Communicated by: Eisuke Nishida
Essential role for ERK2 mitogen-activated protein kinase in placental development
Article first published online: 30 SEP 2003
Genes to Cells
Volume 8, Issue 11, pages 847–856, November 2003
How to Cite
Hatano, N., Mori, Y., Oh-hora, M., Kosugi, A., Fujikawa, T., Nakai, N., Niwa, H., Miyazaki, J., Hamaoka, T. and Ogata, M. (2003), Essential role for ERK2 mitogen-activated protein kinase in placental development. Genes to Cells, 8: 847–856. doi: 10.1046/j.1365-2443.2003.00680.x
- Issue published online: 30 SEP 2003
- Article first published online: 30 SEP 2003
- Received: 11 August 2003 Accepted: 21 August 2003
Background: Extracellular signal-regulated kinase 2 (ERK2) has been implicated in cell proliferation, differentiation, and survival. However, its role in vivo remains to be determined.
Results: Here we show that the targeted disruption of the mouse ERK2 gene results in embryonic lethality by E11.5 and severe abnormality of the placenta. In these animals, the labyrinthine layer of the placenta is very thin and few foetal blood vessels are observed. ERK2 mutants can be rescued by the transgenic expression of ERK2, demonstrating that these abnormalities are caused by ERK2-deficiency. Although ERK2-deficient fetuses are much smaller than wild-type littermates, this seems to be secondary to malfunction of the placenta. When the placental defect is rescued by tetraploid-aggregation, ERK2-deficient foetuses grow as well as littermate controls.
Conclusion: These observations indicate that ERK2 is essential for placental development and suggest that ERK2 in the trophoblast compartment may be indispensable for the vascularization of the labyrinth.