Journal
BLOOD
Volume 108, Issue 12, Pages 3736-3738Publisher
AMER SOC HEMATOLOGY
DOI: 10.1182/blood-2006-07-032847
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Funding
- NIDDK NIH HHS [DK58044, R37 DK058044, R01 DK054937, DK54937, R01 DK058044] Funding Source: Medline
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All 3 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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