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Molecular and Cellular Biology, October 2004, p. 8386-8394, Vol. 24, No. 19
0270-7306/04/$08.00+0     DOI: 10.1128/MCB.24.19.8386-8394.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Early Embryonic Death in Mice Lacking the ß-Catenin-Binding Protein Duplin

Masaaki Nishiyama,1,2 Keiko Nakayama,2,3 Ryosuke Tsunematsu,1,2 Tadasuke Tsukiyama,1,2 Akira Kikuchi,4 and Keiichi I. Nakayama1,2*

Department of Molecular and Cellular Biology, Medical Institute of Bioregulation, Kyushu University, Fukuoka,1 CREST, Japan Science and Technology Corporation, Kawaguchi, Saitama,2 Department of Developmental Biology, Center for Translational and Advanced Animal Research on Human Disease, Graduate School of Medicine, Tohoku University, Sendai,3 Department of Biochemistry, Graduate School of Biomedical Sciences, Hiroshima University, Hiroshima, Japan4

Received 6 February 2004/ Returned for modification 24 April 2004/ Accepted 22 June 2004

The Wnt signaling pathway plays a pivotal role in vertebrate early development and morphogenesis. Duplin (axis duplication inhibitor) interacts with ß-catenin and prevents its binding to Tcf, thereby inhibiting downstream Wnt signaling. Here we show that Duplin is expressed predominantly from early- to mid-stage mouse embryogenesis, and we describe the generation of mice deficient in Duplin. Duplin–/– embryos manifest growth retardation from embryonic day 5.5 (E5.5) and developmental arrest accompanied by massive apoptosis at E7.5. The mutant embryos develop into an egg cylinder but do not form a primitive streak or mesoderm. Expression of ß-catenin target genes, including those for T (brachyury), Axin2, and cyclin D1, was not increased in Duplin–/– embryos, suggesting that the developmental defect is not simply attributable to upregulation of Wnt signaling caused by the lack of this inhibitor. These results suggest that Duplin plays an indispensable role, likely by a mechanism independent of inhibition of Wnt signaling, in mouse embryonic growth and differentiation at an early developmental stage.

* Corresponding author. Mailing address: Department of Molecular and Cellular Biology, Medical Institute of Bioregulation, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka, Fukuoka 812-8582, Japan. Phone: 81-92-642-6815. Fax: 81-92-642-6819. E-mail: nakayak1{at}bioreg.kyushu-u.ac.jp.

Molecular and Cellular Biology, October 2004, p. 8386-8394, Vol. 24, No. 19
0022-538X/04/$08.00+0     DOI: 10.1128/MCB.24.19.8386-8394.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.



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