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Published September 1993 | Published
Journal Article Open

Xwnt-5A: a maternal Wnt that affects morphogenetic movements after overexpression in embryos of Xenopus laevis

Abstract

To contribute to an understanding of the roles and mechanisms of action of Wnts in early vertebrate development, we have characterized the normal expression of Xenopus laevis Wnt-5A, and investigated the consequences of misexpression of this putative signalling factor. Xwnt-5A transcripts are expressed throughout development, and are enriched in both the anterior and posterior regions of embryos at late stages of development, where they are found primarily in ectoderm, with lower levels of expression in mesoderm. Overexpression of Xwnt-5A in Xenopus embryos leads to complex malformations distinct from those achieved by ectopic expression of Xwnts −1, −3A, or −8. This phenotype is unlikely to result from Xwnt-5A acting as an inducing agent, as overexpression of Xwnt-5A does not rescue dorsal structures in UV-irradiated embryos, does not induce mesoderm in blastula caps, and Xwnt-5A does not alter the endogenous patterns of expression of goosecoid, Xbra, or Xwnt-8. To pursue whether Xwnt-5A has the capacity to affect morphogenetic movements, we investigated whether overexpression of Xwnt-5A alters the normal elongation of blastula cap explants induced by activin. Intriguingly, Xwnt-5A blocks the elongation of blastula caps in response to activin, without blocking the differentiation of either dorsal or ventral mesoderm within these explants. The data are consistent with Xwnt-5A having the potential activity of modifying the morphogenetic movements of tissues.

Additional Information

© 1993 The Company of Biologists Limited. Accepted 27 May 1993. We thank D. Melton and M. Ku for communication of unpublished Xwnt-9 data and for the oocyte cDNA library, P. Moore and Genentech for the recombinant human activin A, P. Walter for the prolactin cDNA, R. Perlmutter for the elongation factor cDNA, J. Smith for the Xbra cDNA, C. Kintner for the 12/101 antibody, R. Harland for the beta-galactosidase cDNA and E. Jones and H. Woodland for the 2G9 antibody. We thank A. DeMarais and G. Kelly for helpful comments on the manuscript and for technical assistance, and J. Papkoff and D. Olson for transfecting Xwnt-5A into C57mg cells. This work was supported by Public Health Service Awards (RO1 HD27525, HD29360, and KO4 AR 1837 to R. T. M.) and fellowship HD07528 to L. L. M.

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