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Background  The Eight-Twenty-One ( ETO ) nuclear co-repressor gene belongs to the  ETO  homologue family also containing Myeloid Translocation Gene on chromosome 16 (MTG16) and myeloid translocation Gene-Related protein 1 (MTGR1). By chromosomal translocations ETO and MTG16 become parts of fusion proteins characteristic of morphological variants of acute myeloid leukemia. Normal functions of ETO homologues have as yet not been examined. The goal of this work was to identify structural and functional promoter elements upstream of the coding sequence of the  ETO  gene in order to explore lineage-specific hematopoietic expression and get hints to function.    Results  A putative proximal  ETO  promoter was identified within 411 bp upstream of the transcription start site. Strong ETO promoter activity was specifically observed upon transfection of a promoter reporter construct into erythroid/megakaryocytic cells, which have endogeneous  ETO  gene activity. An evolutionary conserved region of 228 bp revealed potential  cis -elements involved in transcription of  ETO . Disruption of the evolutionary conserved GATA -636 consensus binding site repressed transactivation and disruption of the ETS1 -705 consensus binding site enhanced activity of the  ETO  promoter. The promoter was stimulated by overexpression of GATA-1 into erythroid/megakaryocytic cells. Electrophoretic mobility shift assay with erythroid/megakaryocytic cells showed specific binding of GATA-1 to the GATA -636 site. Furthermore, results from chromatin immunoprecipitation showed GATA-1 binding  in vivo  to the conserved region of the  ETO  promoter containing the -636 site. The results suggest that the GATA -636 site may have a role in activation of the  ETO  gene activity in cells with erythroid/megakaryocytic potential. Leukemia associated  AML1 - ETO  strongly suppressed an  ETO  promoter reporter in erythroid/megakaryocytic cells.    Conclusions  We demonstrate that the GATA-1 transcription factor binds and transactivates the  ETO  proximal promoter in an erythroid/megakaryocytic-specific manner. Thus,  trans -acting factors that are essential in erythroid/megakaryocytic differentiation govern  ETO  expression.

The leukemia associated ETO nuclear repressor gene is regulated by the GATA-1 transcription factor in erythroid/megakaryocytic cells