International Mammalian Genome Society

The 15th International Mouse Genome Conference (2001)


Michel Cohen-Tannoudji
Unite de Biologie du Developpement/CNRS URA 1960.
Institut Pasteur
25, rue du Docteur Roux
75724 Paris Cedex 15

Co-Authors:  Frödin M, Vandormael-Pournin S, Artus J, Le Bras S, Coumailleau F, Baldacci P, Bainet C
Institution:   Unite de Biologie du Developpement/CNRS URA 1960.

Peri-implantation lethality of mice lacking Ovum mutant candidate gene 1 (omcg1)

The locus Ovum mutant (Om), described in the DDK strain of mice, affects the viability of preimplantation embryos. The striking property of this locus is a parent-of-origin effect: embryos from a cross between DDK females x non-DDK males die at the morula to blastocyst stage whereas embryos from the reciprocal cross, non-DDK females x DDK males, are viable. This lethality is caused by an incompatibility, at the one-cell stage, between a maternal factor of DDK origin and a paternal component of non-DDK origin. Both maternal and paternal components segregate as a single mendelian locus, the Om locus, which we have mapped on mouse chromosome 11. We are engaged in the identification of the gene(s) responsible for the observed lethality using a positional cloning strategy. The Omcg1 gene has been isolated by cDNA selection/hybridisation of DDK oocyte cDNAs with a BAC of the Om region. The Omcg1 gene codes for a putative 40 kDa nuclear protein of unknown function. Interestingly, the Omcg1 gene is expressed in both male and female germ cells. In order to elucidate its biological function, we inactivated the Omcg1 gene by gene targeting. Omcg1-null embryos die in utero. They develop normally to the blastocyst stage but present defaults in hatching and/or implantation. Detailed analysis of the phenotype will help to refine the role of Omcg1 in early mammalian development.

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