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Phenotypes Associated with This Genotype
Genotype
MGI:2683464
Allelic
Composition
Myl7tm1(cre)Krc/Myl7tm1(cre)Krc
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * Black Swiss
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Myl7tm1(cre)Krc mutation (0 available); any Myl7 mutation (7 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• all homozygotes die between E10.5 and E11.5 of cardiovascular insufficiency resulting from atrial malfunction

cardiovascular system
• by somite pair 24, mutant intersegmental vessels appear disorganized
• homozygotes display defects in both extraembryonic and intraembryonic vasculature
• by somite pair 24, mutant cranial vessels are less complex and intersegmental vessels appear disorganized
• at E10.0, mutant yolk sacs show absence of both large and small vessels
• mutant atrial cardiomyocytes show myofibrillar disorganization, with loss of a normal parallel alignment of thick and thin filaments
• in contrast, cardiomyocytes from the left ventricle display a normal parallel alignment of thick and thin filaments and normal Z-line formation
• at E10.0-E10.5, homozygtes exhibit a relatively thin walled ventricular myocardium
• at E10.0-E10.5, homozygotes underdeveloped ventricular trabeculae
• at E10.0-E10.5, mutant atrioventricular cushions fail to become seeded by mesenchymal cells
• by somite pair 24-28, homozygotes display enlarged outflow tracts
• at E10.0-E10.5, mutant atrioventricular cushions fail to grow, suggesting defective septation and valve formation
• homozygotes display abnormal looping architecture with alterations in the length, shape and size of each cardiac segment, and their geometrical relationship to each other
• at E8.5 (early linear heart tube stage), homozygotes display enlarged and amorphous hearts, with no clear distinction between the bulbus arteriosus and prospective left ventricle
• by somite pair 22, homozygotes exhibit enlarged atria
• at E10.0-E10.5, homozygotes exhibit a dilated left ventricle
• at E10.5, homozygotes display severe chest edema, indicating heart failure
• at E9.5, homozygotes exhibit severely reduced atrial beating (44 bpm) relative to wild-type embryos (516 bpm)
• in contrast, ventricular beating remains relatively unaffected (5310 and 487 for wild-type and mutant ventricles, respectively)

embryo
• at E10.0, mutant yolk sacs show absence of both large and small vessels
• all homozygotes exhibit growth arrest at approximately somite pair 24-28
• all homozygotes first exhibit growth retardation at ~E9.0-E9.25 (i.e. 15-17 somite pairs)
• at E10.0, mutant yolk sacs display separation of the mesodermal and endodermal layers
• the initial vascular plexus of mutant yolk sacs forms but fails to remodel into a vascular network of larger vessels

growth/size/body
• all homozygotes first exhibit growth retardation at ~E9.0-E9.25 (i.e. 15-17 somite pairs)

homeostasis/metabolism
• at E10.5, homozygotes display severe chest edema, indicating heart failure

muscle
• mutant atrial cardiomyocytes show myofibrillar disorganization, with loss of a normal parallel alignment of thick and thin filaments
• in contrast, cardiomyocytes from the left ventricle display a normal parallel alignment of thick and thin filaments and normal Z-line formation
• at E10.0-E10.5, homozygtes exhibit a relatively thin walled ventricular myocardium
• at E10.0-E10.5, homozygotes underdeveloped ventricular trabeculae


Contributing Projects:
Mouse Genome Database (MGD), Gene Expression Database (GXD), Mouse Models of Human Cancer database (MMHCdb) (formerly Mouse Tumor Biology (MTB)), Gene Ontology (GO)
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last database update
04/09/2024
MGI 6.23
The Jackson Laboratory