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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Med1tm1Rgr
targeted mutation 1, Robert G Roeder
MGI:1861125
Summary 2 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
hm1
Med1tm1Rgr/Med1tm1Rgr either: (involves: 129P2/OlaHsd * C57BL/6J) or (involves: 129P2/OlaHsd * 129X1/SvJ) MGI:2673509
ht2
Med1tm1Rgr/Med1+ either: 129X1/SvJ or (involves: 129X1/SvJ * C57BL/6J) MGI:3588434


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




Genotype
MGI:3588434
ht2
Allelic
Composition
Med1tm1Rgr/Med1+
Genetic
Background
either: 129X1/SvJ or (involves: 129X1/SvJ * C57BL/6J)
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
growth/size/body
• after weaning, heterozygotes are significantly smaller than wild-type mice
• heterozygotes are shorter than wild-type mice; however, no other morphological abnormalities are observed
• heterozygotes display significant growth retardation after weaning
• no significant differences in weight are observed throughout embryogenesis and at birth

homeostasis/metabolism
• at 12 weeks, the serum levels of free T4 are significantly reduced in heterozygous F1 males relative to wild-type levels
• at 12 weeks, the serum levels of free T3 are significantly reduced in heterozygous F1 males relative to wild-type levels
• at 12 weeks, male heterozygotes show a significant decrease in pituitary TSH-beta production without significant changes in TSH-alpha or growth hormone (GH) production
• heterozygotes exhibit widely impaired transcription and post-transcriptional regulation in certain organs

endocrine/exocrine glands
• heterozygotes exhibit pituitary hypothyroidism due to a reduction in pituitary TSH-beta mRNA levels; no changes in TRH mRNA levels are observed





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last database update
11/19/2024
MGI 6.24
The Jackson Laboratory