Phenotypes associated with this allele
Allelic
Composition |
Pak4tm1Amin/Pak4tm1Amin
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Genetic
Background |
either: (involves: 129P2/OlaHsd * C57BL/6J) or (involves: 129S2/SvPas * C57BL/6J) |
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| Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Pak4tm1Amin mutation
(1 available);
any
Pak4 mutation
(91 available)
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embryo
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• at E10.5, vascular invasion fails after chorioallantoic fusion unlike in wild-type mice
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• slightly at E9.5, markedly at E10.5
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• at E10.5, the placenta labyrinth is compact with reduced thickness and fewer embryonic blood vessels compared to in wild-type mice
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• slightly at E9.5, markedly at E10.5
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• at E10.5, yolk sacs are thicker and rougher than wild-type yolk sacs
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• at E10.5, large vitelline vessels are absent with only the honeycomb-like plexus present
• at E10.5, yolk sac vessels are dilated and contain fewer blood cells than in wild-type mice
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growth/size/body
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• slightly at E9.5, markedly at E10.5
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cellular
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• at E10.5, especially in the nervous system
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• at E10.5, especially in the nervous system
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cardiovascular system
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• at E10.5, vascular invasion fails after chorioallantoic fusion unlike in wild-type mice
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integument
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• slightly at E9.5, markedly at E10.5
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Allelic
Composition |
Pak4tm1Amin/Pak4tm1Amin
|
|
Genetic
Background |
either: (involves: 129P2/OlaHsd * C57BL/6) or (involves: 129S2/SvPas * C57BL/6) |
|
| Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Pak4tm1Amin mutation
(1 available);
any
Pak4 mutation
(91 available)
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muscle
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• at E10.5, homozygotes display thinning of the myocardial walls of the bulbus cordis and ventricles
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mortality/aging
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• no homozygotes are obtained after E10.5, putatively due to a defect in the fetal heart
• only partly resorbed embryos are detected at E11.5
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growth/size/body
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• at E9.5, mutant embryos are generally smaller than wild-type embryos
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cardiovascular system
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• at E10.5, homozygotes display thinning of the myocardial walls of the bulbus cordis and ventricles
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• at E10.5, homozygotes display thinning of the primitive ventricular wall
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• at E10.5, the atrium and/or sinus venosus region of the heart appears distended and dilated
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nervous system
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• unlike wild-type embryos where neurofilament positive cells are located at the lateral edge of the hindbrain, mutant embryos display a small number of neurofilament positive cells both medially and laterally, suggesting a defect in neuronal migration
• at E9.5, mutant spinal cord motor neurons are not located in their proper lateral positions, indicating a corresponding defect in motor neuron migration
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• at E9.5, mutant brains appear wavy, probably due to postmortem collapse of the thin neuroepithelial walls
• at E10.5, mutant embryos display a large empty area in the head region in H&E-stained sagittal sections
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• at E9.5, mutant embryos are translucent around the head and neural tube regions
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• at E9.5, homozygotes exhibit lack of neuronal differentiation and a concomittant reduction in cell size due to impaired axonal outgrowth
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• at E9.5, homozygotes display defective axonal outgrowth in the hindbrain, as shown by staining with anti-neurofilament antibody
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• at E9.5, an improper folding appears to occur between the ventral and dorsal parts of the caudal neural tube, resulting in the formation of two neural lumens
• however, the dorsal-ventral patterning appears normal in mutant neural tubes
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• at E9.5, the neuroepithelium around the hindbrain and forebrain is strikingly thinner than normal
• at E9.5, the defects in neuroepithelium are not associated with a severe defect in proliferation or an increase in apoptosis, although sporadic TUNEL-positive staining is observed in tissues outside the neuroepithelium at this stage
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• at E9.5, homozygotes show failure of spinal cord motor neurons to differentiate
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• at E9.5, homozygotes display failure of developing ventral interneurons to differentiate
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embryo
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• at E9.5, mutant embryos are generally smaller than wild-type embryos
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• at E9.5, an improper folding appears to occur between the ventral and dorsal parts of the caudal neural tube, resulting in the formation of two neural lumens
• however, the dorsal-ventral patterning appears normal in mutant neural tubes
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• at E9.5, the neuroepithelium around the hindbrain and forebrain is strikingly thinner than normal
• at E9.5, the defects in neuroepithelium are not associated with a severe defect in proliferation or an increase in apoptosis, although sporadic TUNEL-positive staining is observed in tissues outside the neuroepithelium at this stage
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cellular
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• when grown in serum-free medium, cells isolated from E9.5 mutant, but not wild-type, embryos show significant levels of focal adhesions, as evidenced by large clusters of vinculin
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• at E9.5, homozygotes exhibit lack of neuronal differentiation and a concomittant reduction in cell size due to impaired axonal outgrowth
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• at E9.5, homozygotes display defective axonal outgrowth in the hindbrain, as shown by staining with anti-neurofilament antibody
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• unlike wild-type embryos where neurofilament positive cells are located at the lateral edge of the hindbrain, mutant embryos display a small number of neurofilament positive cells both medially and laterally, suggesting a defect in neuronal migration
• at E9.5, mutant spinal cord motor neurons are not located in their proper lateral positions, indicating a corresponding defect in motor neuron migration
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Analysis Tools