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Phenotypes Associated with This Genotype
Genotype
MGI:2673509
hm1
Allelic
Composition
Med1tm1Rgr/Med1tm1Rgr
Genetic
Background
either: (involves: 129P2/OlaHsd * C57BL/6J) or (involves: 129P2/OlaHsd * 129X1/SvJ)
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Med1tm1Rgr mutation (0 available); any Med1 mutation (83 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• at E9.5 and thereafter, homozygotes show a significant increase in resorption

cardiovascular system
• at E10.5, homozygotes show severe heart failure typified by cardiac and large vessel enlargement; no placental defects are observed
• at E10.5, the vena cava of homozygous embryos becomes significantly enlarged as a result of severe heart failure
• at E10.5, formation of the trabecular layer is severely perturbed
• at E10.5, the thickness of the subepicardial layer is significantly reduced
• at E10.5, the heart of homozygous embryos becomes significantly enlarged as a result of severe heart failure
• after E9.5, most homozygous mutants exhibit severely impaired circulation due to heart hypoplasia
• at E9.5, homozygotes display significant hypoplasia of ventricular trabeculae in spite of a grossly normal compact layer
• by E10.5, mutant embryos display poor trabeculation relative to wild-type
• at E10.5, homozygotes display thin and dilated ventricular walls that presumably arise from effects secondary to severe heart failure
• at E10.5, hypoplastic mutant hearts display a pumping failure as fetal circulation becomes enlarged; as a result, severe heart failure ensues

growth/size/body
• at E10.5, the heart of homozygous embryos becomes significantly enlarged as a result of severe heart failure
• at E10.5, homozygous mutant embryos are significantly smaller than wild-type
• by E9.5, mutant embryos exhibit disproportionally smaller heads than wild-type embryos

nervous system
• at E10.5, mutant embryos exhibit neuronal apoptosis in the cortical plate of neural tubes
• at E9.5, homozygotes display an underdeveloped central nervous system relative to wild-type
• at E9.5, the neuroepithelial layer of cortical neurons is severely reduced
• at E9.5, homozygous embryos show abnormal forebrain development
• at E9.5, homozygotes display an underdeveloped telencephalon
• at E10.5, some cells of the superficial postmitotic telencephalic layer are differentiated into neurons, although their number is significantly reduced

embryo
• at E10.5, homozygous mutant embryos are significantly smaller than wild-type
• at E9.5, the neuroepithelial layer of cortical neurons is severely reduced

muscle
• at E10.5, formation of the trabecular layer is severely perturbed
• at E9.5, homozygotes display significant hypoplasia of ventricular trabeculae in spite of a grossly normal compact layer
• by E10.5, mutant embryos display poor trabeculation relative to wild-type
• at E10.5, the thickness of the subepicardial layer is significantly reduced

cellular
• homozygous mutant MEFs show defective cell cycle regulation with an impaired entrance into S phase
• at E10.5, mutant embryos exhibit neuronal apoptosis in the cortical plate of neural tubes
• homozygous mutant MEFs grow slower than wild-type or heterozygous mutant MEFs

liver/biliary system
• at E10.5, homozygotes display a somewhat reduced liver primordium

respiratory system
• at E10.5, mutant lungs display a grossly normal architecture, albeit with slightly reduced main bronchi


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
12/10/2024
MGI 6.24
The Jackson Laboratory