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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Yap1tm1Smil
targeted mutation 1, Sharon L Milgram
MGI:3608880
Summary 4 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
hm1
Yap1tm1Smil/Yap1tm1Smil either: (involves: 129S/SvEv * C57BL/6J) or (involves: 129S/SvEv * C57BL/6J * CD-1) MGI:3608881
cx2
Tead1tm1Hssk/Tead1+
Tead2tm1Hssk/Tead2tm1Hssk
Yap1tm1Smil/Yap1+
either: (involves: 129S/SvEv * C57BL/6 * CBA) or (involves: 129S/SvEv * C57BL/6 * CBA * CD-1) MGI:3797240
cx3
Tead1tm1Hssk/Tead1tm1Hssk
Tead2tm1Hssk/Tead2+
Yap1tm1Smil/Yap1+
either: (involves: 129S/SvEv * C57BL/6 * CBA) or (involves: 129S/SvEv * C57BL/6 * CBA * CD-1) MGI:3797243
cx4
Wwtr1tm1Hku/Wwtr1tm1Hku
Yap1tm1Smil/Yap1tm1Smil
involves: 129S/SvEv MGI:3840660


Genotype
MGI:3608881
hm1
Allelic
Composition
Yap1tm1Smil/Yap1tm1Smil
Genetic
Background
either: (involves: 129S/SvEv * C57BL/6J) or (involves: 129S/SvEv * C57BL/6J * CD-1)
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Yap1tm1Smil mutation (0 available); any Yap1 mutation (38 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• no homozygous pups were identified among 900 postnatally genotyped progeny of heterozygous intercrosses
• although at E9.5, embryonic genotypes occur in the expected Mendelian ratios, only two, partly resorbed homozygous embryos were observed at E10.5

embryo
• at embryonic day E7.5, about 50% of homozygous embryos exhibit some morphologic abnormality, the rest appearing normal; by E8.5, all mutant embryos have a characteristic phenotype
• midline expression of brachyury (T) in E8.5 mutant embryos occurs in a wide, discontinuous band rather than the narrow, defined band seen in wild-type controls, indicating abnormal development along the mediolateral axis
• E9.5 mutant embryos have failed to turn, retaining the distal point, the bend point of the unturned body axis
• at E8.5, mutant embryos have a strikingly short, wide body axis; by E9.5, failure of elongation of the body axis is even more pronounced
• homozygous mutant E8.5 embryos exhibit caudal dysgenesis
• all mutant embryos are very small at E9.5
• at E8.5, mutant embryos have a strikingly short, wide body axis; by E9.5, failure of elongation of the body axis is even more pronounced
• at E8.5, histologic examination reveals that homozygous embyros have failed to maintain the posterior epiblast-like epithelium in the streak region; the tissue layer overlying the mesoderm is thinner than normal
• perturbations observed in E7.5 mutant embryos include a marked constriction at the embryonic-extraembryonic boundary or total separation of the epiblast from the extraembryonic ectoderm
• histologic examination of E7.5 homozygous embryos reveals disorganization of the yolk sac mesoderm
• although both endothelial cells and erythroblasts, which together normally comprise the yolk sac vasculature, are abundant in the E8.5 mutant yolk sac, they have not organized to form the primitive vascular plexus
• yolk sac visceral endoderm-adjacent mesoderm of mutant E7.5 embryos lacks the organization characteristic of early blood island development
• although mesoderm cells are abundant in E8.5 mutant yolk sac, few defined blood-island-like structures are evident, and endothelial and hematopoietic precursor cells are not clearly distinguishable
• at E9.5, yolk sacs of mutant embryos have a distinctively rippled appearance

growth/size/body
• all mutant embryos are very small at E9.5
• ventral closure has failed to occur in mutant embryos by E9.5

cardiovascular system
• although blood vessels are present in the embryo proper at E8.5, their positioning is aberrant
• although both endothelial cells and erythroblasts, which together normally comprise the yolk sac vasculature, are abundant in the E8.5 mutant yolk sac, they have not organized to form the primitive vascular plexus

nervous system
• mutant embyos at E8.5 exhibit multiple folding, and E9.5 embryos convolution, of the anterior eptithelium
• histologic examination of E8.5 homozygous embryos reveals excessive folding of the neurectoderm, which extends as a single tissue layer into the amniotic cavity




Genotype
MGI:3797240
cx2
Allelic
Composition
Tead1tm1Hssk/Tead1+
Tead2tm1Hssk/Tead2tm1Hssk
Yap1tm1Smil/Yap1+
Genetic
Background
either: (involves: 129S/SvEv * C57BL/6 * CBA) or (involves: 129S/SvEv * C57BL/6 * CBA * CD-1)
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tead1tm1Hssk mutation (1 available); any Tead1 mutation (275 available)
Tead2tm1Hssk mutation (1 available); any Tead2 mutation (34 available)
Yap1tm1Smil mutation (0 available); any Yap1 mutation (38 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
embryo
• mutants exhibit smaller posterior tissues
• defective embryonic turning




Genotype
MGI:3797243
cx3
Allelic
Composition
Tead1tm1Hssk/Tead1tm1Hssk
Tead2tm1Hssk/Tead2+
Yap1tm1Smil/Yap1+
Genetic
Background
either: (involves: 129S/SvEv * C57BL/6 * CBA) or (involves: 129S/SvEv * C57BL/6 * CBA * CD-1)
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tead1tm1Hssk mutation (1 available); any Tead1 mutation (275 available)
Tead2tm1Hssk mutation (1 available); any Tead2 mutation (34 available)
Yap1tm1Smil mutation (0 available); any Yap1 mutation (38 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
embryo
• mutants show essentially the same morphological defects as double Tead1 and Tead2 homozygotes
• embryos develop a posterior-ventral protrusion
• embryos develop a bulbous allantois




Genotype
MGI:3840660
cx4
Allelic
Composition
Wwtr1tm1Hku/Wwtr1tm1Hku
Yap1tm1Smil/Yap1tm1Smil
Genetic
Background
involves: 129S/SvEv
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Wwtr1tm1Hku mutation (0 available); any Wwtr1 mutation (26 available)
Yap1tm1Smil mutation (0 available); any Yap1 mutation (38 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging





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last database update
11/12/2024
MGI 6.24
The Jackson Laboratory