The putative transcription factor DIDO1 contains a pair of zinc finger motifs and is upregulated by apoptotic stimuli. DIDO1 is expressed in the developing limb and may play a role in controlling programmed cell death during development. Nuclear translocation of DIDO1 during apoptosis is associated with its apoptotic activity. Alternative splicing produces the DIDO-1, -2 and -3 isoforms, whose targeted disruption in mice produces a phenotype similar to myelodysplastic/myeloproliferative disease in humans. DIDO3, the largest of the splice variants, is associated with the centrosome and plays a role in mitotic checkpoint and chromosome stability.
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