Gfi-1B (growth factor independence-1B) gene is an erythroid-specific 
transcription factor, whose expression plays an essential role in 
erythropoiesis. Our laboratory has previously defined the human Gfi-1B promoter 
region and shown that GATA-1 mediates erythroid-specific Gfi-1B transcription. 
By further investigating the regulation of the Gfi-1B promoter, here we report 
that (i) Gfi-1B transcription is negatively regulated by its own gene product, 
(ii) GATA-1, instead of Gfi-1B, binds directly to the Gfi-1-like sites in the 
Gfi-1B promoter and (iii) Gfi-1B suppresses GATA-1-mediated stimulation of 
Gfi-1B promoter through their protein interaction. These results not only 
demonstrate that interaction of GATA-1 and Gfi-1B participates in a feedback 
regulatory pathway in controlling the expression of the Gfi-1B gene, but also 
provide the first evidence that Gfi-1B can exert its repression function by 
acting on GATA-1-mediated transcription without direct binding to the Gfi-1 site 
of the target genes. Based on these data, we propose that this negative 
auto-regulatory feedback loop is important in restricting the expression level 
of Gfi-1B, thus optimizing its function in erythroid cells.