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Molecular and Cellular Biology, December 2005, p. 10979-10988, Vol. 25, No. 24
0270-7306/05/$08.00+0     doi:10.1128/MCB.25.24.10979-10988.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Phospholipase C-1 and -3 Are Essential in the Trophoblast for Placental Development

Laboratory of Genome and Biosignal, Tokyo University of Pharmacy and Life Science, 1432-1 Horinouchi, Hachioji, 192-0392 Tokyo, Japan,¹ Tissue and Cell Culture Laboratory, National Institute For Basic Biology, 38 Nishigonaka, Myodaiji, Okazaki, Aichi 444-8585, Japan,² Laboratory Animal Center, Ehime University School of Medicine, Shitsukawa, Shigenobu-cho, Onsen-gun, Ehime 791-0295, Japan,³ Center for Experimental Animals, National Institute for Physiological Sciences, 38 Nishigonaka, Myodaiji, Okazaki 444-8585, Japan,⁴ Laboratory of Cellular Biochemistry, Department of Animal Resource Sciences/Veterinary Medical Sciences, The University of Tokyo, Yayoi 1-1-1, Bukyo-ku, Tokyo 113-8657, Japan,⁵ Department of Pathology, Ehime University School of Medicine, Shitsukawa, Shigenobu-cho, Onsen-gun, Ehime 791-0295, Japan,⁶ Division of Gene Expression and Regulation, The Institute of Medical Science, University of Tokyo, 4-6-1 Shirokanedai, Minato-ku, Tokyo 108-8639, Japan,⁷ Department of Biochemistry, The Institute of Medical Science, University of Tokyo, 4-6-1 Shirokanedai, Minato-ku, Tokyo 108-8639, Japan⁸

Received 19 August 2005/ Returned for modification 2 September 2005/ Accepted 18 September 2005

Phosphoinositide-specific phospholipase C (PLC) is a key enzyme in phosphoinositide turnover and is involved in a variety of physiological functions. We analyzed PLC1 knockout mice and found that PLC1 is required for the maintenance of skin homeostasis. However, there were no remarkable abnormalities except hair loss and runting in PLC1 knockout mice, even though PLC1 is broadly distributed. Here, we report that mice lacking both PLC1 and PLC3 died at embryonic day 11.5 (E11.5) to E13.5. PLC1/PLC3 double-knockout mice exhibited severe disruption of the normal labyrinth architecture in the placenta and decreased placental vascularization, as well as abnormal proliferation and apoptosis of trophoblasts in the labyrinth area. Furthermore, PLC1/PLC3 double-knockout embryos supplied with a normal placenta by the tetraploid aggregation method survived beyond E14.5, clearly indicating that the embryonic lethality is caused by a defect in trophoblasts. On the basis of these results, we conclude that PLC1 and PLC3 are essential in trophoblasts for placental development.

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