Analysis Tools
normal phenotype
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• mice are viable and fertile, with no observable adverse phenotypes
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• mice are viable and fertile, with no observable adverse phenotypes
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• at E11.5, hearts show deficient second heart field (SHF) contribution to the developing muscular interventricular septum between the right (RV) and left ventricle (LV)
• at E12.5 and E15.5, the interventricular septum has a major deficiency of SHF-derived cells, leading to formation of a bifid cardiac apex
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• E12.5 right ventricle (RV) explant cultures exhibit only non-SHF-derived (mT-labeled) cells migrating from the RV explant by day 6 and very few to no SHF-derived (mG-labeled) cell migration
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• about 5% of mutants show a hypoplastic pulmonary trunk at E15.5 and E16.5
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• about 30% of mutants exhibit interrupted aortic arch, type b at E15.5 and E16.5
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• the number of neural crest cells in the proximal outflow tract cushions is reduced at E11.5
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• all mutants exhibit the double outlet right ventricle at E15.5 and E16.5
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• all mutants exhibit a ventricular septal defect at E15.5 and E16.5
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• E17.5 mutants show a smaller frontal bone
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• E17.5 mutants exhibit a smaller mandible
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• E17.5 mutants exhibit a smaller maxilla
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• 30% of mutants show increased cell death in the pharyngeal arch region
• however, no reduction in cell proliferation is seen in the pharyngeal arch regions at E11.5
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• 30% of mutants show increased cell death in the pharyngeal arch region
• however, no reduction in cell proliferation is seen in the pharyngeal arch regions at E11.5
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• marker analysis at E11.5 indicates that differentiation of cranial neural crest cells into smooth muscle cells is reduced
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• cell proliferation in the neural crest cell derivatives, aorta and pulmonary trunk walls, is reduced at E12.5
• 30% of mutants show increased cell death in the pharyngeal arch region
• however, no reduction in cell proliferation is seen in the dorsal neural tube, pharyngeal arch regions and outflow tract cushions at E11.5 and no increase in cell death is seen in the dorsal neural tube and outflow tract cushions at E11.5
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• the number of neural crest cells in the proximal outflow tract cushions is reduced at E11.5 however, no increase in cell death or reduction in cell proliferation is seen in the outflow tract cushions, indicating that cranial neural crest cell migration to outflow tract cushions is reduced
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• marker analysis at E11.5 indicates that differentiation of cranial neural crest cells into smooth muscle cells is reduced
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• E17.5 mutants show a smaller frontal bone
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• E17.5 mutants exhibit a smaller mandible
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• E17.5 mutants exhibit a smaller maxilla
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• the number of neural crest cells in the proximal outflow tract cushions is reduced at E11.5 however, no increase in cell death or reduction in cell proliferation is seen in the outflow tract cushions, indicating that cranial neural crest cell migration to outflow tract cushions is reduced
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• epicardial cells exhibit premature smooth muscle cell differentiation and fail to invade into the right ventricular myocardium unlike in wild-type mice
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• semilunar valves have reduced endocardial-derived mesenchyme
• 2-fold increase in EdU-incorporated mesenchymal cells, indicating increased proliferation of cushion mesenchyme
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
| N |
• lineage-tracing analysis showed no apparent defects in cranial and cardiac neural crest cell migration
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| N |
• lineage-tracing analysis showed no apparent defects in cranial and cardiac neural crest cell migration
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• mice die at a median age of 26 days
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• mice show progressive weight loss after 2 weeks of age
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• mice show hepatosplenomegaly after 2 weeks of age
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• mice exhibit an atrophied thymus
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• mice exhibit an atrophied thymus
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• mice show hepatosplenomegaly after 2 weeks of age
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• mice show thrombocytopenia after 2 weeks of age
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• mice show an increase in the frequency of CD11c+dendritic cells in the bone marrow and spleen, with expansion particularly in the atrophied thymus
• mice show histiocytic infiltrate in the spleen, liver, lung and intestines and an increase in frequency of CD11b+Gr1+ cells in the blood, bone marrow, liver, and spleen
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• frequency of B220+ B lymphocytes is decreased
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• frequency of CD3+ T lymphocytes is decreased
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• atrophied thymus shows a deficit of CD4-CD8-CD25+ committed T cell progenitors
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• atrophied thymus shows a deficit of CD4+CD8+ double-positive cells
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• mice show leukocytosis after 2 weeks of age
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• mice show monocytosis after 2 weeks of age
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• moribund mice show a reduction hematopoietic stem cells (LSK CD150+CD48-) and multipotent progenitors (LSK CD150-CD48+) in the bone marrow and spleen
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• mice exhibit an atrophied thymus
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• mice show hepatosplenomegaly after 2 weeks of age
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• mice show an increase in the frequency of CD11c+dendritic cells in the bone marrow and spleen, with expansion particularly in the atrophied thymus
• mice show histiocytic infiltrate in the spleen, liver, lung and intestines and an increase in frequency of CD11b+Gr1+ cells in the blood, bone marrow, liver, and spleen
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• frequency of B220+ B lymphocytes is decreased
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• frequency of CD3+ T lymphocytes is decreased
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• atrophied thymus shows a deficit of CD4-CD8-CD25+ committed T cell progenitors
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• atrophied thymus shows a deficit of CD4+CD8+ double-positive cells
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• mice show leukocytosis after 2 weeks of age
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• mice show monocytosis after 2 weeks of age
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• mice develop a juvenile myelomonocytic leukemia-like disease
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• mice show hepatosplenomegaly after 2 weeks of age
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Mouse Models of Human Disease |
DO ID | OMIM ID(s) | Ref(s) | |
| juvenile myelomonocytic leukemia | DOID:0050458 |
OMIM:607785 |
J:247853 | |
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
| N |
• loss of Nr0b1 does not impact ability of zona glomerusa cells to contribute to the inner zona fasciculata even at 8 months of age; postnatal zonation and lineage conversion in the adrenal gland are normal
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
| N |
• the size of the first branchial arch is normal at E10.5
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| N |
• the size of the first branchial arch is normal at E10.5
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• after tamoxifen injection, lineage tracing experiments revealed differentiation and proliferation defects in the incisor stem cell compartment at 3 months of age
• GFP+ Gli1 expressing cells are decreased in number and in area in the incisor pulp, indicating decreased hedgehog signaling
• Ki67 immunostaining showed that the proliferation rate of putative mesenchymal stem cells is reduced
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• after tamoxifen injection, lineage tracing experiments revealed differentiation and proliferation defects in the incisor stem cell compartment at 3 months of age
• GFP+ Gli1 expressing cells are decreased in number and in area in the incisor pulp, indicating decreased hedgehog signaling
• Ki67 immunostaining showed that the proliferation rate of putative mesenchymal stem cells is reduced
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• after tamoxifen injection, lineage tracing experiments revealed differentiation and proliferation defects in the incisor stem cell compartment at 3 months of age
• GFP+ Gli1 expressing cells are decreased in number and in area in the incisor pulp, indicating decreased hedgehog signaling
• Ki67 immunostaining showed that the proliferation rate of putative mesenchymal stem cells is reduced
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• in E14 and E17 embryos
• normal in E12 embryos
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• mice treated with tamoxifen at P1-4 show reduced vascular branching in retinal vessels at P5
• mice treated with tamoxifen at P1-4 show fewer distal sprouts with filopodia and fewer number of filopodia in the retinal vasculature
• distal sprouts have fewer side connections in the retinal vasculature of mice treated with tamoxifen at P1-4
• the radial expansion of the vascular plexus is reduced in mice treated with tamoxifen at P1-4
• vessel regression in the retina is increased in tamoxifen treated mice
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• endothelial cell proliferation is reduced
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• mice treated with tamoxifen at P1-4 show reduced vascular branching in retinal vessels at P5
• mice treated with tamoxifen at P1-4 show fewer distal sprouts with filopodia and fewer number of filopodia in the retinal vasculature
• distal sprouts have fewer side connections in the retinal vasculature of mice treated with tamoxifen at P1-4
• the radial expansion of the vascular plexus is reduced in mice treated with tamoxifen at P1-4
• vessel regression in the retina is increased in tamoxifen treated mice
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• decreased apoptosis of cranial neural crest cells that is slight at E8.0, over 30-fold at E9.5 and 4-fold at E10.5
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• considerable at E8.0, modest at E9.5, and 4-fold at E10.5
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• reduced intensity of reporter expressing cells in the frontonasal prominence and pharyngeal arch 1 at E9.5 and throughout the facial processes at E10.5
• absence of obvious NCC streams entering the pharyngeal arches at E10.5
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• decreased apoptosis of cranial neural crest cells that is slight at E8.0, over 30-fold at E9.5 and 4-fold at E10.5
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• considerable at E8.0, modest at E9.5, and 4-fold at E10.5
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• reduced intensity of reporter expressing cells in the frontonasal prominence and pharyngeal arch 1 at E9.5 and throughout the facial processes at E10.5
• absence of obvious NCC streams entering the pharyngeal arches at E10.5
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• in tamoxifen-treated mice following CTX-induced muscle injury
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• starting in E9.5 embryos, worsening with age
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• starting in E9.5 embryos, worsening with age
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| N |
• normal outflow tract septation in E12 embryos
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• median lip notches in some E14-E15 embryos
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• in some E14-E15 embryos
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• in some E14-E15 embryos
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• in some E14-E15 embryos
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• median lip notches in some E14-E15 embryos
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• in some E14-E15 embryos
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• in some E14-E15 embryos
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
| N |
• embryos exposed to tamoxifen
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• delayed vascularization of the superficial retinal vascular plexus at 5-12 days of age
• vessels are unstable
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• endothelial cell proliferation is increased
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• reduced vascular density and decreased number of branch points in the superficial retinal vascular plexus
• capillary network massively reduced in the deep capillary plexus
• capillary orientation in the superficial plexus relative to the deep plexus is disrupted
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• delayed vascularization of the superficial retinal vascular plexus at 5-12 days of age
• vessels are unstable
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• endothelial cell proliferation is increased
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• reduced vascular density and decreased number of branch points in the superficial retinal vascular plexus
• capillary network massively reduced in the deep capillary plexus
• capillary orientation in the superficial plexus relative to the deep plexus is disrupted
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• mice treated with tamoxifen at P1-4 show reduced vascular branching in retinal vessels at P5
• mice treated with tamoxifen at P1-4 show fewer distal sprouts with filopodia and fewer number of filopodia in the retinal vasculature
• distal sprouts have fewer side connections in the retinal vasculature of mice treated with tamoxifen at P1-4
• the radial expansion of the vascular plexus is reduced in mice treated with tamoxifen at P1-4
• vessel regression in the retina is increased in tamoxifen treated mice
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• endothelial cell proliferation is reduced
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• mice treated with tamoxifen at P1-4 show reduced vascular branching in retinal vessels at P5
• mice treated with tamoxifen at P1-4 show fewer distal sprouts with filopodia and fewer number of filopodia in the retinal vasculature
• distal sprouts have fewer side connections in the retinal vasculature of mice treated with tamoxifen at P1-4
• the radial expansion of the vascular plexus is reduced in mice treated with tamoxifen at P1-4
• vessel regression in the retina is increased in tamoxifen treated mice
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• T cells either do not leave thymus or fail to migrate into the blood and to the peripheral lymphoid organs
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• T cells either do not leave thymus or fail to migrate into the blood and to the peripheral lymphoid organs
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• 20-fold increase in pIpC-treated mice
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• expanded long term hematopoietic stem-like cells in pIpC-treated mice
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• reduced +GFP craniofacial neural crest cells in nasal prominences and pharyngeal arches due to increased apoptosis between E9.5 and E10.5
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• reduced +GFP craniofacial neural crest cells in nasal prominences and pharyngeal arches due to increased apoptosis between E9.5 and E10.5
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• 20-fold increase
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• expanded long term hematopoietic stem-like cells
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• tamoxifen-treated mice exhibit increased number of granule cell precursors in the external granule layer
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• tamoxifen-treated mice exhibit disorganized Bergmann glial scaffolds with loose and wavy glial fibers
• endfeet of Bergmann glial fibers in tamoxifen-treated mice fail to maintain adhesion to the basement membrane unlike in control mice
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• granule cells in tamoxifen-treated mice are trapped in the external granule layer unlike in control mice
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• at P19, tamoxifen-treated mice exhibit severely compromised ingression of several fissures compared with control mice
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• tamoxifen-treated mice exhibit the same lobule defects as in Ric8tm1Zhua/Ric8tm1Zhua Tg(GFAP-cre)25Mes mice
• however, fissural basement membrane is normal
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• tamoxifen-treated mice exhibit the same lobule defects as in Ric8tm1Zhua/Ric8tm1Zhua Tg(GFAP-cre)25Mes mice
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• beta-cells show elevated mitochondrial membrane potential (hyperpolarization) under basal conditions that collapses upon elevated glucose exposure; this loss of mitochondrial membrane potential indicates an inability to maintain the mitochondrial electron gradient under high glucose
• acute treatment with rapamycin mitigates the hyperpolarization seen in beta-cells and the loss of mitochondrial membrane potential with high glucose exposure is rescued
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
| N |
• at E9.5 and E10.5, normal patterns of GFP-labeled cranial neural crest cells (CNCCs) are seen in the frontonasal and periocular regions as well as in the branchial arches
• at E10.5, the contribution of GFP-labeled CNCCs in the nasal, maxillary, and mandibular processes is similar to that in control embryos
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• areas of nasal bones is reduced by about 20% at P0
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• areas of nasal bones is reduced by about 20% at P0
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• areas of nasal bones is reduced by about 20% at P0
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• areas of nasal bones is reduced by about 20% at P0
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• in E12 embryos
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• in newborns, owing to blood pooling
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• in E12 embryos
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• shorter in E10 embryos
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• newborn hearts have only single ventricle
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• in newborns, owing to blood pooling
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• in E11.5 embryos
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• in E12 embryos
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• in E12.5 embryos
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• diffuse vascular leakage in E11.5 embryos
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• in E11.5 embryos
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• starting in E9.5 embryos, worsening with age
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• in E11.5 embryos
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• starting in E9.5 embryos, worsening with age
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• in E11.5 embryos
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• in E12 embryos
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• in E12.5 embryos
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• diffuse vascular leakage in E11.5 embryos
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• in E11.5 embryos
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• starting in E9.5 embryos, worsening with age
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• in E11.5 embryos
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• starting in E9.5 embryos, worsening with age
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• in E11.5 embryos
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• in E12 embryos
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• in E12.5 embryos
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• diffuse vascular leakage in E11.5 embryos
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• in E11.5 embryos
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• starting in E9.5 embryos, worsening with age
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• in E11.5 embryos
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• starting in E9.5 embryos, worsening with age
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• in E12 embryos
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• in newborns, owing to blood pooling
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• in E12 embryos
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• shorter in E10 embryos
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• newborn hearts have only single ventricle
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• in newborns, owing to blood pooling
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• in E12 embryos
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• in newborns, owing to blood pooling
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• in E12 embryos
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• shorter in E10 embryos
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• newborn hearts have only single ventricle
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• in newborns, owing to blood pooling
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
| N |
• normal outflow tract septation in E9.5 embryos
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• in E16 and E17 embryos
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• in E16 and E17 embryos
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• mandibular cleft in E14-E17 embryos
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• in E17 embryos
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• in E16 and E17 embryos
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• in E16 and E17 embryos
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• in E16 and E17 embryos
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• in E16 and E17 embryos
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• mandibular cleft in E14-E17 embryos
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• in E16 and E17 embryos
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• in E16 and E17 embryos
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• in E16 and E17 embryos
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• in E16 and E17 embryos
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• in E16 and E17 embryos
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• in E16 and E17 embryos
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• mandibular cleft in E14-E17 embryos
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• in E17 embryos
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• in E16 and E17 embryos
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• normal outflow tract septation in E9.5 embryos
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• in E16 and E17 embryos
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• in E16 and E17 embryos
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• mandibular cleft in E14-E17 embryos
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• in E17 embryos
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• in E16 and E17 embryos
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• in E16 and E17 embryos
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• in E16 and E17 embryos
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• in E16 and E17 embryos
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• mandibular cleft in E14-E17 embryos
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• in E16 and E17 embryos
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• in E16 and E17 embryos
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• in E16 and E17 embryos
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• in E16 and E17 embryos
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• in E16 and E17 embryos
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• in E16 and E17 embryos
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• mandibular cleft in E14-E17 embryos
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• in E17 embryos
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• in E16 and E17 embryos
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
| N |
• cardiopulmonary development is not disrupted
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• animals die at birth, but viable fetuses are observed at E16.5 and E18.5; no Kit protein is detected by Western blot
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• at E16.5, hearts have lower total numbers of EGFP-positive cells compared to controls, and no EGFP-positive cardiomyocytes
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
| N |
• lineage-tracing analysis showed no apparent defects in cranial, cardiac and enteric neural crest cell migration
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| N |
• lineage-tracing analysis showed no apparent defects in cranial, cardiac and enteric neural crest cell migration
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
| N |
• normal IgG secretion
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| N |
• these mice, which have a hemotopoietic conditional null of a gene involved in vesicle transport, develop normally with both endochondral and intramembranous bones being of normal size and mineralization, the osteoblasts have normal Golgi apparatus stack structure and no swelling of the endoplasmic, the humeri at birth show normal trabeculae, cortical bone, and bone marrow, and micro CT measurements at 6 weeks of age are normal, so osteoblast and osteoclast function appear normal
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• despite the absence of a gene invovled in vesicle transport, no swelling of the endoplasmic reticulum cisternae is found in the acinar cells of the adult pancreas
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• humeral osteoblasts have no swelling of the endoplasmic reticulum, but do have an abnormal Golgi apparatus stack structure
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| N |
• despite the osteoblast-specific disruption of a gene invovled in vesicle transport, these mice develop normally with both endochondral and intramembranous bones being of normal size and mineralization, and the osteoblasts having no swelling of the endoplasmic reticulum, although the osteoblast Golgi apparatus stack structure is not normal, and at 6 weeks of age micro CT measurements are normal
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• primary chondrocyte cultures treated with tamoxifen to inactivate the loxP-flanked allele have a change in the protein profile in the proteomes with many of the proteins with altered expression playing a role in membrane trafficking or Golgi/endoplasmic reticulum function, so while chondrocyte secretion continues to function the specific set of secreted proteins differs
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• loss of Golgi apparatus stacking found in humeral chondrocytes
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• histology of newborns shows decreased lung alveolar formation relative to controls, which the authors say appears to be secondary to the small ribcage
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• newborn pups have shorter bones in the extremities
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• assessment of chondrocytes in humeri finds swollen chondrocytes in some areas at E15.5 and widespread just after birth, and electron microscopy shows an increase in the size of the endoplasmic reticulum cisternae and disruption of the Golgi stack structure
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• severe
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• newborn pups have decreased mineralization of the skull and vertebral column relative to controls
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• E15.5 humeri show delayed formation of the primary ossification center
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• although generated at the expected Mendelian frequency, these mice all die shortly after birth with severe chondrodysplasia
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Mouse Models of Human Disease |
DO ID | OMIM ID(s) | Ref(s) | |
| achondrogenesis type IA | DOID:0080054 |
OMIM:200600 |
J:253969 | |
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
Early greying in Pikfyvetm2.1Tssk/Pikfyvetm2.1Tssk Tg(Tyr-cre/ERT2)13Bos/0 Gt(ROSA)26Sortm4(ACTB-tdTomato,-EGFP)Luo/Gt(ROSA)26Sor+ mice
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• after 4-OHT treatment (P21-P50) mice exhibit an early greying phenotype at P50
• however, GFP+ cells associated with hair follicles are present at P100, indicating that melanocyte survival is not significantly affected
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• after 4-OHT treatment (P21-P50) mice exhibit an early greying phenotype at P50
• however, GFP+ cells associated with hair follicles are present at P100, indicating that melanocyte survival is not significantly affected
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• normal outflow tract septation in E9.5 embryos
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• in E16 and E17 embryos
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• in E16 and E17 embryos
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• mandibular cleft in E14-E17 embryos
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• in E17 embryos
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• in E16 and E17 embryos
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• in E16 and E17 embryos
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• in E16 and E17 embryos
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• in E16 and E17 embryos
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• mandibular cleft in E14-E17 embryos
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• in E16 and E17 embryos
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• in E16 and E17 embryos
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• in E16 and E17 embryos
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• in E16 and E17 embryos
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• in E16 and E17 embryos
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• in E16 and E17 embryos
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• mandibular cleft in E14-E17 embryos
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• in E17 embryos
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• in E16 and E17 embryos
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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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