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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Dad1tm1Wnt
targeted mutation 1, Astar Winoto
MGI:2183460
Summary 1 genotype
Jump to Allelic Composition Genetic Background Genotype ID
hm1
Dad1tm1Wnt/Dad1tm1Wnt involves: 129S1/Sv * 129X1/SvJ * C57BL/6 MGI:3639734


Genotype
MGI:3639734
hm1
Allelic
Composition
Dad1tm1Wnt/Dad1tm1Wnt
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Dad1tm1Wnt mutation (0 available); any Dad1 mutation (9 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• homozygous mutant embryos die by E10.5

embryo
• at E8.5, homozygotes exhibit excessive apoptosis in the embryo proper, esp. at the distal tip
• at E9.5, mutant embryos display large regions of TUNEL+ cells in both ectodermal and mesodermal tissues
• excessive apoptosis occurs predominantly in the embryo proper and not typically in the extraembryonic tissues (e.g. parietal cells are TUNEL-)
• at E9.5, homozygous mutant embryos are always unturned
• at E7.5, severely affected homozygotes display a reducion of all three germ layers, with mesoderm formation being most affected
• at E7.5, many homozygotes display fewer mesodermal cells relative to the embryo size; in addition, cells appear to be more closely packed
• by E8.5, some homozygotes display better epiblast cavity expansion and form mesoderm derivatives such as heart and somites but still lag behind in development, being only 50% of wild-type size
• at E9.5, homozygotes exhibit a relatively underdeveloped, undersized posterior axis
• at E8.5, homozygotes are developmentally retarded by one day relative to wild-type or heterozygous embryos
• at E10.5, homozygotes are identical to E9.5 homozygotes, but have begun to deteriorate
• at E8.5, some homozygotes are only 50% of wild-type size
• at E7.5, extraembryonic structures are often not delayed to the same extent as the embryo proper; however, the decidual cavities are typically distorted and reduced both in length and width
• at E9.5, homozygotes display a hydroponic allantois, suggesting an improper chorioallantoic fusion
• at E7.5, extraembryonic structures are often not delayed to the same extent as the embryo proper; however, the exocoelomic cavity is often malformed
• at E7.5, parietal endoderm cells fail to spread on Reichert's membrane and their nuclei appear to be denser than normal
• at E7.5, homozygotes exhibit a thickened Reichert's membrane
• at E7.5, homozygotes exhibit abnormal epiblast cavity formation
• by E8.5, some homozygotes display better epiblast cavity expansion
• at E9.5, homozygotes display a hydroponic allantois, suggesting an improper chorioallantoic fusion
• at E8.5, homozygotes display a discontinuous, usually thicker visceral endoderm layer, with enlarged apical vacuoles

growth/size/body
• at E8.5, homozygotes are developmentally retarded by one day relative to wild-type or heterozygous embryos
• at E10.5, homozygotes are identical to E9.5 homozygotes, but have begun to deteriorate
• at E8.5, some homozygotes are only 50% of wild-type size

cellular
• at E9.5, homozygotes exhibit impaired N-glycosylation of multiple embryonically expressed proteins, such as laminin gamma 1, laminin beta and alpha-fetorprotein
• at E8.5, homozygotes exhibit excessive apoptosis in the embryo proper, esp. at the distal tip
• at E9.5, mutant embryos display large regions of TUNEL+ cells in both ectodermal and mesodermal tissues
• excessive apoptosis occurs predominantly in the embryo proper and not typically in the extraembryonic tissues (e.g. parietal cells are TUNEL-)

homeostasis/metabolism
• at E9.5, homozygotes display a hydroponic allantois, suggesting an improper chorioallantoic fusion





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last database update
11/19/2024
MGI 6.24
The Jackson Laboratory