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Molecular and Cellular Biology, March 2001, p. 1833-1840, Vol. 21, No. 5
0270-7306/01/$04.00+0   DOI: 10.1128/MCB.21.5.1833-1840.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

c-myc Internal Ribosome Entry Site Activity Is Developmentally Controlled and Subjected to a Strong Translational Repression in Adult Transgenic Mice

Laurent Créancier,1 Pascale Mercier,2 Anne-Catherine Prats,1,* and Dominique Morello3

Institut National de la Santé et de la Recherche Médicale U397, Endocrinologie et Communication Cellulaire, Institut Fédératif de Recherche Louis Bugnard, C.H.U. Rangueil, 31403 Toulouse Cedex 04,1 Centre de Biologie du Développement, UMR 5547, Université Paul Sabatier, 31062 Toulouse Cedex 04,3 and Institut de Pharmacologie et Biologie Structurale du Centre National de la Recherche Scientifique, 31077 Toulouse Cedex 04,2 France

Received 11 September 2000/Returned for modification 6 November 2000/Accepted 5 December 2000

The expression of c-myc proto-oncogene, a key regulator of cell proliferation and apoptosis, is controlled at different transcriptional and posttranscriptional levels. In particular, the c-myc mRNA contains an internal ribosome entry site (IRES) able to promote translation initiation independently from the classical cap-dependent mechanism. We analyzed the variations of c-myc IRES activity ex vivo in different proliferating cell types, and in vivo in transgenic mice expressing a bicistronic dual luciferase construct. c-myc IRES efficiency was compared to that of encephalomyocarditis virus (EMCV) IRES under the same conditions. The c-myc IRES was active but with variable efficiency in all transiently transfected cell types; it was also active in the 11-day- old (E11) embryo and in some tissues of the E16 embryo. Strikingly, its activity was undetected or very low in all adult organs tested. In contrast, EMCV IRES was very active in most cell types ex vivo, as well as in embryonic and adult tissues. These data suggest a crucial role of IRES in the control of c-myc gene expression throughout development, either during embryogenesis where its activity might participate in cell proliferation or later on, where its silencing could contribute to the downregulation of c-myc expression, whose deregulation leads to tumor formation.

* Corresponding author. Mailing address: Institut National de la Santé et de la Recherche Médicale U397, Endocrinologie et Communication Cellulaire, Institut Fédératif de Recherche Louis Bugnard, C.H.U. Rangueil, 31403 Toulouse Cedex, France. Phone: 33 (5) 61 32 21 42. Fax: 33 (5) 61 32 21 41. E-mail: pratsac{at}rangueil.inserm.fr.

Molecular and Cellular Biology, March 2001, p. 1833-1840, Vol. 21, No. 5
0270-7306/01/$04.00+0   DOI: 10.1128/MCB.21.5.1833-1840.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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