Analysis Tools
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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absent stapes
(
J:44094
)
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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
absent stapes
(
J:44094
)
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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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absent stapes
(
J:44094
)
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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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growth/size/body
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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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