Phenotypes associated with this allele
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| Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Wnt3atm1Amc mutation
(1 available);
any
Wnt3a mutation
(25 available)
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mortality/aging
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• most homozygotes die around E10.5, but a few survive until just before birth
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skeleton
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• seen in surviving embryos at E18.5
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• cervical vertebra 2 (C2) is fused to C1 in the dorsal region
• C2 has the anterior arcus atlantis that is normally seen on the ventral part of C1
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• homeotic transformation of cervical vertebra 2 (C2) to C1
• C2 has the anterior arcus atlantis that is normally seen on the ventral part of C1
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embryo
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• truncation caudal to the forelimb level
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• only abnormal somite formation is seen posterior to the forelimb bud
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limbs/digits/tail
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• truncation caudal to the forelimb level
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| Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Wnt3atm1Amc mutation
(1 available);
any
Wnt3a mutation
(25 available)
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mortality/aging
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• homozygous mutant embryos die between E10.5 and E12.5
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embryo
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• at E9.5, severe axial truncations suggest impaired gastrulation
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• homozygous mutant embryos exhibit impaired dorsal mesoderm development
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• at E9.5, mutants show massive cell death in the caudal-most region of the axis; cell death is mainly restricted to the dorsal-most mesodermal cells
• at E12.5, caudal development terminates at the level of umbilicus, just anterior to where hindlimbs normally form
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• at E9.5, all mutant embryos exhibit severe axial truncation; however, yolk sac mesoderm and allantois formation appears unaffected
• by E12.5, mutants with little or no caudal development posterior to the forelimb display massive axial truncation
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• at E9.5, mutant embryos have a severely kinked and folded neural tube
• at E9.75, dorsal fusion of the neural tube is often absent
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• at E9.5, mutant notochord is present at the level of forelimbs, but is missing or disrupted in more posterior regions just caudal to the forelimb buds
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• at E9.5, formation of the first 7 to 9 somites up to the level of the forelimb bud is normal; however, no somites are detected from the forelimbs caudal
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• at E9.5, homozygous mutant embryos lack a visible tail bud formation
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nervous system
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• mutant embryos exhibit abnormal CNS morphology and ectopic expression of a dorsal CNS maker
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• at E9.5, mutant embryos have a severely kinked and folded neural tube
• at E9.75, dorsal fusion of the neural tube is often absent
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• at E9.5, the mutant spinal cord is severely dysmorphic (kinked)
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growth/size/body
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• at E9.5, mutant embryos display a shortened trunk caudal to the forelimbs; anterior development proceeds normally
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limbs/digits/tail
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• at E9.5, homozygous mutant embryos lack a visible tail bud formation
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• at E12.5, mutants occasionally display a small degenerate structure just caudal to the forelimbs, i.e. a single midline hindlimb in the normal position of the tail
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Allelic
Composition |
Wnt3atm1Amc/Wnt3avt
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Genetic
Background |
involves: 129S1/Sv * C3H/HeJ * C57BL/6J * C57BR |
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mortality/aging
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• only about 50% of compound heterozygotes live longer than 4 weeks compared to 90% of Wnt3avt heterozygotes
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limbs/digits/tail
skeleton
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• deformities seen as far anterior as the 7th thoracic vertebra
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• the most severely affected mutants have a reduction in the number of thoracic vertebrae
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• none of the compound heterozygotes have all of the lumbar vertebrae
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• no normal sacral vertebrae are seen
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embryo
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• the most severely affected mutants are smaller than wild-type littermates
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• the most severely affected mutants display spina bifida of the posterior neural tube
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• somites do not extend as far caudally as in wild-type embryos and malformed somites are seen rostral to the last somite
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nervous system
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• the most severely affected mutants display spina bifida of the posterior neural tube
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behavior/neurological
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• the most severely affected mutants display hindlimb paralysis
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growth/size/body
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• the most severely affected mutants are smaller than wild-type littermates
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renal/urinary system
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• in several cases severely affected mutants displayed accumulation of urine in the kidneys and ureters
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digestive/alimentary system
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• in several cases severely affected mutants displayed hyperextended intestines
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Allelic
Composition |
Tbx6tm2Pa/Tbx6+
Wnt3atm1Amc/Wnt3a+
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Genetic
Background |
involves: 129 * 129S1/Sv * 129X1/SvJ * ICR |
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embryo
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N |
• despite decrease in Wnt3a expression in Tbx6 null mice, no defects in somite formation are detected
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cardiovascular system
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N |
• unlike in Tbx6 null mice, the direction of heart looping is similar to controls
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cardiovascular system
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• 92% of embryos (n=12) display cardiac defects
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craniofacial
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• in 14% of embryos (n=14)
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digestive/alimentary system
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• in 14% of embryos (n=14)
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growth/size/body
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• in 14% of embryos (n=14)
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cardiovascular system
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• 37% of embryos (n=16) display cardiac defects
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| Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Wnt1tm1Brd mutation
(0 available);
any
Wnt1 mutation
(30 available)
Wnt3atm1Amc mutation
(1 available);
any
Wnt3a mutation
(25 available)
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mortality/aging
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• double homozygotes are obtained at the expected Mendelian frequency between E9.0 and E10.5; however, only a few survive to E18.5
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• double homozygotes are obtained at the expected Mendelian frequency between E9.0 and E10.5; however, only a few survive to E18.5
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nervous system
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• double homozygotes show defects in major neural crest derivatives, including components of the head skeleton, cranial and dorsal root ganglia, and melanocyte precursors, suggesting that a broad loss of dorsal Wnt signaling in the neural tube affects neural crest formation
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• at E11.5, double homozygotes show show virtual loss of dopachrome tautomerase-positive (DCT+), neural crest-derived melanoblasts within the hindbrain region; a few DCT+ cells remain at the dorsal midline
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• at E9.0, double homozygotes exhibit loss of forebrain tissue
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• at E9.0, double homozygotes exhibit loss of midbrain tissue
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• at E9.0. double homozygotes exhibit loss of rostral hindbrain r1, which is typical of Wnt3atm1Amc homozygotes
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• at E10.5, double homozygotes show a 60% reduction in the cellular content of the dorsal root ganglia; in contrast, sympathetic ganglia remain normal
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skeleton
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• at E18.5, the basisphenoid bone is somewhat reduced
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• at E18.5, the alisphenoid bone is somewhat reduced
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• at E18.5, the presphenoid bone is somewhat reduced
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• at E18.5, the squamosal bone is somewhat reduced
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• at E18.5, the main body of the hyoid bone including the greater horn, which originates from neural crest cells derived from r6-r7, is absent
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• at E18.5, the stapes, which originates from neural crest cells derived from r3-r5, is absent
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• at E18.5, the thyroid cartilage is consistently malformed
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embryo
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• double homozygotes display a severe reduction of dorsolateral neural precursors within the neural tube
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• similar to Wnt3atm1Amc homozygotes, double homozygotes exhibit severe posterior axial truncation at the forelimb level
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• double homozygotes show defects in major neural crest derivatives, including components of the head skeleton, cranial and dorsal root ganglia, and melanocyte precursors, suggesting that a broad loss of dorsal Wnt signaling in the neural tube affects neural crest formation
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• at E11.5, double homozygotes show show virtual loss of dopachrome tautomerase-positive (DCT+), neural crest-derived melanoblasts within the hindbrain region; a few DCT+ cells remain at the dorsal midline
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hearing/vestibular/ear
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• at E18.5, the stapes, which originates from neural crest cells derived from r3-r5, is absent
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• at E18.5, the otic capsule is somewhat reduced
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craniofacial
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• at E18.5, the basisphenoid bone is somewhat reduced
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• at E18.5, the alisphenoid bone is somewhat reduced
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• at E18.5, the presphenoid bone is somewhat reduced
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• at E18.5, the squamosal bone is somewhat reduced
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• at E18.5, the main body of the hyoid bone including the greater horn, which originates from neural crest cells derived from r6-r7, is absent
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• at E18.5, the stapes, which originates from neural crest cells derived from r3-r5, is absent
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respiratory system
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• at E18.5, the thyroid cartilage is consistently malformed
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muscle
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• at E10.0, the length of dermomyotome in the mediolateral direction is reduced and the myotome layer is not clearly identifiable
• by E11.0, only small clusters of myotomal cells are observed instead of a condensed cell layer
• notably, expression of a myogenic gene, Myf5, is reduced at E9.5 but recovered at E11.0, indicating that early differentiation of myotomal cells is impaired
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• at E9.5, double homozygotes show absence of medial dermomyotome formation caused by a loss of cells that normally form the medial lip, with no notable changes in cell proliferation or cell survival
• in addition, mediolateral patterning of the dermomyotome is defective and dermomyotome appears to be lateralized
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