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Nucleic Acids Research Advance Access originally published online on July 10, 2008
Nucleic Acids Research 2008 36(14):4609-4620; doi:10.1093/nar/gkn432
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Nucleic Acids Research, 2008, Vol. 36, No. 14 4609-4620
© 2008 The Author(s)
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.0/uk/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Molecular Biology

Development of an isoform-specific gene suppression system: the study of the human Pax-5B transcriptional element

Gilles A. Robichaud1,2,3, Jean-Pierre Perreault1,* and Rodney J. Ouellette2

1Département de biochimie, RNA Group/Groupe ARN, Faculté de médecine et des sciences de la santé, Université de Sherbrooke, Sherbrooke, Québec, J1H 5N4, Canada, 2Atlantic Cancer Research Institute, Moncton, NB, E1C 8X3 Canada and 3Département de chimie et biochimie, Université de Moncton, Moncton, NB, E1A 3E9 Canada

*To whom correspondence should be addressed. Tel: (819) 564 5310; Fax: (819) 564 5340; Email: Jean-Pierre.Perreault{at}USherbrooke.ca Correspondence may also be addressed to Rodney J. Ouellette. Tel: (506) 862 7512; Fax: (506) 862 7571; Email: rodneyo{at}canceratl.ca

Received February 22, 2008. Revised May 31, 2008. Accepted June 23, 2008.

The transcription factor Pax-5, is vital during B lymphocyte differentiation and is known to contribute to the oncogenesis of certain cancers. The Pax-5 locus generates multiple yet structurally related mRNA transcripts through the specific activation of alternative promoter regions and/or alternative splicing events which poses challenges in the study of specific isoform function. In this study, we investigated the function of a major Pax-5 transcript, Pax-5B using an enhanced version of the Hepatitis Delta Virus ribozyme (HDV Rz) suppression system that is specifically designed to recognize and cleave the human Pax-5B mRNA. The activity of these ribozymes resulted in the specific suppression of the Pax-5B transcripts without altering the transcript levels of other closely related Pax-5 isoforms mRNAs both in vitro and in an intracellular setting. Following stable transfection of the ribozymes into a model B cell line (REH), we showed that Pax-5B suppression led to an increase of CD19 mRNA and cell surface protein expression. In response to this Pax-5B specific deregulation, a marked increase in apoptotic activity compared to control cell lines was observed. These results suggest that Pax-5B has distinct roles in physiological processes in cell fate events during lymphocyte development.


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