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Published December 15, 1999 | Published
Journal Article Open

Polarity of the mouse embryo is anticipated before implantation

Abstract

In most species, the polarity of an embryo underlies the future body plan and is determined from that of the zygote. However, mammals are thought to be an exception to this; in the mouse, polarity is generally thought to develop significantly later, only after implantation. It has not been possible, however, to relate the polarity of the preimplantation mouse embryo to that of the later conceptus due to the lack of markers that endure long enough to follow lineages through implantation. To test whether early developmental events could provide cues that predict the axes of the postimplantation embryo, we have used the strategy of injecting mRNA encoding an enduring marker to trace the progeny of inner cell mass cells into the postimplantation visceral endoderm. This tissue, although it has an extraembryonic fate, plays a role in axis determination in adjacent embryonic tissue. We found that visceral endoderm cells that originated near the polar body (a marker of the blastocyst axis of symmetry) generally became distal as the egg cylinder formed, while those that originated opposite the polar body tended to become proximal. It follows that, in normal development, bilateral symmetry of the mouse blastocyst anticipates the polarity of the later conceptus. Moreover, our results show that transformation of the blastocyst axis of symmetry into the axes of the postimplantation conceptus involves asymmetric visceral endoderm cell movement. Therefore, even if the definitive axes of the mouse embryo become irreversibly established only after implantation, this polarity can be traced back to events before implantation.

Additional Information

© 1999 The Company of Biologists. Accepted 12 October; published on WWW 24 November 1999. We are grateful to Robin Lovell-Badge for very helpful discussions of the results of this work, to David Glover for his interest and support throughout the course of this work, and to our colleagues who provided helpful comments and support, including John Gurdon, Chris Graham, Jonathan Pines, Kirstie Lawson, Anne McLaren, Azim Surani, Ian Pearson and Nadia Rosenthal. We also thank to Richard Gardner for his encouragement in the initiation of these studies. We thank Brian Tom for statistical consultation and analysis. Erin Browne illustrated the model shown in Fig. 5. Luis Sanchez Palazon participated in preliminary pilot experiments. M. Z.-G. is a Senior Research Fellow of the Lister Institute for Preventative Medicine, and a Stanley Elmore Fellow of Sydney Sussex College. This work was also supported by Wellcome Trust Project Grant (M. Z.-G.), CRC Project Grant (M. Z.-G. and M. J. E.), NIH Grant HD 26732 (R. A. P.) and Wellcome Trust Project grant (M. J. E.).

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