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Hematopoietic specific transcription factor GATA-1 is essential for hematopoietic development.Misregulation of GATA-1 is linked to hematologic diseases including leukemia.GATA-1 activity is required for erythroid and megakaryoeytic cell differentiation.However, recent discoveries indicate that GATA-1 is associated with HDAC 1 containing corepressor complexes throughout differentiation of erythroid cells.We hypothesize that GATA-1 associated deacetylase activity is attenuated during erythroid differentiation.We previously found that HDAC1 can be acetylated in vivo and acetylated HDAC 1 completely lost deacetylase activity (Qiu et al, 2006).In this study, we investigate the role of HDAC 1 in erythroid differentiation.Our results indicate that during erythroid differentiation, GATA-1 associated deacetylase activity is significantly decreased and further diminished at day 5 of DMSO induction in MEL cells.More interestingly, acetylated form of HDAC 1 within the GATA-1 complex increases during erythroid differentiation.Overexpresion of HDAC1 mutant mimicking the acetylated HDAC1 promotes erythriod differentiation.These observations suggest a novel but rather general regulation mechanism of histone deacetylase containing complexes.Further studies will allow us to understand the molecular basis of the regulation of deacetylation of HDACs and their roles in hematopoiesis and general transcription regulation.