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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Ccnftm1.1Sje
targeted mutation 1.1, Stephen J Elledge
MGI:3040863
Summary 3 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
hm1
Ccnftm1.1Sje/Ccnftm1.1Sje involves: 129S7/SvEvBrd * C57BL/6 MGI:3041854
cn2
Ccnftm1Sje/Ccnftm1.1Sje
Tg(Col1a1-cre)1Kry/0
involves: 129S7/SvEvBrd * C57BL/6 * FVB MGI:3041866
cn3
Ccnftm1Sje/Ccnftm1.1Sje
Tg(Fabp1-cre)1Jig/0
involves: 129S7/SvEvBrd * C57BL/6 * FVB/N MGI:3041859


Genotype
MGI:3041854
hm1
Allelic
Composition
Ccnftm1.1Sje/Ccnftm1.1Sje
Genetic
Background
involves: 129S7/SvEvBrd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ccnftm1.1Sje mutation (0 available); any Ccnf mutation (51 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• homozygotes die between E9.5 and 10.5 due to defects in the maturation of the yolk sac and chorioallantoic placenta

growth/size/body
• at E8.5, mutant embryos appear grossly normal but are ~10% smaller than wild-type embryos
• by E9.5, mutant embryos display a number of gross morphological defects and are ~3-fold smaller than wild-type embryos

embryo
• by E9.5, the number of vitelline vessels is reduced and the vessel walls appear significantly thickened
• only small amounts of blood are detected in these vessels
• by E9.5, mutant yolk sacs lack a rich nucleated hematopoietic component
• by E9.5, mutant vitelline vessels appear as a disorganized meshwork lacking organized branching patterns
• at E9.5, 90% of mutant embryos exhibit no axial rotation; their bodies appear kinked, suggesting that axial rotation is initiated but fails to complete
• by E9.5, homozygotes exhibit underdeveloped posterior structures, including the posterior limb bud and allantois
• in contrast, the first branchial arch, otic cup, eye primordia, and anterior limb bud, appear developmentally normal
• at E8.5, mutant embryos appear grossly normal but are ~10% smaller than wild-type embryos
• by E9.5, mutant embryos display a number of gross morphological defects and are ~3-fold smaller than wild-type embryos
• by E9.5, the mutant posterior limb bud appears underdeveloped relative to wild-type
• by E9.5, all homozygotes exhibit defects and/or delays in neural tube closure
• by E9.5, the leading edges which fuse during neural tube closure appear thickened and kinked
• at E8.5, the allantois fails to fuse with the chorion and appears rounded
• by E9.5, the allantois appears as a bulbous knot
• by E8.5, mutant yolk sacs already appear thinner and more fragile than normal
• homozygotes exhibit failure of placental development and maturation
• at E9.5, a significant reduction in BrdU incorporation by trophoblast cells is observed at the chorionic plate adjacent to the area of labyrinthine branching
• at E8.5, all homozygotes fail to initiate chorioallantoic fusion
• at E9.5, mutant yolk sacs fail to exhibit a rich mature vascular network

nervous system
• by E9.5, all homozygotes exhibit defects and/or delays in neural tube closure
• by E9.5, the leading edges which fuse during neural tube closure appear thickened and kinked
• by E9.5, mutant hindbrain regions appear underdeveloped relative to wild-type
• by E9.5, brain development is severely retarded and/or defective
• by E9.5, mutant forebrain regions appear underdeveloped relative to wild-type
• by E9.5, mutant midbrain regions appear underdeveloped relative to wild-type

cellular
• mutant MEFs are viable but exhibit cell cycle defects, including reduced population-doubling time and a delay in cell cycle reentry from quiescence
• proliferative defects are observed in vivo in the placenta and in vitro in MEFs

limbs/digits/tail
• by E9.5, the mutant posterior limb bud appears underdeveloped relative to wild-type

cardiovascular system
• by E9.5, the number of vitelline vessels is reduced and the vessel walls appear significantly thickened
• only small amounts of blood are detected in these vessels
• by E9.5, mutant yolk sacs lack a rich nucleated hematopoietic component
• by E9.5, mutant vitelline vessels appear as a disorganized meshwork lacking organized branching patterns




Genotype
MGI:3041866
cn2
Allelic
Composition
Ccnftm1Sje/Ccnftm1.1Sje
Tg(Col1a1-cre)1Kry/0
Genetic
Background
involves: 129S7/SvEvBrd * C57BL/6 * FVB
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ccnftm1.1Sje mutation (0 available); any Ccnf mutation (51 available)
Ccnftm1Sje mutation (0 available); any Ccnf mutation (51 available)
Tg(Col1a1-cre)1Kry mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
skeleton
N
• no developmental or physiological defects are detected in bone




Genotype
MGI:3041859
cn3
Allelic
Composition
Ccnftm1Sje/Ccnftm1.1Sje
Tg(Fabp1-cre)1Jig/0
Genetic
Background
involves: 129S7/SvEvBrd * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ccnftm1.1Sje mutation (0 available); any Ccnf mutation (51 available)
Ccnftm1Sje mutation (0 available); any Ccnf mutation (51 available)
Tg(Fabp1-cre)1Jig mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
N
• no developmental or physiological defects are detected in the distal small intestine, cecum, colon, or bladder





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last database update
04/16/2024
MGI 6.23
The Jackson Laboratory