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Nucleic Acids Research Advance Access published online on June 27, 2008
Nucleic Acids Research, doi:10.1093/nar/gkn368
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© 2008 The Author(s)
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.0/uk/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Molecular Biology

The role of transcriptional activator GATA-1 at human β-globin HS2

Youngran Cho1, Sang-Hyun Song2, Jong Joo Lee3, Narae Choi1, Chul Geun Kim3, Ann Dean2 and AeRi Kim1,*

1Department of Molecular Biology, College of Natural Sciences, Pusan National University, Pusan 609-735, Korea, 2Laboratory of Cellular and Developmental Biology, NIDDK, NIH, Bethesda, MD 20892, USA and 3Department of Life Science, College of Natural Sciences, Hanyang University, Seoul 133-791, Korea

*To whom correspondence should be addressed. Tel: +82 51 510 3683; Fax: +82 51 513 9258; Email: kimaeri{at}pusan.ac.kr

Received March 17, 2008. Revised May 9, 2008. Accepted May 22, 2008.

GATA-1 is an erythroid activator that binds β-globin gene promoters and DNase I hypersensitive sites (HSs) of the β-globin locus control region (LCR). We investigated the direct role of GATA-1 interaction at the LCR HS2 enhancer by mutating its binding sites within minichromosomes in erythroid cells. Loss of GATA-1 in HS2 did not compromise interaction of NF-E2, a second activator that binds to HS2, nor was DNase I hypersensitivity at HS2 or the promoter of a linked {varepsilon}-globin gene altered. Reduction of NF-E2 using RNAi confirmed the overall importance of this activator in establishing LCR HSs. However, recruitment of the histone acetyltransferase CBP and RNA pol II to HS2 was diminished by GATA-1 loss. Transcription of {varepsilon}-globin was severely compromised with loss of RNA pol II from the transcription start site and reduction of H3 acetylation and H3K4 di- and tri-methylation in coding sequences. In contrast, widespread detection of H3K4 mono-methylation was unaffected by loss of GATA-1 in HS2. These results support the idea that GATA-1 interaction in HS2 has a prominent and direct role in co-activator and pol II recruitment conferring active histone tail modifications and transcription activation to a target gene but that it does not, by itself, play a major role in establishing DNase I hypersensitivity.


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