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Nucleic Acids Research 2005 33(21):6805-6815; doi:10.1093/nar/gki985
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Published online 2 December 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

Krüppel-like zinc finger protein Gli-similar 2 (Glis2) represses transcription through interaction with C-terminal binding protein 1 (CtBP1)

Seong-Chul Kim, Yong-Sik Kim and Anton M. Jetten*

Cell Biology Section, Division of Intramural Research, National Institute of Environmental Health Sciences, National Institutes of Health Research Triangle Park, NC 27709, USA

*To whom correspondence should be addressed. Tel: +1 919 541 2768; Fax: +1 919 541 4133; Email: jetten{at}niehs.nih.gov

Received November 9, 2005. Accepted November 10, 2005.

Glis2 is a member of the Gli-similar (Glis) subfamily of Krüppel-like zinc finger transcription factors. It functions as an activator and repressor of gene transcription. To identify potential co-activators or co-repressors that mediate these actions of Glis2, we performed yeast two-hybrid analysis using Glis2 as bait. C-terminal binding protein 1 (CtBP1) was identified as one of the proteins that interact with Glis2. This interaction was confirmed by mammalian two-hybrid analysis. CtBP1 did not interact with other members of the Glis subfamily suggesting that this interaction is specific for Glis2. Pulldown analysis with GST-CtBP1 demonstrated that CtBP1 physically interacts with Glis2. Analysis of CtBP1 and Glis2 deletion mutants identified several regions important for this interaction. CtBP1 repressed transcriptional activation induced by Glis2(1–171). Repression by Glis2 appears to involve the recruitment of both CtBP1 and histone deacetylase 3 (HDAC3). Confocal microscopic analysis demonstrated that Glis2 localized to nuclear speckles while in most cells CtBP1 was found diffusely in both cytoplasm and nucleus. However, when CtBP1 and Glis2 were co-expressed, CtBP1 was restricted to nuclear speckles and co-localized with Glis2. Our observations suggest that the co-repressor CtBP1 and HDAC3 are part of transcription silencing complex that mediates the transcriptional repression by Glis2.

Correspondence may also be addressed to Yong-Sik Kim. Tel: +1 919 541 4702; Fax: +1 919 541 4133; Email: kim13{at}niehs.nih.gov


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