Analysis Tools
taste/olfaction
| N |
• axons of OLFR151 expressing olfactory sensory neurons appear to co-converge and coalesce in glomerular formation correctly despite G-protein disruption during development
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Allele Symbol Allele Name Allele ID |
Gnastm5.1Lsw targeted mutation 5.1, Lee S Weinstein MGI:3609165 |
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| Summary |
7 genotypes
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
| N |
• axons of OLFR151 expressing olfactory sensory neurons appear to co-converge and coalesce in glomerular formation correctly despite G-protein disruption during development
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
| N |
• formation of olfactory bulb glomeruli appears normal despite G-protein disruption in basal stem cells and some immature olfactory sensory neurons
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• approximately 25% greater than control
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• in the fed state
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| N |
• food intake measured over 14 days was normal
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• in fed mutant mice
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• very high glucagon and glucagon-like peptide-1
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• in fed mutant mice
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• in fasted mutant mice
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• mutant mice had resting and total energy expenditure rate at 30 degree
• resting or total energy expenditure rate or activity level at ambient temperature are normal
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• increased glucose-stimulated insulin secretion
• increased insulin sensitivity in liver and muscle
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• in the fed state
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• reduced adiposity
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• alpha cell hyperplasia with les uniform cellular size and appearance
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• mutant mice had increased pancreas weights
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• mutant mice had increased pancreas weights
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• approximately 25% greater than control
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• mice are born at expected Mendelian ratios; however, all neonates die within hours after birth
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• at P0, the nasal capsule is missing
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• at E17.5, the nasal septum cartilage is abnormally ossified and malformed
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• thyroid cartilage is abnormally ossified at P0
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• newborns are unable to suckle
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• at P0, all mice exhibit severe craniofacial malformations
• however, embryos are grossly normal at E10.5 and E12.5
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• newborns show severe craniofacial skeleton defects due to accelerated osteochondrogenic differentiation; the NCC-derived nasal capsule, maxilla, premaxilla, mandible, tympanic ring and body of hyoid bone are absent or severely malformed
• in contrast, mesoderm-derived skeleton elements including the parietal, lateral portion of the interparietal, supraoccipital, exoccipital, basioccipital and otic capsule are formed normally
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• hyoid bone is heavily ossified at P0
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• newborns exhibit an over-ossified body of the hyoid bone
• premature ossification in the body of hyoid bone is first seen at E15.5
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• incisor tip is abnormally ossified at E14.5 and E15.5
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• newborns exhibit a hypoplastic and malformed mandible
• mandibular bone is heavily ossified at P0
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• at P0, the angular process is missing
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• at P0, the condylar process is missing
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• at P0, the coronoid process is missing
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• at E16.5, E18.5 and P0, the mandible is severely shortened
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• newborns exhibit a hypoplastic and malformed maxilla
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• newborns exhibit a hypoplastic and malformed premaxilla
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• at E16.5, E18.5 and P0, the maxilla is severely shortened
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• at P0, mice exhibit a domed skull
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• neonatal palatal bones are severely hypoplastic and thus palate is cleft
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• at P0, the nasal capsule is missing
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• palatal shelves are well developed and elevate to the horizontal position above tongue but fail to elongate or fuse at E14.5
• however, in vitro, palatal shelves show complete fusion with normal disappearance of the medial edge epithelium after 72 hours in organ culture
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• at E14.5, embryos exhibit a round face
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• newborns exhibit a complete cleft palate caused by craniofacial skeleton defects
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• at E16.5 and E18.5, the tongue is arched rather than flat
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• at E16.5, E18.5 and P0, mice exhibit an exposed (protuberant) tongue
|
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• at E17.5, the nasal septum cartilage is abnormally ossified and malformed
|
|
• at E14.5, embryos exhibit a short snout
|
|
• newborns show severe craniofacial skeleton defects due to accelerated osteochondrogenic differentiation; the NCC-derived nasal capsule, maxilla, premaxilla, mandible, tympanic ring and body of hyoid bone are absent or severely malformed
• in contrast, mesoderm-derived skeleton elements including the parietal, lateral portion of the interparietal, supraoccipital, exoccipital, basioccipital and otic capsule are formed normally
|
|
• hyoid bone is heavily ossified at P0
|
|
• newborns exhibit an over-ossified body of the hyoid bone
• premature ossification in the body of hyoid bone is first seen at E15.5
|
|
• incisor tip is abnormally ossified at E14.5 and E15.5
|
|
• newborns exhibit a hypoplastic and malformed mandible
• mandibular bone is heavily ossified at P0
|
|
• at P0, the angular process is missing
|
|
• at P0, the condylar process is missing
|
|
• at P0, the coronoid process is missing
|
|
• at E16.5, E18.5 and P0, the mandible is severely shortened
|
|
• newborns exhibit a hypoplastic and malformed maxilla
|
|
• newborns exhibit a hypoplastic and malformed premaxilla
|
|
• at E16.5, E18.5 and P0, the maxilla is severely shortened
|
|
• at P0, mice exhibit a domed skull
|
|
• neonatal palatal bones are severely hypoplastic and thus palate is cleft
|
|
• at P0, the nasal capsule is missing
|
|
• at E17.5, the nasal septum cartilage is abnormally ossified and malformed
|
|
• thyroid cartilage is abnormally ossified at P0
|
|
• mice exhibit abnormal ossification within the maxilla and mandible, nasal septum, hyoid and laryngeal cartilages
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• premature ossification in the body of hyoid bone is first seen at E15.5
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• newborns exhibit premature frontal suture closure (craniosynostosis)
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• at E14.5, embryos exhibit hypertelorism
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• neonatal tympanic rings are thickened and deformed
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| N |
• morphology of cranial nerves is grossly normal at E10.5 and E12.5
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• size of sympathetic ganglia is reduced at E16.5 and E17.5
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• size of dorsal root ganglia is reduced at E16.5 and E17.5
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• neonatal palatal bones are severely hypoplastic and thus palate is cleft
|
|
• palatal shelves are well developed and elevate to the horizontal position above tongue but fail to elongate or fuse at E14.5
• however, in vitro, palatal shelves show complete fusion with normal disappearance of the medial edge epithelium after 72 hours in organ culture
|
|
• newborns exhibit a complete cleft palate caused by craniofacial skeleton defects
|
|
• at E16.5 and E18.5, the tongue is arched rather than flat
|
|
• at E16.5, E18.5 and P0, mice exhibit an exposed (protuberant) tongue
|
|
• incisor tip is abnormally ossified at E14.5 and E15.5
|
|
• neonatal palatal bones are severely hypoplastic and thus palate is cleft
|
|
• at P0, the nasal capsule is missing
|
|
• palatal shelves are well developed and elevate to the horizontal position above tongue but fail to elongate or fuse at E14.5
• however, in vitro, palatal shelves show complete fusion with normal disappearance of the medial edge epithelium after 72 hours in organ culture
|
|
• at E14.5, embryos exhibit a round face
|
|
• newborns exhibit a complete cleft palate caused by craniofacial skeleton defects
|
|
• at E16.5 and E18.5, the tongue is arched rather than flat
|
|
• at E16.5, E18.5 and P0, mice exhibit an exposed (protuberant) tongue
|
|
• at E17.5, the nasal septum cartilage is abnormally ossified and malformed
|
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• at E14.5, embryos exhibit a short snout
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| N |
• morphology of the cardiac outflow tract and cardiac development is grossly normal at E17.5
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| N |
• both cranial neural crest cell (CNCC) migration and CNCC proliferation are normal
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
| N |
• newborns exhibit normal craniofacial structures and completely fused palates; no cleft palate phenotype is observed
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• the reduction of plasma phosphate 2 hours after parathyroid hormone injection is about 30% of that in controls, however this difference does not reach significance
• serum FGF23 is increased, although this is not statistically significant
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• blood ionized calcium is reduced
• however, serum phosphate and index of fractional phosphate excretion is similar to controls
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• males show a reduction in serum 1,25-dihydroxyvitamin D levels
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• parathyroid hormone-induced urinary cAMP excretion is significantly blunted
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• parathyroid hormone-induced urinary cAMP excretion is significantly blunted
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Mouse Models of Human Disease |
DO ID | OMIM ID(s) | Ref(s) | |
| pseudohypoparathyroidism | DOID:4184 |
OMIM:612462 |
J:233851 | |
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• by 14 weeks in severely affected mice
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| N |
• surviving mice exhibit normal food intake, energy expenditure and respiratory ratio at ambient or cold temperatures
• mice exhibit normal T4 levels
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• in the muscle of mice fed a high-fat diet
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• in response to cold exposure on a high fat diet, mice exhibit reduced body temperature and a 3-fold increase in energy expenditure compared with control mice
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• under basal fed conditions
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• under basal fed conditions
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• at 3 months in surviving mice
• however, adiponectin levels are normal
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• increased norephinephrine excretion
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• 3-fold in response to cold exposure on a high fat diet
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• when fed a high-fat diet
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• almost completely absent in severely affected mice
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• at 3 months in surviving mice
• however, no macrophage infiltration is observed
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• embryonic cells exhibit reduced adipogenesis compared with control cells
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• at 3 months in surviving mice
• however, weights of brown adipose tissue, liver, kidney and heart are normal
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• in epididymal WAT
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• almost completely absent in severely affected mice
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• almost completely absent in severely affected mice
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• almost completely absent in severely affected mice
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• almost completely absent in severely affected mice
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• isoproterenol-treated white adipose tissue adipocytes exhibit reduced lipolytic response compared with control cells
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• at 3 months in surviving mice
• however, weights of brown adipose tissue, liver, kidney and heart are normal
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• at 3 months in surviving mice
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• when fed a high-fat diet
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• in severely affected mice
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• at 3 months in surviving mice
• however, weights of brown adipose tissue, liver, kidney and heart are normal
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• at 3 months in surviving mice
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• in cold-exposed mice
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• increased norephinephrine excretion
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• almost completely absent in severely affected mice
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• in the muscle of mice fed a high-fat diet
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Mouse Genome Database (MGD), Gene Expression Database (GXD), Mouse Models of Human Cancer database (MMHCdb) (formerly Mouse Tumor Biology (MTB)), Gene Ontology (GO) |
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last database update 04/23/2024 MGI 6.23 |
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