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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Altered interaction of HDAC5 with GATA-1 during MEL cell differentiation.

The transcription factor GATA-1 plays a significant role in erythroid differentiation and association with CBP stimulates its activity by acetylation. It is possible that histone deacetylases (HDACs) repress the activity of GATA-1. In the present study, we investigated whether class I and class II HDACs interact with GATA-1 to regulate its function and indeed, GATA-1 is directly associated with HDAC3, HDAC4 and HDAC5. The expression profiling and our previous observation that GATA-2 interacts with members of the HDAC family prompted us to investigate further the biological relevance of the interaction between GATA-1 and HDAC5. Coexpression of HDAC5 suppressed the transcriptional potential of GATA-1. Our results demonstrated that GATA-1 and HDAC5 colocalized to the nucleus of murine erythroleukemia (MEL) cells. Furthermore, a portion of HDAC5 moved to the cytoplasm concomitant with MEL cell erythroid differentiation, which was induced by treatment with N,N'-hexamethylenebisacetamide. These observations support the suggestion that control of the HDAC5 nucleocytoplasmic distribution might be associated with MEL cell differentiation, possibly through regulated GATA-1 transactivation.[1]


  1. Altered interaction of HDAC5 with GATA-1 during MEL cell differentiation. Watamoto, K., Towatari, M., Ozawa, Y., Miyata, Y., Okamoto, M., Abe, A., Naoe, T., Saito, H. Oncogene (2003) [Pubmed]
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