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First published online 9 April 2008
doi: 10.1242/dev.018853

Development 135, 1791-1801 (2008)
Published by The Company of Biologists 2008
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Dkk1 and Wnt3 interact to control head morphogenesis in the mouse

Samara L. Lewis1, Poh-Lynn Khoo1, R. Andrea De Young1, Kirsten Steiner1, Chris Wilcock2, Mahua Mukhopadhyay3, Heiner Westphal3, Robyn V. Jamieson1,2, Lorraine Robb4 and Patrick P. L. Tam1,2,*

1 Embryology Unit, Children's Medical Research Institute, University of Sydney, Locked Bag 23, Wentworthville, New South Wales, NSW 2145, Australia.
2 Faculty of Medicine, University of Sydney, Locked Bag 23, Wentworthville, New South Wales, NSW 2145, Australia.
3 Laboratory of Mammalian Genes and Development, National Institute of Child Health and Human Development, National Institute of Health, Bethesda, MD 20892, USA.
4 The Walter and Eliza Hall Institute of Medical Research, 1G, Royal Parade, Parkville, Victoria 3050, Australia.

* Author for correspondence (e-mail: ptam{at}cmri.usyd.edu.au)

Accepted 14 March 2008

Loss of Dkk1 results in ectopic WNT/β-catenin signalling activity in the anterior germ layer tissues and impairs cell movement in the endoderm of the mouse gastrula. The juxtaposition of the expression domains of Dkk1 and Wnt3 is suggestive of an antagonist-agonist interaction. The downregulation of Dkk1 when Wnt3 activity is reduced reveals a feedback mechanism for regulating WNT signalling. Compound Dkk1;Wnt3 heterozygous mutant embryos display head truncation and trunk malformation, which are not found in either Dkk1+/- or Wnt3+/- embryos. Reducing the dose of Wnt3 gene in Dkk1-/- embryos partially rescues the truncated head phenotype. These findings highlight that head development is sensitive to the level of WNT3 signalling and that DKK1 is the key antagonist that modulates WNT3 activity during anterior morphogenesis.

Key words: Head development, WNT signalling, DKK1, WNT3, Mouse


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