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 Blood, 15 July 2008, Vol. 112, No. 2, pp. 406-414.
Prepublished online as a Blood First Edition Paper on April 25, 2008; DOI 10.1182/blood-2007-12-128983.

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RED CELLS

H3 K79 dimethylation marks developmental activation of the β-globin gene but is reduced upon LCR-mediated high-level transcription

Tomoyuki Sawado1, Jessica Halow1, Hogune Im2, Tobias Ragoczy1, Emery H. Bresnick2, M. A. Bender3,4, and Mark Groudine1,5

1 Division of Basic Sciences, Fred Hutchinson Cancer Research Center, Seattle, WA; 2 Department of Pharmacology, University of Wisconsin School of Medicine and Public Health, Madison; 3 Division of Clinical Research, Fred Hutchinson Cancer Research Center, Seattle, WA; 4 Department of Pediatrics, University of Washington School of Medicine, Seattle; and 5 Department of Radiation Oncology, University of Washington School of Medicine, Seattle

Genome-wide analyses of the relationship between H3 K79 dimethylation and transcription have revealed contradictory results. To clarify this relationship at a single locus, we analyzed expression and H3 K79 modification levels of wild-type (WT) and transcriptionally impaired β-globin mutant genes during erythroid differentiation. Analysis of fractionated erythroid cells derived from WT/{Delta} locus control region (LCR) heterozygous mice reveals no significant H3 K79 dimethylation of the β-globin gene on either allele prior to activation of transcription. Upon transcriptional activation, H3 K79 di-methylation is observed along both WT and {Delta}LCR alleles, and both alleles are located in proximity to H3 K79 dimethylation nuclear foci. However, H3 K79 di-methylation is significantly increased along the {Delta}LCR allele compared with the WT allele. In addition, analysis of a partial LCR deletion mutant reveals that H3 K79 dimethylation is inversely correlated with β-globin gene expression levels. Thus, while our results support a link between H3 K79 dimethylation and gene expression, high levels of this mark are not essential for high level β-globin gene transcription. We propose that H3 K79 dimethylation is destabilized on a highly transcribed template.


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