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Molecular and Cellular Biology, July 2003, p. 4778-4787, Vol. 23, No. 14
0270-7306/03/$08.00+0     DOI: 10.1128/MCB.23.14.4778-4787.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

Mek2 Is Dispensable for Mouse Growth and Development

Louis-François Bélanger,1 Sophie Roy,1 Michel Tremblay,1 Barbara Brott,2 Ann-Muriel Steff,3 Walid Mourad,4 Patrice Hugo,3 Raymond Erikson,2 and Jean Charron1*

Centre de recherche en cancérologie de l'Université Laval, Centre Hospitalier Universitaire de Québec, Québec, Québec, Canada G1R 2J6,1 Department of Molecular and Cellular Biology, Harvard University, Cambridge, Massachusetts 02138,2 MetrioGene BioSciences, Montréal, Québec, Canada H4P 2R2,3 Centre de recherche du CHUL, Sainte-Foy, Québec, Canada G1V 4G24

Received 10 February 2003/ Returned for modification 10 April 2003/ Accepted 26 April 2003

MEK is a dual-specificity kinase that activates the extracellular signal-regulated kinase (ERK) mitogen-activated protein (MAP) kinase upon agonist binding to receptors. The ERK/MAP kinase cascade is involved in cell fate determination in many organisms. In mammals, this pathway is proposed to regulate cell growth and differentiation. Genetic studies have shown that although a single Mek gene is present in Caenorhabditis elegans, Drosophila melanogaster, and Xenopus laevis, two Mek homologs, Mek1 and Mek2, are present in the mammalian cascade. The inactivation of the Mek1 gene leads to embryonic lethality and has revealed the unique role played by Mek1 during embryogenesis. To investigate the biological function of the second homolog, we have generated mice deficient in Mek2 function. Mek2 mutant mice are viable and fertile, and they do not present flagrant morphological alteration. Although several components of the ERK/MAP kinase cascade have been implicated in thymocyte development, no such involvement was observed for MEK2, which appears to be nonessential for thymocyte differentiation and T-cell-receptor-induced proliferation and apoptosis. Altogether, our findings demonstrate that MEK2 is not necessary for the normal development of the embryo and T-cell lineages, suggesting that the loss of MEK2 can be compensated for by MEK1.

* Corresponding author. Mailing address: Centre de recherche de L'Hôtel-Dieu de Québec, 9 rue McMahon, Québec, QC, Canada G1R 2J6. Phone: (418) 525-4444. Fax: (418) 691-5439. E-mail: jean.charron{at}crhdq.ulaval.ca.

Molecular and Cellular Biology, July 2003, p. 4778-4787, Vol. 23, No. 14
0022-538X/03/$08.00+0     DOI: 10.1128/MCB.23.14.4778-4787.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.



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