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Nucleic Acids Research Advance Access published online on April 24, 2008
Nucleic Acids Research, doi:10.1093/nar/gkn207
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© 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.

RNA

A G-tract element in apoptotic agents-induced alternative splicing

Yan Hai1,2, Wenguang Cao2, Guodong Liu2, Say-Pham Hong2, Sherif Abou Elela3, Roscoe Klinck3, Jiayou Chu1 and Jiuyong Xie2,*

1Institute of Medical Biology, Chinese Academy of Medical Sciences & Peking Union Medical College. Kunming, China, 2Department of Physiology, Faculty of Medicine, University of Manitoba, Winnipeg and 3Département de microbiologie et d'infectiologie, and Laboratoire de Génomique Fonctionnelle de l’Université de Sherbrooke, Sherbrooke, Canada

*To whom correspondence should be addressed. Tel: 204 975 7774; Fax: 204 789 3934; Email: xiej{at}cc.umanitoba.ca

Received January 19, 2008. Revised April 7, 2008. Accepted April 8, 2008.

Alternative splicing of a single pre-mRNA transcript can produce protein isoforms that promote either cell growth or death. Here we show that Ro-31-8220 (Ro), an apoptotic agent that inhibits protein kinase C and activates the c-Jun N terminal kinase, decreased the proportion of the cell growth-promoting Bcl-xL splice variant. Targeted mutagenesis analyses narrowed down a critical sequence to a 16-nt G-tract element (Gt16). Transferring this element to a heterologous gene conferred Ro response on an otherwise constitutive exon. The Ro effect was reduced by okadaic acid, an inhibitor of protein phosphatases PP1 and PP2A, in a concentration-dependent manner. Search in the human genome followed by RT–PCR identified a group of genes that contain similar exonic G-tract elements and are responsive to Ro. Moreover, the Gt16 element also mediates the regulation of alternative splicing by other cell apoptosis-inducers particularly retinoic acid. Therefore, the G-tract element likely plays a role in the apoptotic agents-induced alternative splicing of a group of genes. The functions of these genes imply that this regulation will have impact on cell growth/death.


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