Phenotypes associated with this allele
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| Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Foxm1tm1.1Rhc mutation
(0 available);
any
Foxm1 mutation
(26 available)
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cardiovascular system
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• E13.5-18.5 hearts exhibit thinning of the ventricular myocardium
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• severe accumulation of polyploid cardiomyocytes is seen in E13.5-18.5 heart tissues, including ventricular myocardium, interventricular septum, atrium, and heart trabeculae
• increase in the size of cardiomyocyte nuclei is noted at E15.5 and E18.5
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• reduced number of cardiomyocytes at E13.5 and E18.5
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• enlarged cardiomyocytes are seen in the atrium and ventricle as early as E9.5
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• 25% reduction in heart size at E15.5 but not at E13.5
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• 1.3-fold increase in thickness of heart valve leaflets at E13.5
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• thickening of atrioventricular (A/V) valves (mitral valve leaflets) at E13.5
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• hearts show a 43% reduction in the thickness of the left ventricle at E13.5 and a 57% reduction at E15.5
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• embryos display dilated heart ventricles
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• developing cardiomyocytes show diminished DNA replication and mitosis at E15.5
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cellular
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• developing cardiomyocytes show diminished DNA replication and mitosis at E15.5
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muscle
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• E13.5-18.5 hearts exhibit thinning of the ventricular myocardium
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• developing cardiomyocytes show diminished DNA replication and mitosis at E15.5
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| Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Foxm1tm1.1Rhc mutation
(0 available);
any
Foxm1 mutation
(26 available)
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mortality/aging
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• 75% were dead by E17.5 and all were dead by E18.5
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cardiovascular system
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• disruption in the organization of liver sinusoids
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• reduction in the number of large hepatic veins
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• enlarged polyploid embryonic cardiomyocytes were observed
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• at E17.5 embryos were transparent with hemorrhagic lesions
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cellular
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• decrease in BrdU incorporation without increase in apoptosis suggesting a block in mitosis; a decrease in expression of proteins required for cell cycle progression and cytokinesis was observed
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homeostasis/metabolism
liver/biliary system
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• disruption in the organization of liver sinusoids
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• abnormal development of the intrahepatic bile ducts
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• presence of abnormal hepatoblast cells with enlarged polyploid nuclei
• decrease in BrdU incorporation without increase in apoptosis suggesting a block in mitosis; a decrease in expression of proteins required for cell cycle progression and cytokinesis was observed
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• reduced numbers of hepatoblasts; 75% reduction in the number of hepatoblasts compared to controls, but no decrease in overall size of liver suggesting a hypertrophy of remaining hepatoblasts
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• disruption in the organization of hepatic cords
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muscle
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• enlarged polyploid embryonic cardiomyocytes were observed
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endocrine/exocrine glands
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• abnormal development of the intrahepatic bile ducts
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| Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Foxm1tm1.1Rhc mutation
(0 available);
any
Foxm1 mutation
(26 available)
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Foxm1tm1.1Rhc/Foxm1tm1.1Rhc embryonic lungs exhibit pulmonary artery hypertrophy
cardiovascular system
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• at E18.5, homozygotes exhibit severe hypertrophy of pulmonary arteries, associated with a 5-fold increase in arterial muscularity
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• at E18.5, homozygotes display severe hypertrophy of vascular smooth muscle cells of the aorta
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• at E18.5, homozygotes display severe hypertrophy of vascular smooth muscle cells of the carotid artery
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• at E17.5, homozygotes show a significant reduction in the number of peripheral pulmonary capillaries
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• at E15.5 and E17.5, homozygotes show a significant reduction in the number of large pulmonary vessels (arteries and veins with diameter = 25 um) and peripheral pulmonary capillaries, with no evidence of increased apoptosis
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• at E18.5, homozygotes display severe hypertrophy of vascular smooth muscle cells of the pulmonary arteries, with abnormally large DAPI-stained nuclei
• many extrapulmonary arteries (e.g. the carotid artery and aorta) display severe hypertrophy of smooth muscle cells
• however, airway smooth muscle cells of E18.5 mutant pulmonary bronchi exhibit normal morphology
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respiratory system
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• at E15.5 and E17.5, homozygotes show a significant reduction in the number of large pulmonary vessels (arteries and veins with diameter = 25 um) and peripheral pulmonary capillaries, with no evidence of increased apoptosis
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• homozygotes display defective lung development associated with aberrant expression of pulmonary genes involved in extracellular matrix remodeling, mesenchyme proliferation, and vasculogenesis
• however, mutant lung size, lobular architecture, and sacculation appear unaffected
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• at E15.5, homozygotes display reduced proliferation of mesenchymal cells around the distal lung epithelium
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muscle
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• at E18.5, homozygotes display severe hypertrophy of vascular smooth muscle cells of the pulmonary arteries, with abnormally large DAPI-stained nuclei
• many extrapulmonary arteries (e.g. the carotid artery and aorta) display severe hypertrophy of smooth muscle cells
• however, airway smooth muscle cells of E18.5 mutant pulmonary bronchi exhibit normal morphology
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cellular
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• at E15.5, homozygotes display reduced proliferation of mesenchymal cells around the distal lung epithelium
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Analysis Tools