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Nucleic Acids Research 2005 33(16):5331-5342; doi:10.1093/nar/gki838
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Published online 21 September 2005

© The Author 2005. Published by Oxford University Press. All rights reserved
The online version of this article has been published under an open access model. Users are entitled to use, reproduce, disseminate, or display the open access version of this article for non-commercial purposes provided that: the original authorship is properly and fully attributed; the Journal and Oxford University Press are attributed as the original place of publication with the correct citation details given; if an article is subsequently reproduced or disseminated not in its entirety but only in part or as a derivative work this must be clearly indicated. For commercial re-use, please contact journals.permissions{at}oxfordjournals.org

Article

GATA-1 mediates auto-regulation of Gfi-1B transcription in K562 cells

Duen-Yi Huang, Yuan-Yeh Kuo and Zee-Fen Chang*

Institute of Biochemistry and Molecular Biology, College of Medicine, National Taiwan University No. 1 Jen Ai Road 1st Section, Taipei, Taiwan, R.O.C.

*To whom correspondence should be addressed. Fax/Tel: +886 2 2395 8904; Email: zfchang{at}ha.mc.ntu.edu.tw

Received May 4, 2005. Revised July 20, 2005. Accepted August 30, 2005.

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.


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