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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Stk11tm2.1Tpm
targeted mutation 2.1, Tomi P Makela
MGI:2387005
Summary 1 genotype
Jump to Allelic Composition Genetic Background Genotype ID
hm1
Stk11tm2.1Tpm/Stk11tm2.1Tpm involves: BALB/c * C57BL/6 MGI:3790878


Genotype
MGI:3790878
hm1
Allelic
Composition
Stk11tm2.1Tpm/Stk11tm2.1Tpm
Genetic
Background
involves: BALB/c * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Stk11tm2.1Tpm mutation (0 available); any Stk11 mutation (5 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• no viable embryos are observed past E11.0

embryo
• rudimentary vessels are seen between the parietal and visceral leaves of yolk sac; vessels are congested with nucleated embryonic blood cells
• vitelline artery is completely atretic
• large vessels and extensive capillary network fail to develop in mutant yolk sac
• absent in some embryos after E8.25
• hypoplastic in some embryos after E8.25
• after E8.25, failure of embryo turning is observed
• cephalic mesenchyme of E9.5 head folds has lower cell density and fewer capillaries than controls; cell density is result of increased cell death assayed by TUNEL staining and this apoptosis phenotype is limited to the E9.5 embryos
• at E9.5 folds often display large cystic degenerations near dorsal aorta with some containing embryonic blood cells
• defect in neural tube closure is observed after E8.25
• misaligned and contorted along anterior/posterior axis of embryo at E9.25
• somitogenesis is defective resulting in dimorphic protrusive somites at E9.5
• at E9.5, placentas are hemorrhagic and edematous
• blood lacunae have ruptured causing massive hemorrhaging by E10.5
• invasion of placenta by embryonic blood vessels does not occur; at E9.5 lack of fetal blood vessels in rudimentary labyrinth layer is shown by absence of VEGF signal
• less organized than in wild-type and contains larger number of abnormal (flt-1 negative) giant cells
• diameter of placenta is smaller at E9.5
• fusion is delayed in mutant conceptuses compared to controls, but occurs by E9.5

cardiovascular system
• at E8.5, vessel is thin and discontinuous especially in the anterior part
• at E9.5 lumen remains thin with intersomitic branches ending prematurely in the mesenchyme
• blood lacunae have ruptured causing massive hemorrhaging by E10.5
• invasion of placenta by embryonic blood vessels does not occur; at E9.5 lack of fetal blood vessels in rudimentary labyrinth layer is shown by absence of VEGF signal
• rudimentary vessels are seen between the parietal and visceral leaves of yolk sac; vessels are congested with nucleated embryonic blood cells
• vitelline artery is completely atretic
• large vessels and extensive capillary network fail to develop in mutant yolk sac
• complete absence of vascular smooth muscle cell (VSMC) staining is observed in mutant dorsal aorta and somites at E9.5
• strong ectopic VSMC signal is observed in head folds

craniofacial
• absent in some embryos after E8.25
• hypoplastic in some embryos after E8.25

muscle
• complete absence of vascular smooth muscle cell (VSMC) staining is observed in mutant dorsal aorta and somites at E9.5
• strong ectopic VSMC signal is observed in head folds

nervous system
• defect in neural tube closure is observed after E8.25

growth/size/body
• cephalic mesenchyme of E9.5 head folds has lower cell density and fewer capillaries than controls; cell density is result of increased cell death assayed by TUNEL staining and this apoptosis phenotype is limited to the E9.5 embryos





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last database update
11/13/2018
MGI 6.13
The Jackson Laboratory