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International Immunology Advance Access published online on February 5, 2008
International Immunology, doi:10.1093/intimm/dxn005
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© The Japanese Society for Immunology. 2008. All rights reserved. For permissions, please e-mail: journals.permissions@oxfordjournals.org

Regulation of the plasma cell transcription factor Blimp-1 gene by Bach2 and Bcl6

Kyoko Ochiai1, Akihiko Muto1, Hiromu Tanaka1, Shinichiro Takahashi2 and Kazuhiko Igarashi1

1 Department of Biochemistry, Tohoku University Graduate School of Medicine, Seiryo-machi 2-1, Sendai 980-8575, Japan
2 Department of Molecular Hematology, Kitasato University Graduate School of Medical Sciences, Sagamihara 228-8555, Japan

Correspondence to: Correspondence to: K. Igarashi; E-mail: igarak{at}mail.tains.tohoku.ac.jp

B lymphocyte-induced maturation protein 1 (Blimp-1) is a key regulator for plasma cell differentiation. Prior to the terminal differentiation into plasma cells, Blimp-1 expression is suppressed in B cells by transcription repressors BTB and CNC homology 2 (Bach2) and B cell lymphoma 6 (Bcl6). Bach2 binds to the Maf recognition element (MARE) of the promoter upstream region of the Blimp-1 gene (Prdm1) by forming a heterodimer with MafK. Bach2 and Bcl6 were found to interact with each other in B cells. While both Bach2 and Bcl6 possess the BTB domain which mediates protein–protein interactions, they interacted in a BTB-independent manner. Bcl6 is known to repress Prdm1 through a Bcl6 recognition element 1 in the intron 5, in which a putative, evolutionarily conserved MARE was identified. Both repressed the expression of a reporter gene containing the intron 5 region depending on the presence of the respective binding sites in 18-81 pre-B cells. Co-expression of Bach2 and Bcl6 resulted in further repression of the reporter plasmid. Chromatin immunoprecipitation assays showed MafK to bind to the intron MARE in various B cell lines, thus suggesting that it binds as a heterodimer with Bach2. Therefore, the interaction between Bach2 and Bcl6 might be crucial for the proper repression of Prdm1 in B cells.

Keywords: B cells, gene regulation, Maf, transcription factor

Transmitting editor: H. Karasuyama

Received 27 September 2007, accepted 7 January 2008.


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