Context-dependent regulation of GATA-1 by friend of GATA-1.

ABSTRACT: The transcription factor GATA-1 and its cofactor, friend of GATA-1 (FOG-1), are essential for normal erythroid development. FOG-1 physically interacts with GATA-1 to augment or inhibit its activity. The mechanisms by which FOG-1 regulates GATA-1 function are unknown. By using an assay that is based on the phenotypic rescue of a GATA-1-null erythroid cell line, we found that a conditional form of GATA-1 (GATA-1-ER) strongly induced histone acetylation at the beta-major globin promoter in vivo, consistent with previous results. In contrast, GATA-1 bearing a point mutation that impairs FOG-1 binding [GATA-1(V205M)-ER] failed to induce high levels of histone acetylation at this site. However, at DNase I-hypersensitive site (HS)3 of the beta-globin locus control region, GATA-1-induced histone a

SUBMITTER: Letting DL 

PROVIDER: S-EPMC327172 | biostudies-literature | 2004 Jan

REPOSITORIES: biostudies-literature