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First published online 19 December 2007
doi: 10.1242/dev.014894

Development 135, 425-429 (2008)
Published by The Company of Biologists 2008
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Research Report

Constitutive PtdIns(3,4,5)P3 synthesis promotes the development and survival of early mammalian embryos

Guillaume Halet1,*, Patricia Viard2 and John Carroll1

1 Department of Physiology, University College London, Gower Street, London WC1E 6BT, UK.
2 Department of Pharmacology, University College London, Gower Street, London WC1E 6BT, UK.

* Author for correspondence (e-mail: g.halet{at}ucl.ac.uk)

Accepted 30 October 2007

SUMMARY

Mammalian preimplantation embryos develop in the oviduct as individual entities, and can develop and survive in vitro, in defined culture media lacking exogenous growth factors or serum. Therefore, early embryos must generate intrinsic signals that promote their development and survival. In other cells, activation of class I phosphoinositide 3-kinase (PI3K) is a universal mechanism to promote cell proliferation and survival. Here, we examined whether PI3K is intrinsically activated during preimplantation development. Using GFP-tagged pleckstrin homology domains to monitor PtdIns(3,4,5)P3 synthesis, we show that PI3K is constitutively activated in mouse preimplantation embryos. E-cadherin ligation promotes PtdIns(3,4,5)P3 synthesis at sites of blastomere adhesion at all cleavage stages. In addition, in culture conditions that promote autocrine signalling, a second pool of PtdIns(3,4,5)P3 is generated in the apical membrane of early stage blastomeres. We show that constitutive PtdIns(3,4,5)P3 synthesis is necessary for optimal development to blastocyst and to prevent large-scale apoptosis at the time of cavitation.

Key words: Preimplantation development, PI 3-kinase, PIP3, E-cadherin, Apoptosis






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