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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Foxp1tm1Eem
targeted mutation 1, Edward E Morrisey
MGI:3056542
Summary 3 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
hm1
Foxp1tm1Eem/Foxp1tm1Eem involves: 129S6/SvEvTac * C57BL/6 MGI:3056578
cx2
Foxp1tm1Eem/Foxp1tm1Eem
Foxp2tm1Bux/Foxp2tm1Bux
involves: 129X1/SvJ * C57BL/6 MGI:4889124
cx3
Foxp1tm1Eem/Foxp1+
Foxp2tm1Bux/Foxp2tm1Bux
involves: 129X1/SvJ * C57BL/6 MGI:4889125


Genotype
MGI:3056578
hm1
Allelic
Composition
Foxp1tm1Eem/Foxp1tm1Eem
Genetic
Background
involves: 129S6/SvEvTac * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Foxp1tm1Eem mutation (0 available); any Foxp1 mutation (75 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• embryos die around E14.5
• Background Sensitivity: the penetrance of this phenotype increases with successive backcrosses to C57BL/6 (59% die after 1 generation versus 92% after 4 generations)

cardiovascular system
• the compact zone of the ventricular wall is thinner at E11.5 and E14.5
• at E11.5 the myocytes in the compact zone are disorganized
• persistent truncus arteriosis is seen in 80% of mutant embryos at E11.5 -E14.5
• a 3-fold increase in cell proliferation is seen in the trabecular zone after E12.5
• more cushion mesenchyme is seen in the pulmonary and aortic valves in all mutant embryos at E14.5
• about a 70% decrease in apoptosis in the valve cushions is seen at E14.5
• more cushion mesenchyme is seen in the mitral and tricuspid valves in 45% of mutant embryos at E14.5
• about a 70% decrease in apoptosis in the valve cushions is seen at E14.5
• at E14.5, 20% of mutant embryos display double outlet right ventricle
• at E14.5 ventricular septal defects are seen
• perivascular hemorrhage is seen at E14.5
• at E13.5 and E14.5 the heart rate is slower compared to wild-type embryos
• at E13.5 and E14.5 an irregular heartbeat is detected

homeostasis/metabolism
• edema is seen at E14.5

muscle
• the compact zone of the ventricular wall is thinner at E11.5 and E14.5
• at E11.5 the myocytes in the compact zone are disorganized




Genotype
MGI:4889124
cx2
Allelic
Composition
Foxp1tm1Eem/Foxp1tm1Eem
Foxp2tm1Bux/Foxp2tm1Bux
Genetic
Background
involves: 129X1/SvJ * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Foxp1tm1Eem mutation (0 available); any Foxp1 mutation (75 available)
Foxp2tm1Bux mutation (0 available); any Foxp2 mutation (52 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• double homozygotes die prior to E11.5

growth/size/body
• double homozygous mutant embryos are severely runted

embryo
• double homozygous mutant embryos are severely runted




Genotype
MGI:4889125
cx3
Allelic
Composition
Foxp1tm1Eem/Foxp1+
Foxp2tm1Bux/Foxp2tm1Bux
Genetic
Background
involves: 129X1/SvJ * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Foxp1tm1Eem mutation (0 available); any Foxp1 mutation (75 available)
Foxp2tm1Bux mutation (0 available); any Foxp2 mutation (52 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• no live mutants are observed at P0-P14, although at least some survive gestation

respiratory system
• severe defects in lung airway development are observed at E14.5, E16.5 and E18.5
• >40% reduction in cell proliferation in both the lung epithelia and mesenchyme is observed, without any significant changes in apoptosis
• however, proximal-distal epithelial patterning of the lung airways is normal at E18.5
• >40% reduction of cell proliferation in lung mesenchyme, without any significant changes in apoptosis
• branching morphogenesis is reduced as shown by the dilated nature of developing airways
• overall lung size is reduced at both E14.5 and E18.5
• lung-to-body weight ratios are significantly reduced at both E17.5 and P0
• distal airspace luminal area is significantly increased at both E14.5 (~3-fold) and E18.5 (~2-fold)

digestive/alimentary system
• both smooth and skeletal muscle differentiation is disrupted in mutant esophagi
• at E14.5, the smooth muscle surrounding the mutant esophagus is thinner than normal
• by E18.5, mutants display severely dilated esophagi with a very thin muscular layer
• however, no differences in apoptosis or cell proliferation are observed in mutant esophagi at E14.5
• at E14.5, the smooth muscle surrounding the mutant esophagus is thinner than normal
• by E18.5, mutants display severely dilated esophagi

muscle
• at E14.5, the smooth muscle surrounding the mutant esophagus is thinner than normal

cellular
• >40% reduction of cell proliferation in lung mesenchyme, without any significant changes in apoptosis





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last database update
03/19/2024
MGI 6.23
The Jackson Laboratory