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Vertebrate reproductive science and technology
RESEARCH ARTICLE

The role of insulin-like growth factor II and its receptor in mouse preimplantation development

M. Pantaleon A , H. Jericho A B , G. Rabnott A and P. L. Kaye A C
+ Author Affiliations
- Author Affiliations

A Department of Physiology and Pharmacology, School of Biomedical Sciences, The University of Queensland, Brisbane, Queensland 4072, Australia.

B Current address: Melbourne IVF, Freemason’s Medical Centre, 320 Victoria Parade, East Melbourne, Victoria 3002, Australia.

C To whom correspondence should be addressed. email: p.kaye@uq.edu.au

Reproduction, Fertility and Development 15(1) 37-45 https://doi.org/10.1071/RD02031
Submitted: 6 May 2002  Accepted: 16 December 2002   Published: 16 December 2002

Abstract

Insulin-like growth factor II (IGF-II) and its receptor, the IGF-II/mannose-6-phosphate (IGF-II/M6P) receptor, are first expressed from the zygotic genome at the two-cell stage of mouse development. However, their role is not clearly defined. Insulin-like growth factor II is believed to mediate growth through the heterologous type 1 IGF and insulin receptors, whereas the IGF-II/M6P receptor is believed to act as a negative regulator of somatic growth by limiting the availability of excess levels of IGF-II. These studies demonstrate that IGF-II does have a role in growth regulation in the early embryo through the IGF-II/M6P receptor. Insulin-like growth factor II stimulated cleavage rate in two-cell embryos in vitro. Moreover, this receptor is required for the glycaemic response of two-cell embryos to IGF-II and for normal progression of early embryos to the blastocyst stage. Improved development of embryos in crowded culture supports the concept of an endogenous embryonic paracrine activity that enhances cell proliferation. These responses indicate that the IGF-II/M6P receptor is functional and likely to participate in such a regulatory circuit. The functional role of IGF-II and its receptor is discussed with reference to regulation of early development.

Extra keywords: antisense inhibition


Acknowledgments

We thank Drs Carolyn Scott and Robert Baxter (Kolling Institute of Medical Research, St Leonards, NSW, Australia) for generously donating the IFG-II receptor antiserum used in the study.


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