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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Med1tm1Jkr
targeted mutation 1, Janardan K Reddy
MGI:1861123
Summary 1 genotype
Jump to Allelic Composition Genetic Background Genotype ID
hm1
Med1tm1Jkr/Med1tm1Jkr involves: 129P2/OlaHsd * C57BL/6 MGI:2673511


Genotype
MGI:2673511
hm1
Allelic
Composition
Med1tm1Jkr/Med1tm1Jkr
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Med1tm1Jkr mutation (0 available); any Med1 mutation (83 available)
phenotype observed in females
phenotype observed in males
N normal phenotype

Histological and ultrastructural alterations in Med1tm1Jkr/Med1tm1Jkr placenta

mortality/aging
• at E11.5, most homozygotes are still viable; however, a small number of embryos are either moribund, dead or degenerating
• no homozygous embryos are detected at E12.5 or beyond

cardiovascular system
• at E11.5, mutant livers show significantly dilated sinusoids
• at E11.5, homozygotes display significant differences in fetal and maternal vascular channels; vascular channels are scant and contain few erythrocytes (J:62272)
• at E11.5, mutant placentas fail to develop a complex capillary network; however, reduced placental angiogenesis is in marked contrast with the excessive systemic vascularization observed in hyperemic mutant embryos (J:74328)
• reduced network of embryonic capillary blood vessels at E11.5
• at E11.5, homozygotes display a hypoplastic myocardium relative to wild-type embryos
• at E11.5, homozygous embryos display trabecular hypoplasia
• at E11.5, homozygotes fail to compact the ventricular myocardium into the multilayer structure that is required to sustain cardiac function
• at E10.5 and E11.5, homozygotes display reduced thickness of the myocardium
• at E11.5, homozygotes show an significant increase in vascularization along the paraspinal region, within the developing brain and the retina; as a result, all mutant embryos appear grossly hyperemic
• at E11.5, the endothelial cells of the mutant endocardium fail to make direct contact with the underlying myocardial cells which appear pyknotic rather than stratified
• at E11.5, mutant hearts display contact gaps at the endocardial-myocardial junction possibly accounting for the loss of myocytes that result in ventricular hypoplasia
• at E11.5, myocardial cells fail to stratify normally resulting in a thin ventriular wall
• at E11.5, homozygotes display significant pericardial effusion associated with an enlarged, blood-filled ventricle
• embryonic lethality at E11.5 is attributed to severe cardiac failure resulting from abnormal cardiovascular development (J:74328)
• in some cases, vascular permeability is impaired with extravazation of erythrocytes into adjacent tissue

embryo
• at E11.5, viable homozygous embryos exhibit an overall growth retardation relative to wild-type or heterozygous embryos
• at E11.5, viable homozygous embryos are smaller than wild-type embryos
• at E11.5, homozygotes display significant differences in fetal and maternal vascular channels; vascular channels are scant and contain few erythrocytes (J:62272)
• at E11.5, mutant placentas fail to develop a complex capillary network; however, reduced placental angiogenesis is in marked contrast with the excessive systemic vascularization observed in hyperemic mutant embryos (J:74328)
• reduced network of embryonic capillary blood vessels at E11.5
• at E11.5, mutant placentas lack the distinct separation between fetal and maternal sinuses due to the presence of densely packed trophoblast cells
• placental trophoblast cells display erythrophagocytic activity indicative of vascular defects
• at E11.5, mutant placentas exhibit less vascularized spongiotrophoblast layers
• at E11.5, the labyrinth zone is poorly developed

hematopoietic system
• at E11.5, homozygotes display failure of megakaryocyte and erythroid differentiation
• at E11.5, mutant livers contain excessive nucleated erythrocytes in dilated sinusoids
• at E11.5, mutant livers lack mature megakaryocytes; a significant number of cells display fragmented nuclei suggestive of apoptosis

vision/eye
• at E11.5, mutant eyes are difficult to visualize due to a paucity of retinal pigmention
• at E11.5, mutant eyes exhibit defective lens formation
• at E11.5, mutant lenses fail to form a lining epithelium
• mutant rudimentary lenses are surrounded by excessively abundant small vessels relative to wild-type lenses

muscle
• at E11.5, homozygotes display a hypoplastic myocardium relative to wild-type embryos
• at E11.5, homozygous embryos display trabecular hypoplasia
• at E11.5, homozygotes fail to compact the ventricular myocardium into the multilayer structure that is required to sustain cardiac function
• at E10.5 and E11.5, homozygotes display reduced thickness of the myocardium

growth/size/body
• at E11.5, viable homozygous embryos exhibit an overall growth retardation relative to wild-type or heterozygous embryos
• at E11.5, viable homozygous embryos are smaller than wild-type embryos

liver/biliary system
• at E11.5, mutant livers show significantly dilated sinusoids

pigmentation
• at E11.5, mutant eyes are difficult to visualize due to a paucity of retinal pigmention

homeostasis/metabolism
• at E11.5, homozygotes display significant pericardial effusion associated with an enlarged, blood-filled ventricle





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last database update
11/12/2024
MGI 6.24
The Jackson Laboratory