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Phenotypes Associated with This Genotype
Genotype
MGI:2676189
Allelic
Composition
Juntm1Wag/Juntm1Wag
Genetic
Background
involves: 129S2/SvPas * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Juntm1Wag mutation (0 available); any Jun mutation (15 available)
phenotype observed in females
phenotype observed in males
N normal phenotype

Juntm1Wag/Juntm1Wag fetuses exhibit increased apoptosis in the liver

liver/biliary system
• at E13.0, 8 of 19 mutant fetal livers show significantly increased apoptosis of both hepatoblasts and erythroid cells; however, no deregulation of apoptosis is noted at E12.5
• mutant fetal liver cells are able to reconstitute all hematopoietic compartments of lethally irradiated recipient mice, indicating that hematopoietic cell apoptosis is likely not due to a cell-autonomous defect
• in vitro, primary hepatoblasts and fibroblasts obtained from E12.5 homozygotes show a ~4-fold increase in apoptosis relative to wild-type cells
• in vitro, primary hepatoblasts and fibroblasts obtained from E12.5 homozygotes display a ~50% reduction in mitotic capacity as shown by [3H]thymidine incorporation

cardiovascular system
• at E12.5, some homozygotes display abnormal remodeling of the aortic arch arteries resulting in a right-sided aortic arch
• at E12.5, all (19 of 19) homozygotes exhibit a single outflow vessel arising from the right ventricle
• at E14.5, homozygotes display incomplete septation of the left and right ventricles
• at E12.5, homozygotes display a thinner right ventricular wall

embryo
• at E12.5, homozygotes exhibit reduced migration of neural crest cells in the outflow tract of the right ventricle

cellular
• at E13.0, 8 of 19 mutant fetal livers show significantly increased apoptosis of both hepatoblasts and erythroid cells; however, no deregulation of apoptosis is noted at E12.5
• mutant fetal liver cells are able to reconstitute all hematopoietic compartments of lethally irradiated recipient mice, indicating that hematopoietic cell apoptosis is likely not due to a cell-autonomous defect
• in vitro, primary hepatoblasts and fibroblasts obtained from E12.5 homozygotes show a ~4-fold increase in apoptosis relative to wild-type cells
• at E12.5, homozygotes exhibit reduced migration of neural crest cells in the outflow tract of the right ventricle
• in vitro, primary hepatoblasts and fibroblasts obtained from E12.5 homozygotes display a ~50% reduction in mitotic capacity as shown by [3H]thymidine incorporation


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
03/31/2026
MGI 6.24
The Jackson Laboratory