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Blood, 1 December 2006, Vol. 108, No. 12, pp. 3736-3738.
Prepublished online as a Blood First Edition Paper on August 3, 2006; DOI 10.1182/blood-2006-07-032847.


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Submitted July 5, 2006
Accepted July 14, 2006

Acetylation of GATA-1 is required for chromatin occupancy

Janine M Lamonica, Christopher R Vakoc, and Gerd A Blobel*

University of Pennsylvania, Philadelphia, PA, USA
University of Pennsylvania Medical Center, Philadelphia, PA, USA

* Corresponding author; email: blobel{at}email.chop.edu.

All three hematopoietic GATA transcription factors GATA-1, GATA-2, and GATA-3 are acetylated, although the in vivo role of this modification remains unclear. We examined the functions of an acetylation-defective mutant of GATA-1 in maturing erythroid cells. We found that removal of the acetylation sites in GATA-1 does not impair its nuclear localization, steady state protein levels, or its ability to bind naked GATA elements in vitro. However, chromatin immunoprecipitation (ChIP) experiments revealed that mutant GATA-1 was dramatically impaired in binding to all examined cellular target sites in vivo, including genes that are normally activated and repressed by GATA-1. Together, these results suggest that acetylation regulates chromatin occupancy of GATA-1. These findings point to a novel function for transcription factor acetylation, perhaps by facilitating protein interactions required for stable association with chromatin templates in vivo.


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