Phenotypes associated with this allele
cardiovascular system
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• cardiomyocytes of older mutants (9 months of age) exhibit increased length but not width
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• myocardium of older mutants (9 months of age) shows disorganized myofibrils with increased nonmyofibrillar space filled with swelled mitochondria
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• develop eccentric cardiac hypertrophy (normal left ventricle wall thickness and increased left chamber dimension) upon stimulation with angiotensin II or pressure overload by transverse aortic constriction, exhibiting an increase in heart/body weight ratios and elevated markers of cardiac hypertrophy
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• older mutants develop spontaneous cardiac chamber dilation
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• develop multifocal interstitial fibrosis upon stimulation with angiotensin II
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muscle
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• cardiomyocytes of older mutants (9 months of age) exhibit increased length but not width
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• myocardium of older mutants (9 months of age) shows disorganized myofibrils with increased nonmyofibrillar space filled with swelled mitochondria
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growth/size/body
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• develop eccentric cardiac hypertrophy (normal left ventricle wall thickness and increased left chamber dimension) upon stimulation with angiotensin II or pressure overload by transverse aortic constriction, exhibiting an increase in heart/body weight ratios and elevated markers of cardiac hypertrophy
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cellular
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• develop multifocal interstitial fibrosis upon stimulation with angiotensin II
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| Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ptk2tm1.1Guan mutation
(1 available);
any
Ptk2 mutation
(90 available)
Tg(Tek-cre)12Flv mutation
(1 available)
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mortality/aging
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• fewer mutant embryos than Mendelian ratio at E13.5
• no live mutant embryos at E14.5
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cellular
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• increased apoptosis in the liver, brain, placenta and skin at E13.5
• presence of apoptotic endothelial cells (ECs) in the blood vessel of the brain and skin
• increased apoptosis after recombinant adenoviruses encoding Cre (Ad-Cre) infection of the ECs in vitro
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growth/size/body
embryo
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• lack of vessels containing nucleated red blood cells in placenta at E13.5
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• reduced vascular network in mutant yolk sac at E13.5
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• decrease in the thickness of the labyrinth layer of the placenta at E13.5
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cardiovascular system
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• fewer blood vessels in the brain, spinal cord and skin at E13.5
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• lack of vessels containing nucleated red blood cells in placenta at E13.5
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• reduced vascular network in mutant yolk sac at E13.5
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• dilation of vessels in the brain, spinal cord and skin at E12.5
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• perivascular hemorrhages at E13.5
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• increased permeability after Ad-Cre infection of ECs in vitro
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homeostasis/metabolism
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| Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ptk2tm1.1Guan mutation
(1 available);
any
Ptk2 mutation
(90 available)
Ptk2tm1.2Guan mutation
(0 available);
any
Ptk2 mutation
(90 available)
Tg(Tek-cre)12Flv mutation
(1 available)
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mortality/aging
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• mutant embryos are progressively lost starting at E13.5 with only 3% of pups at birth having the conditional null genotype
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cardiovascular system
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• endothelial cells lining small capillaries have pyknotic and karyorrhetic changes and many are rounded, detached, and sloughing off into the lumen
• apoptotic and necrotic endothelial cells are seen
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• many capillaries with abnormal endothelial cells are collapsed
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• arterial canals and canal branches lack fetal red blood cells and some of the vessels appear collapsed; however the heart appears normal
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• at E13.5, the vascular network in the head is reduced and no clear outlines of viscera or axial skeleton with PECAM-1 staining
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• fewer branched vessels and a marked decrease in sprouting angiogenesis are seen in the yolk sac
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• at E13.5, multifocal, scattered, and variably sized hemorrhages are seen and at E14.5 these are large and superficial
• at E13.5, the thickened dermis also has numerous perivascular hemorrhages
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embryo
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• arterial canals and canal branches lack fetal red blood cells and some of the vessels appear collapsed; however the heart appears normal
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• fewer branched vessels and a marked decrease in sprouting angiogenesis are seen in the yolk sac
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• seen in about 5% of embryos at E10.5
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• thickening of the amnion as a result of edema
• prominent amniotic blood vessels are not seen
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• the thickness of the placental labyrinth is reduced
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homeostasis/metabolism
growth/size/body
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• seen in about 5% of embryos at E10.5
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integument
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• at E13.5, thickening and expansion of the dermis with loosely arranged mesenchymal cells mixed with acellular pale esosinophilic material
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mortality/aging
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• fewer mutant embryos are recovered than Mendelian ratios starting at embryonic day (E)14.5; none are alive at birth
• no perivascular hemorrhages, normal vessels containing nucleated red blood cells, normal vascularization in placenta at E13.5
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cardiovascular system
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• decreased number of vessels in the brain, spinal cord and skin at E13.5
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• dilated vessels in the brain, spinal cord and skin at E12.5
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• increased permeability after recombinant adenoviruses encoding Cre infection of endothelial cells in vitro
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cellular
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• a slight increase in apoptosis in the liver at E13.5
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Analysis Tools