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Originally published In Press as doi:10.1074/jbc.M011769200 on March 1, 2001

J. Biol. Chem., Vol. 276, Issue 20, 17597-17602, May 18, 2001
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Dimethyl Sulfoxide Affects the Selection of Splice Sites*

Lucie BolducDagger , Benoit Labrecque, Mélanie Cordeau, Marco Blanchette§, and Benoit Chabot

From the Département de Microbiologie et d'Infectiologie, Faculté de Médecine, Université de Sherbrooke, Sherbrooke, Québec, Canada J1H 5N4

Depending on the cell lines and cell types, dimethyl sulfoxide (Me2SO) can induce or block cell differentiation and apoptosis. Although Me2SO treatment alters many levels of gene expression, the molecular processes that are directly affected by Me2SO have not been clearly identified. Here, we report that Me2SO affects splice site selection on model pre-mRNAs incubated in a nuclear extract prepared from HeLa cells. A shift toward the proximal pair of splice sites was observed on pre-mRNAs carrying competing 5'-splice sites or competing 3'-splice sites. Because the activity of recombinant hnRNP A1 protein was similar when added to extracts containing or lacking Me2SO, the activity of endogenous A1 proteins is probably not affected by Me2SO. Notably, in a manner reminiscent of SR proteins, Me2SO activated splicing in a HeLa S100 extract. Moreover, the activity of recombinant SR proteins in splice site selection in vitro was improved by Me2SO. Polar solvents like DMF and formamide similarly modulated splice site selection in vitro but formamide did not activate a HeLa S100 extract. We propose that Me2SO improves ionic interactions between splicing factors that contain RS-domains. The direct impact of Me2SO on alternative splicing may explain, at least in part, the different and sometimes opposite effects of Me2SO on cell differentiation and apoptosis.

* This work was supported in part by a grant from the National Cancer Institute of Canada with funds from the Canadian Cancer Society (to B. C.).The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

Dagger Recipient of a studentship from the Fonds pour la Formation de Chercheurs et l'Aide à la Recherche (FCAR).

§ Recipient of a studentship from the Medical Research Council of Canada. Present Address: Dept. of Molecular and Cell Biology, University of California, Berkeley, CA 94720-3204.

Research Scholar from the Fond de la Recherche en Santé du Québec and member of the Sherbrooke RNA/RNP group supported by the FCAR. To whom correspondence should be addressed. Tel.: 819-564-5295; Fax: 819-564-5392; E-mail: b.chabot@courrier.usherb.ca.

Copyright © 2001 by The American Society for Biochemistry and Molecular Biology, Inc.
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