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| Caption | Excessive Wnt/beta-catenin signaling results in anterior head defects during embryonic development. (A) Whole mounts of E9.5 wild-type (WT, +/+) and ApcMin/Apctm1Tno (min/fl) mutant embryos and E17.5 Apc+/Apctm1Tno(+/fl) and ApcMin/Apctm1Tno (min/fl) mutant embryos. (B) Whole mounts of E13.5 wild-type and mutant embryos of the indicated genotypes. Genetic ablation of one allele of beta-catenin in (min/fl) headless mutant (ApcMin/Apctm1Tno Ctnnb1tm4.1Wbm/Ctnnb1+) rescues normal head morphology in (min/fl; +/-) mice. (C) Histological cross sections of E12 wild-type (+/+) and mutant (min/fl) embryos. (D) Confocal cross section of E3.5-5.5 (+/fl) and (min/fl) embryos stained for beta-catenin protein. The arrowheads demarcate the outer layer (anterior visceral endoderm) of the embryo which shows increased and expanded beta-catenin expression in the (min/fl) mutant. A, Anterior; P, Posterior. (E) Whole mount in vivo X-gal staining of E16 embryos to monitor canonical Wnt/beta-catenin dependent activity in compound mutant mice harboring the corresponding BAT::gal reporter transgene. Genotypes are as follows: wild-type (+/+); Apc+/fl (+/fl); Apcfl/fl (fl/fl); Apcmin/+ (min/+); Apcmin/fl (min/fl); Apcmin/fl;Ctnnb1+/- (min/fl; +/-). | ||||||||
| Copyright | This image is from Buchert M, PLoS Genet 2010 Jan;6(1):e1000816, and is displayed under the terms of the Creative Commons Attribution 4.0 International License. J:156864 | ||||||||
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Associated Genotypes |
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Mouse Genome Database (MGD), Gene Expression Database (GXD), Mouse Models of Human Cancer database (MMHCdb) (formerly Mouse Tumor Biology (MTB)), Gene Ontology (GO) |
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last database update 12/17/2024 MGI 6.24 |
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