Phenotypes associated with this allele

• Allele Symbol: Tek^tm1Sato
• Allele Name: targeted mutation 1, Thomas N Sato
• Allele ID: MGI:2159358
• Summary: 2 genotypes

Jump to	Allelic Composition	Genetic Background	Genotype ID
hm1	Tek^tm1Sato/Tek^tm1Sato	either: (involves: 129S1/Sv * 129T2/SvEmsJ) or (involves: 129S1/Sv * C57BL/6J)	MGI:3612282
hm2	Tek^tm1Sato/Tek^tm1Sato	involves: 129S1/Sv * C57BL/6J	MGI:3612285

Genotype
MGI:3612282

hm1

• Allelic Composition: Tek^tm1Sato/Tek^tm1Sato
• Genetic Background: either: (involves: 129S1/Sv * 129T2/SvEmsJ) or (involves: 129S1/Sv * C57BL/6J)

• ♀: phenotype observed in females
• ♂: phenotype observed in males
• N: normal phenotype

mortality/aging

embryonic lethality during organogenesis, complete penetrance ( J:26844 )

• homozygotes all die by E10.5

cardiovascular system

abnormal angiogenesis ( J:26844 )

• at E9.0, vessels in the head are uniformly dilated with no distinction between large and small vessels

abnormal vascular branching morphogenesis ( J:26844 )

• beginning at E8.5, vessels that form the myocardial circulation fail to form extensive branches

• at E9.0, no capillary sprouts into the neuroectoderm are seen

abnormal vitelline vasculature morphology ( J:26844 )

• vasodilation and malformations of the vascular network are seen similar to those in the embryo proper

embryo

abnormal vitelline vasculature morphology ( J:26844 )

• vasodilation and malformations of the vascular network are seen similar to those in the embryo proper

embryonic growth retardation ( J:26844 )

• embryos appear growth retarded, especially in the head region and heart at E9.5

growth/size/body

embryonic growth retardation ( J:26844 )

• embryos appear growth retarded, especially in the head region and heart at E9.5

Genotype
MGI:3612285

hm2

• Allelic Composition: Tek^tm1Sato/Tek^tm1Sato
• Genetic Background: involves: 129S1/Sv * C57BL/6J

cardiovascular system

abnormal blood vessel morphology ( J:79305 )

• collapsed vessels lined by extremely thin endothelial extensions are seen in the heart, sinus venosus, and many smaller vessels throughout the embryo

abnormal vascular endothelial cell morphology ( J:79305 )

• round-shaped endothelial cells are more frequently seen protruding into the vessel lumen, compared to wild-type vessels

• these cells may block the lumen resulting in vessel collapse subsequent invasion of mesenchymal cells may result in vessel division

abnormal angiogenesis ( J:79305 )

• the primary vascular plexus is not transformed to a more complex vascular network

• only rudimentary perineural vascular loops are formed and more frequent blind-ending sprout like structures are seen

failure of vascular branching ( J:79305 )

• at E9.5 the number of tissue folds (involved in vessel division) are reduced and these folds are malformed, no periendothelial cells are seen, and mesenchymal cells remain distant from the endothelial cells

• many of these tissue folds are too short and unstable to result in proper vessel division

absent trabeculae carneae ( J:79305 )

• ventricular trabecular muscles do not form

abnormal heart development ( J:79305 )

• cells of the endocardium and sinus venosus remain separated from the surrounding mesenchyme

• endocardial endothelial cells unsupported by mesenchyme collapse into the lumen and fuse together forming occlusions of the sinus venosus, bulbo-truncal canal, or the area between the atrium and ventricle of the primitive heart

muscle

absent trabeculae carneae ( J:79305 )

• ventricular trabecular muscles do not form

embryo

embryo tissue necrosis ( J:79305 )

• necrosis is seen in the neuroectoderm and mesenchymal cells