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Nucleic Acids Research 2006 34(5):1342-1350; doi:10.1093/nar/gkl022
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Published online 3 March 2006

© The Author 2006. 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@oxfordjournals.org

Article

An isoform of ZBP-89 predisposes the colon to colitis

David J. Law1,*, Edwin M. Labut1, Rachael D. Adams1 and Juanita L. Merchant1,2

1Department of Internal Medicine, University of Michigan 1150 W. Medical Center Dr., MSRB I, Rm. 3510, Ann Arbor, MI 48109-0650, USA 2Department of Physiology, University of Michigan 1150 W. Medical Center Dr., MSRB I, Rm. 3510, Ann Arbor, MI 48109-0650, USA

*To whom correspondence should be addressed. Tel: +1 734 936 6363; Fax: +1 734 763 4686; Email: davelaw{at}umich.edu

Received November 21, 2005. Revised February 15, 2006. Accepted February 15, 2006.

Alternative splicing enables expression of functionally diverse protein isoforms. The structural and functional complexity of zinc-finger transcription factor ZBP-89 suggests that it may be among the class of alternatively spliced genes. We identified a human ZBP-89 splice isoform (ZBP-89{Delta}N), which lacks amino terminal residues 1–127 of the full-length protein (ZBP-89FL). ZBP-89{Delta}N mRNA was co-expressed with its ZBP-89FL cognate in gastrointestinal cell lines and tissues. Similarly, ZBP-89{Delta}N protein was expressed. To define its function in vivo, we generated ZBP-89{Delta}N knock-in mice by targeting exon 4 that encodes the amino terminus. Homozygous ZBP-89{Delta}N mice, expressing only ZBP-89{Delta}N protein, experienced growth delay, reduced viability and increased susceptibility to dextran sodium sulfate colitis. We conclude that ZBP-89{Delta}N antagonizes ZBP-89FL function and that over-expression of the truncated isoform disrupts gastrointestinal homeostasis.

DDBJ/EMBL/GenBank accession nos+

+DQ090088, DQ090089 and DQ144540


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