The leukaemia-associated transcription factors EVI-1 and MDS1/EVI1 represstranscription and interact with histone deacetylase

EVI-1 and its variant form, MDS1/EVI1, have been reported to act in an anta gonistic manner and be differentially regulated in samples from patients wi th acute myeloid leukaemia and rearrangements of the long arm of chromosome 3. Here, we show that both EVI-1 and MDS1/EVI1 can repress transcription f rom a reporter construct containing EVI-1 binding sites and interact with h istone deacetylase in mammalian cells. This interaction can be recapitulate d in vitro and is mediated by a previously characterized transcription repr ession domain, whose activity is alleviated by the histone deacetylase inhi bitor trichostatin A.