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First published online 3 August 2006
doi: 10.1242/dev.02526

Development 133, 3429-3440 (2006)
Published by The Company of Biologists 2006
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Requirement for Map2k1 (Mek1) in extra-embryonic ectoderm during placentogenesis

Vickram Bissonauth, Sophie Roy, Mathieu Gravel, Stéphanie Guillemette and Jean Charron*

Centre de recherche en cancérologie de l'Université Laval, Centre Hospitalier Universitaire de Québec, L'Hôtel-Dieu de Québec, Québec, QC G1R 2J6, Canada.

* Author for correspondence (e-mail: jean.charron{at}crhdq.ulaval.ca)

Accepted 28 June 2006

Map2k1-/- embryos die at mid-gestation from abnormal development and hypovascularization of the placenta. We now show that this phenotype is associated with a decreased labyrinth cell proliferation and an augmented cell apoptosis. Although the activation of MAP2K1 and MAP2K2 is widespread in the labyrinthine region, MAPK1 and MAPK3 activation is restricted to the cells lining the maternal sinuses, suggesting an important role for the ERK/MAPK cascade in these cells. In Map2k1-/- placenta, ERK/MAPK cascade activation is perturbed. Abnormal localization of the syncytiotrophoblasts is also observed in Map2k1-/- placenta, even though this cell lineage is specified at the correct time during placentogenesis. The placental phenotype can be rescued in tetraploid experiments. In addition, Map2k1-specific deletion in the embryo leads to normal embryo development and to the birth of viable Map2k1-/- mice. Altogether, these data enlighten the essential role of Map2k1 in extra-embryonic ectoderm during placentogenesis. In the embryo, the Map2k1 gene function appears dispensable.

Key words: MAP2K1, Map kinase cascade, Conditional deletion, Placenta, Labyrinthine morphogenesis, Syncytiotrophoblast, Mouse






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