American Society of Hematology
Publisher Date	2006-08-15
Access Restriction	Open
Rights Holder	The American Society of Hematology
Subject Keyword	Immunology Cell Biology Biochemistry Hematology Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Cell Biology Hematology Biochemistry Immunology

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