Abstract:
:The Wnt signaling pathway plays a pivotal role in vertebrate early development and morphogenesis. Duplin (axis duplication inhibitor) interacts with beta-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 beta-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.
journal_name
Mol Cell Bioljournal_title
Molecular and cellular biologyauthors
Nishiyama M,Nakayama K,Tsunematsu R,Tsukiyama T,Kikuchi A,Nakayama KIdoi
10.1128/MCB.24.19.8386-8394.2004subject
Has Abstractpub_date
2004-10-01 00:00:00pages
8386-94issue
19eissn
0270-7306issn
1098-5549pii
24/19/8386journal_volume
24pub_type
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