Phenotypes associated with this allele
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| Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Myh10tm2Rsad mutation
(1 available);
any
Myh10 mutation
(95 available)
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The hydrocephalus seen in Myh10tm2Rsad/Myh10tm2Rsad mice is rescued by Myh9 expression in Myh10tm6(Myh9/GFP)Rsad/Myh10tm6(Myh9/GFP)Rsad mice
cardiovascular system
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• epicardial cells exhibit normal migration in vitro in a scratch wound assay
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• authors state that mice exhibit similar heart defects as observed in
Myh10ehc homozygotes
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• does not display organized clusters of smooth muscle cells or vascular structures unlike wild-type myocardium
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• the percentage of binucleated cells is increased to 23% from 1% in wild-type
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• at E14.5, the number of cardiac myocytes is reduced by about 70% relative to that in wild-type controls
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• the size of myocytes is increased at E12.5
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• at E12.5 the number of cell layers in the ventricles is reduced to 2 - 3 compared to 4 - 5 in wild-type hearts
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• proliferation of cardiac myocytes is decreased at E14.5
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• in the myocardium at E14.5
• however, there is no statistically significant change in apoptosis in the epicardium or in the heart at E9.5
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cellular
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• proliferation of cardiac myocytes is decreased at E14.5
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• in the myocardium at E14.5
• however, there is no statistically significant change in apoptosis in the epicardium or in the heart at E9.5
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muscle
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• does not display organized clusters of smooth muscle cells or vascular structures unlike wild-type myocardium
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• proliferation of cardiac myocytes is decreased at E14.5
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• in the myocardium at E14.5
• however, there is no statistically significant change in apoptosis in the epicardium or in the heart at E9.5
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nervous system
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• the spinal cord is obstructed in mutants
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| Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Myh10tm2Rsad mutation
(1 available);
any
Myh10 mutation
(95 available)
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nervous system
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• mice show severe hydroencephaly
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• mice show protrusion of facial neurons into fourth ventricle
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cardiovascular system
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• E14.5 hearts exhibit defects in outflow tract (OFT) alignment
• at E11.5, cardiac myocytes do not invade the underlying cardiac cushions, indicating defective myocardialization of the developing OFT
• at E11.5, cardiac myocytes show abnormal enrichment of N-cadherin at the cell-cell boundaries, indicating defects in the disassembly of cell-cell adhesions
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• 13% of cardiomyocytes exhibit an abnormal shape and 15% are binucleated
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• at E13.5, hearts exhibit a marked reduction in cardiomyocytes
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• atrioventricular cushions exhibit normal fusion at E12.5 but show a delay in further maturation into mitral and tricuspid valves at E14.5
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growth/size/body
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N |
• embryos DO NOT exhibit defects in ventral body wall closure or midline fusion
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| Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Myh10tm2Rsad mutation
(1 available);
any
Myh10 mutation
(95 available)
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Cardiac defects in newborn Myh10tm2Rsad/Myh10tm2Rsad mice
mortality/aging
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• homozygotes that survive to term exhibit congestive heart failure and die during the first postnatal day
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• ~65% of homozygotes die prior to birth
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cardiovascular system
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• newborn hearts show mild to moderate myofibrillar disarray as well as clear areas of cytoplasm corresponding to accumulations of glycogen particles
• right atrial myocytes are enlarged and contain significantly more cisterns of endoplasmic reticulum and Golgi complexes, as well as abundant glycogen particles
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• newborn hearts show mild to moderate myofibrillar disarray
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• as early as E12.5, homozygotes exhibit cardiac myocyte hypertrophy throughout the ventricles and atria, as shown by a significant increase in RV+LV cardiomyocyte diameter
• newborn hearts show enlarged right atrial myocytes
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• newborn homozygotes show right atrial dilatation
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• 6 of 7 newborn homozygotes exhibit a VSD located beneath the aortic valve; the muscular portion of the ventricular septum remains intact
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• newborn homozygotes display abnormal rounded hearts
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• 6 of 7 homozygotes exhibit a rightward malposition of the aortic valve, so that it straddles the ventricular septum and the septal defect or emanates almost entirely from the right ventricle; the defect is found in the membranous portion of the ventricular septum
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• in 6 of 7 newborn homozygotes, the right ventricular outflow tract is narrowed by hypertrophic muscle
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• newborn homozygotes die of congestive heart failure with secondary tissue changes noted in the liver, kidney, and spleen
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craniofacial
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• newborn homozygotes exhibit dome-shaped heads due to hydrocephalus involving the lateral ventricles
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liver/biliary system
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• newborn homozygotes exhibit a dark purple, congested liver that is visible through the skin
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nervous system
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• newborn homozygotes display hydrocephalus involving the lateral ventricles
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• newborn homozygotes fail to develop the bipolar layer of retinal ganglion cells
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behavior/neurological
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• all moribund pups are unable to nurse
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growth/size/body
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• newborn homozygotes exhibit a variable body size
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vision/eye
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• newborn homozygotes display retinal dysplasia with rosette formation
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• newborn homozygotes fail to develop the bipolar layer of retinal ganglion cells
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skeleton
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• newborn homozygotes exhibit dome-shaped heads due to hydrocephalus involving the lateral ventricles
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Allelic
Composition |
Myh10tm2Rsad/Myh10+
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Genetic
Background |
involves: 129S4/SvJae * 129S6/SvEvTac * BALB/c * C57BL/6 |
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| Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Myh10tm2Rsad mutation
(1 available);
any
Myh10 mutation
(95 available)
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growth/size/body
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N |
• embryos DO NOT exhibit defects in ventral body wall closure
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cardiovascular system
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• mutants develop postnatal cardiac hypertrophy however at E13.5 no increase in the number of binucleated cardiac myocytes or in the size of cardiac myocytes is seen
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growth/size/body
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• mutants develop postnatal cardiac hypertrophy however at E13.5 no increase in the number of binucleated cardiac myocytes or in the size of cardiac myocytes is seen
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Allelic
Composition |
Myh10ehc/Myh10tm2Rsad
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Genetic
Background |
involves: 129S4/SvJae * 129S5/SvEvBrd * 129S7/SvEvBrd * C57BL/6J |
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| Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Myh10ehc mutation
(0 available);
any
Myh10 mutation
(95 available)
Myh10tm2Rsad mutation
(1 available);
any
Myh10 mutation
(95 available)
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mortality/aging
cardiovascular system
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• authors state that mice exhibit similar heart defects as observed in Myh10ehc homozygotes
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• does not display organized clusters of smooth muscle cells or vascular structures unlike wild-type myocardium
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muscle
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• does not display organized clusters of smooth muscle cells or vascular structures unlike wild-type myocardium
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growth/size/body
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• embryos exhibit defects in ventral body wall closure
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nervous system
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• mice show severe hydroencephaly
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• mice show protrusion of facial neurons into fourth ventricle
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| Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Myh10tm2Rsad mutation
(1 available);
any
Myh10 mutation
(95 available)
Myh10tm5Rsad mutation
(0 available);
any
Myh10 mutation
(95 available)
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nervous system
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• mice show severe hydroencephaly
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• mice show protrusion of facial neurons into fourth ventricle
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mortality/aging
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• embryos die as a result of cardiomyopathy after E14.5
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cellular
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• cardiomyocytes show an increase in acetylated tubulin staining suggesting an increase in microtubule stability
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• at E13.5, gamma-tubulin staining showed abnormal formation of multiple centrosomes in mitotic cardiac myocytes
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• cardiomyocytes exhibit impaired karyokinesis and multiple centrosomes
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• mitotic cardiomyocytes lack a bipolar spindle at metaphase; instead, spindles are deformed with irregular aggregated chromosomes
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cardiovascular system
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• at E13.5, 91% of cardiomyocytes exhibit an abnormal shape
• 9% of cardiomyocytes are binucleated
• nuclei are irregular and significantly larger, sometimes exhibiting a multilobed appearance
• mitotic cardiomyocytes lack a bipolar spindle; instead, spindles are deformed with irregular aggregated chromosomes
• however, sarcomere formation is normal in E13.5 cardiac myocytes
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• at E13.5, hearts exhibit a marked reduction in cardiomyocytes
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• embryonic heart is severely hypoplastic; however, numbers of cardiac myocytes are sufficient to support life to E14.5
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muscle
Analysis Tools