Mouse Genome Informatics
hm1
    Cxadrtm1.1Mds/Cxadrtm1.1Mds
involves: 129S1/Sv * 129S4/SvJae * 129X1/SvJ * C57BL/6J
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
mortality/aging
• all homozygous embryos are dead or undergoing resorption at E12.5 and later times; only one homozygote was identified among living animals at 4 weeks of age

embryogenesis
N
• yolk sac and yolk sac vessels appear normal (J:121400)

cardiovascular system
N
• no definite abnormalities are seen in endocardial cushions, right ventricular wall, right ventricular outflow tract, or other derivatives of the secondary hear field (J:121400)
• at E10.5 and E11.5, engorgement of the cardinal veins is apparent, suggesting cardiac dysfunction
• hyperplasia of proximal heart tube is seen at E10.5
• many embryos show moderate thickening of the atrial myocardium
• junctions between left ventricular cardiomyocytes are abnormal; cells have short membrane contact sites while controls show long stretches of membrane contacts with electron density
• junctions between epicardial and endocardial cells appear normal
• myofilament bundles are thinner than in wild-type and appear less compact
• thickened left ventricle is result of increased cell numbers
• at E10.5 and 11.5, null embryos can be identified by prominence of the left ventricular silhouette
• left ventricular wall is abnormally thickened, with partial obliteration of the ventricular lumen
• proliferation rate of left ventricular cardiomyocytes is twice that in wild-type hearts

muscle
• junctions between left ventricular cardiomyocytes are abnormal; cells have short membrane contact sites while controls show long stretches of membrane contacts with electron density
• junctions between epicardial and endocardial cells appear normal
• myofilament bundles are thinner than in wild-type and appear less compact
• proliferation rate of left ventricular cardiomyocytes is twice that in wild-type hearts

cellular
• proliferation rate of left ventricular cardiomyocytes is twice that in wild-type hearts


Mouse Genome Informatics
cn2
    Cxadrtm1Mds/Cxadrtm1.1Mds
Tg(Tnnt2-cre)5Blh/0

involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * DBA/2
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
mortality/aging
• no live conditional null mice are found at 4 weeks after birth; embryos at E10.5; mice display identical phenotype to Cxadrtm1.1Mds homozygotes

cardiovascular system
• at E10.5, engorgement of the cardinal veins is apparent
• hyperplasia of proximal heart tube is seen at E10.5
• sinuatrial valves located at junction between sinus venosus and atrium in wild-type embryos, are absent


Mouse Genome Informatics
cn3
    Cxadrtm1Mds/Cxadrtm1.1Mds
Tg(Myh6-cre)2182Mds/0

involves: 129S1/Sv * 129X1/SvJ * FVB/N
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
mortality/aging
N
• many conditional null mice are born alive and survive to adulthood (20/102) (J:121400)

cardiovascular system
• sinuatrial valves show mild abnormalities in embryos, with only 1 embryo showing absence or attenuation comparable to constitutive null mice
• embryos show only mild or no abnormal ventricular thickening with little or no increase in proliferating cells