mortality/aging
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• all homozygotes die within 24 hrs of birth from failure to suckle
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craniofacial
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• newborn homozygotes display lethal craniofacial abnormalities
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• as early as E14.5, Meckel's cartilage is noticeably truncated
• at P1, the distal symphysis of Meckel's cartilage is present but smaller than normal
• at P1, Meckel's cartilage is disrupted at the proximal end closer to the junction to the malleus
• however, all inner ear structures and middle ear ossicles are present
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• as early as E14.5, Meckel's cartilage is noticeably truncated
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• at P1, the palatine processes are not formed causing the presphenoid to be exposed in ventral view
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• at P1, the pterygoid bones are deformed causing the relative angle to the basisphenoid bone to be abnormal
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• at E14.5, the lesser horns of the hyoid are laterally projected
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• at P1, mutant mandibular bones are displaced laterally and appear deformed relative to those of wild-type mice
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• at P1, the angle between the right and left mandibular bones is wider than normal
• at P1, the angular process is markedly reduced, and an ectopic process is noted extending from the ventral surfaces of the mandible
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• at P1, mutant mandibular bones are hypoplastic relative to those of wild-type mice
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• at P1, the palatine processes are nearly absent; only small remnants are observed by close examination
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• at P1, middle ear ossicles are only mildly affected
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• at P1, the gonial bone is mildly hypoplastic
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• at P1, the projection of the malleal manubrium is abnormal
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• newborn homozygotes display failure of palatal shelf elevation and fusion (cleft palate)
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• at P1, the secondary palate of the mutants fails to fuse along the midline of the oral shelf
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• at P1, mutant tongue muscle fibers are sparse and less organized, and appear to be randomly oriented relative to those of wild-type mice
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skeleton
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• newborn homozygotes display lethal craniofacial abnormalities
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|
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• as early as E14.5, Meckel's cartilage is noticeably truncated
• at P1, the distal symphysis of Meckel's cartilage is present but smaller than normal
• at P1, Meckel's cartilage is disrupted at the proximal end closer to the junction to the malleus
• however, all inner ear structures and middle ear ossicles are present
|
|
|
• as early as E14.5, Meckel's cartilage is noticeably truncated
|
|
|
• at P1, the palatine processes are not formed causing the presphenoid to be exposed in ventral view
|
|
|
• at P1, the pterygoid bones are deformed causing the relative angle to the basisphenoid bone to be abnormal
|
|
|
• at E14.5, the lesser horns of the hyoid are laterally projected
|
|
|
• at P1, mutant mandibular bones are displaced laterally and appear deformed relative to those of wild-type mice
|
|
|
• at P1, the angle between the right and left mandibular bones is wider than normal
• at P1, the angular process is markedly reduced, and an ectopic process is noted extending from the ventral surfaces of the mandible
|
|
|
• at P1, mutant mandibular bones are hypoplastic relative to those of wild-type mice
|
|
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• at P1, the palatine processes are nearly absent; only small remnants are observed by close examination
|
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• at P1, middle ear ossicles are only mildly affected
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• at P1, the gonial bone is mildly hypoplastic
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• at P1, the projection of the malleal manubrium is abnormal
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behavior/neurological
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• newborn homozygotes fail to suckle and do not contain milk in their stomachs
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hearing/vestibular/ear
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• at P1, middle ear ossicles are only mildly affected
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• at P1, the gonial bone is mildly hypoplastic
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• at P1, the projection of the malleal manubrium is abnormal
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• at P1, the tympanic rings are thickened and malformed
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• at P1, the tympanic rings are shorter than normal
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muscle
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• at P1, mutant tongue muscle fibers are sparse and less organized, and appear to be randomly oriented relative to those of wild-type mice
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digestive/alimentary system
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• at P1, the palatine processes are nearly absent; only small remnants are observed by close examination
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• newborn homozygotes display failure of palatal shelf elevation and fusion (cleft palate)
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• at P1, the secondary palate of the mutants fails to fuse along the midline of the oral shelf
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• at P1, mutant tongue muscle fibers are sparse and less organized, and appear to be randomly oriented relative to those of wild-type mice
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cardiovascular system
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N |
• homozygotes do not display any gross abnormalities in the cardiac outflow tract or great vessels
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growth/size/body
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• at P1, the palatine processes are nearly absent; only small remnants are observed by close examination
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• newborn homozygotes display failure of palatal shelf elevation and fusion (cleft palate)
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|
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• at P1, the secondary palate of the mutants fails to fuse along the midline of the oral shelf
|
|
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• at P1, mutant tongue muscle fibers are sparse and less organized, and appear to be randomly oriented relative to those of wild-type mice
|
Analysis Tools