Analysis Tools
mortality/aging
|
• all homozygous null mice died within 12 hours after birth
|
respiratory system
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• most homozygous null pups gasped for breath
• soon after birth, mutant pups displayed a gradual swelling of their stomach and small bowel with air
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behavior/neurological
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• the cleft was wide and prevented mutant pups from nursing, leading to dehydration
|
homeostasis/metabolism
dehydration
(
J:78077
)
craniofacial
|
• neonatal anterior and posterior palatine processes were reduced in size
|
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• the mutant maxilla appeared to be slightly narrow relative to wild-type
• however, no defects in any of the other bones and cartilage derived from the first pharyngeal arch were observed
|
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• neonatal vomer bones were reduced in size
|
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• in homozygous null mice, the small palatal shelves were present at either side and the nasal and oral cavities appeared contiguous
|
|
• all homozygous null pups exhibited complete cleft of the secondary palate regardless of strain background
(J:78077)
• the cleft was wide and prevented mutant pups from nursing, leading to dehydration
(J:78077)
• other facial midline structures appeared unaffected
(J:78077)
|
skeleton
|
• neonatal anterior and posterior palatine processes were reduced in size
|
|
• the mutant maxilla appeared to be slightly narrow relative to wild-type
• however, no defects in any of the other bones and cartilage derived from the first pharyngeal arch were observed
|
|
• neonatal vomer bones were reduced in size
|
cardiovascular system
|
• inwardly rectifying K+ currents were absent in arterial myocytes isolated from homozygous null mice, whereas voltage-dependent K+ currents appeared unaffected relative to wild-type
• when the extracellular K+ concentration was increased from 6 to 15 mmol/L, cerebral arteries from homozygous null mice failed to dilate, unlike neonatal arteries from wild-type mice
• however, mutant cerebral arteries were responsive to forskolin and to changes in Ca2+ influx, indicating that other vasodilatory mechanisms remained intact
|
muscle
|
• inwardly rectifying K+ currents were absent in arterial myocytes isolated from homozygous null mice, whereas voltage-dependent K+ currents appeared unaffected relative to wild-type
• when the extracellular K+ concentration was increased from 6 to 15 mmol/L, cerebral arteries from homozygous null mice failed to dilate, unlike neonatal arteries from wild-type mice
• however, mutant cerebral arteries were responsive to forskolin and to changes in Ca2+ influx, indicating that other vasodilatory mechanisms remained intact
|
limbs/digits/tail
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• all homozygous null newborns exhibited digit defects
|
|
• newborns exhibited preaxial digit duplication of the forelimb
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growth/size/body
|
• neonatal anterior and posterior palatine processes were reduced in size
|
|
• in homozygous null mice, the small palatal shelves were present at either side and the nasal and oral cavities appeared contiguous
|
|
• other facial midline structures appeared unaffected
(J:78077)
• all homozygous null pups exhibited complete cleft of the secondary palate regardless of strain background
(J:78077)
• the cleft was wide and prevented mutant pups from nursing, leading to dehydration
(J:78077)
|
digestive/alimentary system
|
• neonatal anterior and posterior palatine processes were reduced in size
|
|
• in homozygous null mice, the small palatal shelves were present at either side and the nasal and oral cavities appeared contiguous
|
|
• all homozygous null pups exhibited complete cleft of the secondary palate regardless of strain background
(J:78077)
• the cleft was wide and prevented mutant pups from nursing, leading to dehydration
(J:78077)
• other facial midline structures appeared unaffected
(J:78077)
|
