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Allele Symbol Allele Name Allele ID |
Gt(ROSA)26Sortm1Sor targeted mutation 1, Philippe Soriano MGI:1861932 |
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| Summary |
99 genotypes
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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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• no abnormal phenotype is detected in the absence or presence of tamoxifen
• tamoxifen expression leads to beta-galactosidase expression in numerous tissues
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• at E12.5, the number of neural crest cells in the outflow tract cushions are less than in wild-type mice
• at E17.5, the number of neural crest cells in the proximal outflow tract is less than in wild-type mice
• however, initial proliferation and migration are normal
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• cranial neural crest cells fail to differentiate into osteoblasts unlike in wild-type mice
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• at E12.5, the number of neural crest cells in the outflow tract cushions are less than in wild-type mice
• at E17.5, the number of neural crest cells in the proximal outflow tract is less than in wild-type mice
• however, initial proliferation and migration are normal
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• cranial neural crest cells fail to differentiate into osteoblasts unlike in wild-type mice
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• at E12.5, the number of neural crest cells in the outflow tract cushions are less than in wild-type mice
• at E17.5, the number of neural crest cells in the proximal outflow tract is less than in wild-type mice
• however, initial proliferation and migration are normal
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• at 5 weeks of age, mice exhibit fewer lacZ+ cells in tail scales compared with control mice
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• dorsal CNS hyperproliferation at E13.5 after being exposed at E8.5 to tamoxifen
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• observed at E13.5 after being exposed at E8.5 to tamoxifen
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• the ventral pancreas fails to form at E11.5 with the precursor cells reverting to an intestinal epithelial fate
• growth retardation of the dorsal epithelial bud is evident at E11.5
• the dorsal epithelial bud is significantly smaller at E12.5
• at E17.5, the dorsal pancreatic epithelium is a truncated, poorly branched, duct like structure without islet or acinar tissues
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• mice injected with an adenovirus expressing cre (adeno-cre) into the lateral ventricle predominantly develop poorly differentiated, well-circumscribed neoplasms with similarity to supratentorial primitive neuroectodermal tumors (sPNET)
• expression profiles of tumors resemble human atypical teratoid/rhabdoid tumor
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• mice injected with an adenovirus expressing cre (adeno-cre) into the lateral ventricle predominantly develop poorly differentiated, well-circumscribed neoplasms with similarity to supratentorial primitive neuroectodermal tumors (sPNET)
• expression profiles of tumors resemble human atypical teratoid/rhabdoid tumor
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• mice injected with an adenovirus expressing cre (adeno-cre) into the lateral ventricle predominantly develop poorly differentiated, well-circumscribed neoplasms with similarity to supratentorial primitive neuroectodermal tumors (sPNET)
• expression profiles of tumors resemble human atypical teratoid/rhabdoid tumor
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• mice injected with an adenovirus expressing cre (adeno-cre) into the lateral ventricle predominantly develop poorly differentiated, well-circumscribed neoplasms with similarity to supratentorial primitive neuroectodermal tumors (sPNET)
• expression profiles of tumors resemble human atypical teratoid/rhabdoid tumor
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• in MEFs at later time points after OHT treatment and serum addition cells develop large aberrant nuclei with frequent micronuclei
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• in MEFS after OHT treatment and serum addition increases in the population of cells with 4N and 8N DNA content are seen
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• live cell imaging indicates a median 8 h delay in mitotic entry in MEFS after OHT treatment and serum addition compared to controls
• in MEFS after OHT treatment and serum addition more cells are in prophase and most of these show an early prophase phenotype
• in MEFS after OHT treatment and serum addition almost no cells in metaphase, anaphase, and telophase are detected
• in MEFS after OHT treatment and serum addition cells in prometaphase have a monopolar spindle with closely adjacent chromosomes, the presence of these monopolar spindles activates the spindle checkpoint
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• in MEFS 28 h after OHT treatment and serum addition the percent of cells positive for PH3 is increased about 3 fold compared to controls
• however, the timing of the peak in PH3 positive cells is similar to controls
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• growth defect in MEFs following OHT treatment and serum addition
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• mice are present at E9.5 but dead by E12.5
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• at E9.5
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• mice lack networks of vessels at all stages
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• at E9.5, mice appear delayed by 1 day
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• yolk sacs possess greater numbers of vascular smooth muscle cells than in wild-type yolk sacs
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• at E9.5, mice appear delayed by 1 day
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• at E9.5
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• mice lack networks of vessels at all stages
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• at E9.5, hearts exhibit pericardial effusion
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• at E9.5, hearts exhibit pericardial effusion
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• mice are present at E9.5 but dead by E12.5
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• at E9.5
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• mice lack networks of vessels at all stages
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• at E9.5
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• at E9.5, mice appear delayed by 1 day
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• at E9.5, mice appear delayed by 1 day
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• at E9.5
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• at E9.5
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• mice lack networks of vessels at all stages
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• at E9.5, hearts exhibit pericardial effusion
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• at E9.5, hearts exhibit pericardial effusion
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• at E12.5, mice exhibit narrowed outflow tract and hypoplastic outlet or subpulmonary conus compared with wild-type mice
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• at E14.5, the right ventricular cavity is smaller than in wild-type mice
• however, the right ventricular muscle wall thickness is normal
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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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• temporarily delayed at E10.5
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• at E10.5, atrioventricular cushions exhibit rounded endocardial-derived cells that accumulate at the cushion interface and less dense, hypoplastic areas unlike in control mice
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• arrested
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• at E10.5, atrioventricular cushions exhibit rounded endocardial-derived cells that accumulate at the cushion interface and less dense, hypoplastic areas unlike in control mice
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• at 9.5 months, mice exhibit failure in motor coordination during walking and incapability to maintain balance on a rod
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• mice exhibit shorter and more variable strides with more frequent additional steps made by both forepaw and hindpaw compared with wild-type mice
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• and more variable
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• at 6 months in the cerebellum
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• in the cerebellum of aged mice
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• at 6 months in the cerebellum
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• at 6 months in the cerebellum
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• massive cell death in the branchial arches without a decrease in cell proliferation
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• at E12.5
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• at E12.5
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• rudimentary at E12.5
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• absent at E10.5
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• absence of midbrain structures at E10.5
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• absence of hindbrain structures at E10.5
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• rudimentary at E12.5
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• at E12.5
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• at E12.5
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• not developed at E10.5
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• absent at E10.5
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• hypoplastic and malformed
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• hypoplastic and malformed
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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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• disorganized tongue muscle fibers at E14
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• die around the time of birth
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• poor colonization of the outflow tract by cardiac neural crest cells at E10.5
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• poor colonization of the outflow tract by cardiac neural crest cells at E10.5
• at E11 the outflow tract has a lower density of cardiac neural crest cells and these cells are disorganized
• however, septation occurs normally
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• in some embryos
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• malformed outflow tract valves in 90% of mice at E12
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• poor colonization of the outflow tract by cardiac neural crest cells at E10.5
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• smaller and misshapen
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• less affected compared to germline null mice
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• at E17
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• fail to grow and close over the eye bulb at E17
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• boundary of ossification is abnormal
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• severely malformed
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• poorly developed
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• severely malformed palatal cartilage in 33% of mice with less severe malformations in the remaining 67% of mice
• otic capsule cartilage is absent at E16 in 33% of mice and reduced in 66% of mice
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• cartilage is absent at E16 in 33% of mice and reduced in 66% of mice
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• boundary of ossification is abnormal
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• severely malformed
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• poorly developed
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• severely malformed cartilage in 33% of mice with less severe malformations in the remaining 67% of mice
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• disorganized tongue muscle fibers at E14
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• small tongue at E14
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• severely malformed cartilage in 33% of mice with less severe malformations in the remaining 67% of mice
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• disorganized tongue muscle fibers at E14
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• small tongue at E14
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• severely malformed cartilage in 33% of mice with less severe malformations in the remaining 67% of mice
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• disorganized tongue muscle fibers at E14
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• small tongue at E14
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• poor colonization of the outflow tract by cardiac neural crest cells at E10.5
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
| N |
• following tamoxifen-treatment, injury-induced myogenesis and satellite cell characteristics are normal
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• in culture, tamoxifen-treated P0 myoblasts exhibit defective expansive and myogenic potentials compared with control Pax7tm2.1(cre/ERT2)Fan heterozygous myoblasts
• however, myoblasts from tamoxifen-treated adults exhibit normal expansive and myogenic potentials
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• following tamoxifen treatment between P7 and P11, regeneration is severely compromised compared to in control Pax7tm2.1(cre/ERT2)Fan heterozygotes
• however, following tamoxifen treatment between P14 to P18 and P21 to P25 regeneration capacity gradually increased to levels in control Pax7tm2.1(cre/ERT2)Fan heterozygotes
• following tamoxifen treatment, myofibers continue to be incorporated into a regenerating muscle beyond P31 longer than in control Pax7tm2.1(cre/ERT2)Fan heterozygotes
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• mice die between E12.5 and E16.5; only resorbed homozygous embryos are recovered at E16.5
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• while yolk sacs are normal at E9.5 by E12.5 yolk sacs are pale, anemic and possess obvious vasculature defects
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• at E12.5, yolk sacs are pale and anemic
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• while yolk sacs are normal at E9.5 by E12.5 yolk sacs are pale, anemic and possess obvious vasculature defects
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• mice exhibit delayed underdeveloped hearts
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• mice exhibit delayed underdeveloped brains
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
 |
• after ureteral ligation, mice exhibit reduced fibrosis and inflammation compared with similarly treated Hif1atm3Rsjo/Hif1atm3Rsjo Gt(ROSA)26Sortm1Sor/Gt(ROSA)26Sor+ mice
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• after ureteral ligation, mice exhibit reduced fibrosis and inflammation compared with similarly treated Hif1atm3Rsjo/Hif1atm3Rsjo Gt(ROSA)26Sortm1Sor/Gt(ROSA)26Sor+ mice
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• hypoxic primary tubular epithelial cells fails to undergo an epithelial to mesenchyme transition unlike similarly treated cells from Hif1atm3Rsjo/Hif1atm3Rsjo Gt(ROSA)26Sortm1Sor/Gt(ROSA)26Sor+ mice
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• after ureteral ligation, mice exhibit reduced fibrosis and inflammation compared with similarly treated Hif1atm3Rsjo/Hif1atm3Rsjo Gt(ROSA)26Sortm1Sor/Gt(ROSA)26Sor+ mice
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• after ureteral ligation, mice exhibit reduced fibrosis and inflammation compared with similarly treated Hif1atm3Rsjo/Hif1atm3Rsjo Gt(ROSA)26Sortm1Sor/Gt(ROSA)26Sor+ mice
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• 3 of 16 mice injected with endoxifen develop glial tumors with lesions of different sizes and varying extents of infiltration
• small neoplastic lesions in endoxifen-induced mice arise from beneath the SVZ and extend into the striatum and dorsally into the corpus callosum
• larger tumors of endoxifen-induced mice show expansion into and a diffuse infiltration of the entire caudate nucleus
• some tumors contain areas of necrosis and occasional microvascular proliferations similar to those in malignant gliomas
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• endoxifen-induced tumors show glial morphology with features typical of astrocytomas and oligodendrogliomas
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• endoxifen-induced tumors show glial morphology with features typical of astrocytomas and oligodendrogliomas
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• 3 of 16 mice injected with endoxifen develop glial tumors with lesions of different sizes and varying extents of infiltration
• small neoplastic lesions in endoxifen-induced mice arise from beneath the SVZ and extend into the striatum and dorsally into the corpus callosum
• larger tumors of endoxifen-induced mice show expansion into and a diffuse infiltration of the entire caudate nucleus
• some tumors contain areas of necrosis and occasional microvascular proliferations similar to those in malignant gliomas
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• endoxifen-induced tumors show glial morphology with features typical of astrocytomas and oligodendrogliomas
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• endoxifen-induced tumors show glial morphology with features typical of astrocytomas and oligodendrogliomas
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Mouse Models of Human Disease |
DO ID | OMIM ID(s) | Ref(s) | |
| high grade glioma | DOID:3070 |
OMIM:PS137800 |
J:229481 | |
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• mice injected with an adenovirus expressing cre recombinase (Ad-Cre) into the left ventricle exhibit a 33.3% incidence of glioma
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• in left ventricle Ad-cre injected mice
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• in left ventricle Ad-cre injected mice
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• mice injected with an adenovirus expressing cre recombinase (Ad-Cre) into the left ventricle exhibit a 33.3% incidence of glioma
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• in left ventricle Ad-cre injected mice
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• in left ventricle Ad-cre injected mice
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Mouse Models of Human Disease |
DO ID | OMIM ID(s) | Ref(s) | |
| high grade glioma | DOID:3070 |
OMIM:PS137800 |
J:229481 | |
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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 |
|
• anterior heart field (AHF) cells are lost compared to controls; numbers of B-gal +ve cells in splanchnic mesoderm (SM) and pharyngeal endoderm are significantly reduced, causing thinning of these cell layers
• number of positive cells in pharyngeal arch core mesoderm (CM) is significantly decreased also
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• thinning of splanchnic mesoderm due to significantly reduced numbers of B-gal +ve cells
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• reduced cycling and proliferation of intestinal stem cells
• however, proliferation rates are normal
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• reduced cycling and proliferation of intestinal stem cells
• however, proliferation rates are normal
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• impaired intestinal epithelial renewal in tamoxifen treated mice
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• mice injected with an adenovirus expressing cre (adeno-cre) into the lateral ventricle develop a spectrum of gliomas, including anaplastic astrocytomas, oligodendrogliomas, and most commonly, anaplastic oligoastrocytomas
• however, adeno-cre injected mice do not develop glioblastoma with palisading necrosis or microvascular proliferation
• tumors in adeno-cre injected mice resemble The Cancer Genome Atlas (TCGA) classical glioblastomas, Phillips proneural and TACG neural gliomas
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• mice injected with an adeno-cre into the lateral ventricle develop anaplastic oligoastrocytoma
• oligoastrocytomas do not resemble any human gliobastoma subtypes
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• mice injected with an adeno-cre into the lateral ventricle develop oligodendrogliomas
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• mice injected with an adenovirus expressing cre (adeno-cre) into the lateral ventricle develop a spectrum of gliomas, including anaplastic astrocytomas, oligodendrogliomas, and most commonly, anaplastic oligoastrocytomas
• however, adeno-cre injected mice do not develop glioblastoma with palisading necrosis or microvascular proliferation
• tumors in adeno-cre injected mice resemble The Cancer Genome Atlas (TCGA) classical glioblastomas, Phillips proneural and TACG neural gliomas
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• mice injected with an adeno-cre into the lateral ventricle develop anaplastic oligoastrocytoma
• oligoastrocytomas do not resemble any human gliobastoma subtypes
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• mice injected with an adeno-cre into the lateral ventricle develop oligodendrogliomas
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
| N |
• unlike mice homozygous for Fgf8tm2.1Jyhl, mice are normal in size
|
| N |
• unlike mice homozygous for Fgf8tm2.1Jyhl, the size of the midbrain and cerebellum are normal
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• telencepepahlic vesicle development is often asymmetric in embryos, with the right side being more severely affected
• very small telencephalic vesicle is sometimes observed at the 8-10 somite stage
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• development of optic vesicles is often asymmetric with right side more severely affected
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• when tamoxifen is administered at E10.5, rhombomere 1 (r1) is reduced in size in mutants at E12.5
• anterior r1 cells contribute to more lateral regions of vermis than normal
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• when tamoxifen is administered at E10.5, mesencephalon is reduced in size at E12.5 relative to normal
• marked cells in posterior mesencephalon do not expand normally
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• when tamoxifen is administered at E10.5, size of marked domain is smaller than wild-type at E16.5
• in adults, marked domain in tectum is greatly reduced compared to wild-type; marked domain is restricted to remaining region of inferior colliculus
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• when tamoxifen is administered at E10.5, size of marked cell population is wider in mutants than in controls at E16.5
• in adults, marked domain is broader than normal
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• in adults, vermis is reduced in size
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• anterior r1 cells contribute to more lateral regions of vermis than normal
• when tamoxifen is administered at E10.5, rhombomere 1 (r1) is reduced in size in mutants at E12.5
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• in E13.5 embryos
• cardiomyocytes smaller, rounded and loosely attached to each other with thin cellular projections in conotruncal regions
• absent thick protrusions from leading edges of cardiomyocytes invading non-myocardial tissue
• cardiomyocytes randomly distributed and mixed with endocardial cells at bases of blood vessels
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• in E13.5 embryos
• cardiomyocytes smaller, rounded and loosely attached to each other with thin cellular projections in conotruncal regions
• absent thick protrusions from leading edges of cardiomyocytes invading non-myocardial tissue
• cardiomyocytes randomly distributed and mixed with endocardial cells at bases of blood vessels
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• embryos exposed to tamoxifen at E10.5-12.5 show some blood-filled dermal lymphatic vessels
• embryos exposed to tamoxifen show reduced number of superficial vessels (X-gal stained); severity of reduction increases with early tamoxifen treatment
• tamoxifen treatment at E10.5 or E11.5 results in severely reduced lymphatic endothelial cell numbers and lack of lymphatic vessels
• embryos exposed to tamoxifen at E10.5 or 11.5 display drastically mispatterned lymph sacs that are reduced in size compared to controls
• when tamoxifen exposure occurs at E13.5, few embryos show any lymphatic defects, while exposure later in development or postnatally causes no obvious defects despite reduction in Nr2f2 expression in LECs
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• reduced proliferation in the mesoderm compartment of both paraxial mesoderm and ectopic ventral mass
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• precursors normally fated to become amacrine and horizontal cells switch to ganglion cell fates, resulting in an increase in ganglion cells
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• precursors normally fated to become amacrine and horizontal cells switch to ganglion cell fates, resulting in an increase in ganglion cells
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• exhibit a switch of pancreatic progenitors such that their progeny proliferate in and adopt the normal fates of duodenal epithelium, including its stem-cell compartment
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• at E10.5, E12.5, E14.5, E16.5, and E18.5, exocrine acini are completely absent
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• at E10.5, E12.5, E14.5, E16.5, and E18.5, exocrine acini are completely absent
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• conversion of pancreatic precursors into duodenal fates; form rudimentary pancreatic tissue that contains ductal and endocrine cell types
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• embryos do not develop intramyocardial coronary arteries
|
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• at E11.5, endocardial cells cannot respond to Vegf120 and fail to migrate, sprout, and form endothelial networks
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• at E12.5, homozygotes exhibit successful septation of the distal outflow tract; however, the number of NCCs contributing to the proximal outflow tract is significantly reduced
|
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• at E9.5, cardiac NCCs migrate to the developing caudal pharyngeal arches of mutant embryos in numbers comparable to those of wild-type embryos; however, at E11.5, NCCs fail to invaginate on the right side of the proximal aortic sac at the level of its connection with the 6th aortic arch arteries
• as a result, the conotruncal cushions remain oriented laterally relative to one another
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|
• at E12.5, homozygotes exhibit successful septation of the distal outflow tract; however, the number of NCCs contributing to the proximal outflow tract is significantly reduced
|
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• homozygotes exhibit abnormal NCC behavior during outflow tract remodeling
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• at E12.5, homozygotes exhibit successful septation of the distal outflow tract; however, the number of NCCs contributing to the proximal outflow tract is significantly reduced
|
|
• at E9.5, cardiac NCCs migrate to the developing caudal pharyngeal arches of mutant embryos in numbers comparable to those of wild-type embryos; however, at E11.5, NCCs fail to invaginate on the right side of the proximal aortic sac at the level of its connection with the 6th aortic arch arteries
• as a result, the conotruncal cushions remain oriented laterally relative to one another
|
|
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• hypoplastic, particularly the trigeminal ganglion
|
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• maxillary branch is consistently narrower than in controls
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• devoid of pigment except for a cone shaped region in the anterior segment
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• retinal pigment layer is normal at E10.5 but pigment loss begins at E12.5
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• corneal stroma and epithelium are absent
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• hypomorphic hyaloid blood vessels
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• muscle bundles present adjacent to the anterior segment
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• eye stalk fails to extend at E12.5
• eyes directly attached to ventral diencephalon by E14.5
• retinal ganglion cell axons enter ventral thalamus and form an optic chiasma-like structure
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• eyes are not visible externally at E16.5
• eyes present but buried within the skull near the midline directly beneath the brain
• lens and retina present
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• devoid of pigment except for a cone shaped region in the anterior segment
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• retinal pigment layer is normal at E10.5 but pigment loss begins at E12.5
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• muscle bundles present adjacent to the anterior segment
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• E17.5 embryos often have hemorrhaging in the lung
|
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• at E12, moderate increases in apoptosis are observed in the primary bronchi of both lungs
• cell death extended farther into the medial and accessory branches and there was a small area of ectopic death observed in the mesenchyme of either the vestigial rostral lobe or at the distal tip of the accessory lobe
|
|
• all lobes exhibit reduced branching following outgrowth of the initial branch that established the lobe
• mesenchymal protrusions without an accompanying epithelial branch are occasionally observed during embryonic development
• such protrusions are observed only in the right lung in positions that correspond to lobes
|
|
• at E17.5, mutant lobes are smaller and much flatter than control lobes
|
|
• at E12.5, the accessory lobe is reduced in size and often misshapen
|
|
• most E11.5 embryos have a reduction or absence of the nascent rostral lobe
• at E12.5, the rostral lobe is absent in the majority of mice
|
|
• at E12.5, the medial lobe is reduced in size and often misshapen
|
|
• at E17.5, mutant lobes are smaller than control lobes
|
|
• at E12.5, mutant lungs are smaller than control lungs
|
|
• at E17.5, mutant lungs are severely hypoplastic
|
|
• E17.5 embryos often have hemorrhaging in the lung
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• maxillary processes are slightly reduced at E10.5
|
|
• frontonasal prominence is slightly reduced at E10.5
• cranial neural crest (CNC) cell participation in the frontonasal prominence is markedly reduced
• however, neural tube formation is normal
|
|
• maxillary processes are slightly reduced at E10.5
|
|
• maxillary processes are slightly reduced at E10.5
|
|
• maxillary processes are slightly reduced at E10.5
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• mice express cre in all mineralcorticoid target tissues, as determined by reporter expression
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• mice die within a few hours of birth
|
|
• cutaneous branch of the ventral ramus is absent in E14.5 embryos
• innervation of the distal limbs at E14.5 confirmed a nearly complete loss of fine cutaneous sensory fibers with only a single sensory branch innervating one side of digits 1, 2 and 5 in both the forelimb and hindlimb
|
|
• there is an increased rate of apoptosis within the trigeminal ganglia of E11.5 and E12.5 embryos
|
|
• the dorsal root ganglion (DRG) of E12.5 embryos do not express Isl1 protein
• TrkA+ neurons are lower in number starting at E12.5 and by E14.5 are less than one-third of what is found in controls
• TrkB+ neurons are also lower in number starting at E12.5 and are markedly reduced at E14.5 and birth
• TrkC+ neurons do not appear until E12.5, a delay of two days compared to controls
|
|
• the DRG of E14.5 embryos is markedly smaller than controls with a smaller number neurons found within the ganglion
• an increased rate of apoptosis is noted in the E12.5 DRG
|
|
• mice have a reduced response to a mild noxious stimulus that was applied to the skin of the trunk or limbs
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• at E14.5, cells expressing lacZ are found across the dorsal and posterior borders of the thalamus expanding into the epithalamus and pretectum
• ectopic lacZ expressing cells from the thalamus are mainly found in the lateral habenular nuclei and anterior part of the pretectum at E18.5
|
|
• at E10.5 the thalamus is smaller in the mediolateral dimension and larger in the ventrodorsal dimension
• thalamus morphology is severely disrupted after E14.5
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• following tamoxifen treatment mild defects in thalamus morphology are seen in some mutants with high levels of recombination but for the most part defects in establishment of dorsal and posterior thalamic boundaries seen in null mice are not seen
• this result and chimera experiments suggest that the function of Gbx2 is cell nonautonomous
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• fewer neurons arising in hippocampus from radial glial cells after treatment with tamoxifen survive to become mature neurons
• axon elongation is unaffected
|
|
• dendritic branching and lengths are reduced in neurons arising in the hippocampus from radial glial cells after treatment with tamoxifen
• reduced dendritic complexity 90 um from soma
• spine density is significantly reduced
|
|
• lasts only 30-40 minutes as compared to over 90 minutes for controls
|
|
• studied between 28 and 42 days after tamoxifen treatment
• enter the center in an open field test less frequently and spend less time there
• more time spent on the periphery in an open field test
• in an elevated + maze, fewer entries into the open arms and less time spent in the open arms
|
|
• studied between 28 and 42 days after tamoxifen treatment
• less spontaneous activity in an open field test
|
|
• fewer neurons arising in hippocampus from radial glial cells after treatment with tamoxifen survive to become mature neurons
• axon elongation is unaffected
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• the formation of the epicardium is severely compromised in E12.5 embryos
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• numbers of stained spots in intestines is not increased compared to mice without the Kras allele, but size of stained patches increases suggesting sporadic cre activation of Kras which might have a selective advantage for mutant stem cells resulting in clonal expansion and crypt fission
|
|
• animals become moribund at 5 weeks of age due to high lung tumor burden
|
|
• numbers of stained spots in intestines is not increased compared to mice without the Kras allele, but size of stained patches increases suggesting sporadic cre activation of Kras which might have a selective advantage for mutant stem cells resulting in clonal expansion and crypt fission
|
|
• animals become moribund at 5 weeks of age due to high lung tumor burden
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• at E14.5, the number of LacZ+ neural crest cell-derived cells in the skin is lower in both the head and belly regions than that in NCC-specific heterozygous knockout littermates carrying only one Resttm1.1Yasu allele
|
|
• at E14.5, the number of LacZ+ neural crest cell-derived cells in the skin is lower in both the head and belly regions than that in NCC-specific heterozygous knockout littermates carrying only one Resttm1.1Yasu allele
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• persistent adherence of the lens vesicle to the corneal ectoderm hinders the migration of neural crest cells across the stromal space between the surface ectoderm and endothelium
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• no developmental abnormalities are detected
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• DNA mismatch repair (measured by cre reversion and activation of the lacZ reporter) is increased about 100 fold relative to mice heterozygous form the Pms2 allele
• average numbers of gastrointestinal tract spots (stained villi) in homozygous Pms2 mutants is 3300 compared to 26 in Pms2 heterozygotes
|
|
• DNA mismatch repair (measured by cre reversion and activation of the lacZ reporter) is increased about 100 fold relative to mice heterozygous form the Pms2 allele
• average numbers of gastrointestinal tract spots (stained villi) in homozygous Pms2 mutants is 3300 compared to 26 in Pms2 heterozygotes
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• die within about 3 hours of birth
|
|
• lack differentiated amacrine cells at E18.5
• almost no GABAergic or glycinergic positive amacrine cells are found in retinal explants cultured for 12 days; however some syntaxin- and calbindin-positive cells do develop indicating retention of a small subpopulation of differentiated amacrine cells
|
|
• in retinal explants cultured for 12 days, syntaxin-, PKCalpha- and calbindin-positive cells are disorganized
|
|
• at E18.5, beta-gal expressing cells are found scattered in the inner retina, unlike in control mice where these cells are localized in the innermost zone of the neuroblastic layer
|
|
• fusion of the ganglion cell layer and the neuroblastic layer results in loss of the inner plexifom layer
|
|
• lack differentiated amacrine cells at E18.5
• almost no GABAergic or glycinergic positive amacrine cells are found in retinal explants cultured for 12 days; however some syntaxin- and calbindin-positive cells do develop indicating retention of a small subpopulation of differentiated amacrine cells
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
| N |
• fate mapping of Pax3 derivatives showed normal heart septation and cellular contributions to the outflow tract in newborn pups
|
| N |
• fate mapping of Pax3 derivatives showed normal patterning of enteric ganglia in the stomach and gastrointestinal tract of newborn pups
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
| N |
• X-Gal staining of E9.5 embryos showed no obvious defects in neural crest contribution to the branchial arches or craniofacial mesenchyme relative to control embryos
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
| N |
• at E10.5, E14.5 and E18.5, secondary heart field development is normal
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
 |
• neural tube defects after deletion of Nap1l2 at E9
|
|
|
• neural tube defects after deletion of Nap1l2 at E9
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
|
• neural tube defects after deletion of Nap1l2 at E9
|
|
|
• neural tube defects after deletion of Nap1l2 at E9
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• the coronal suture adjacent to the frontal bone has a curvilinear appearance and fails to fuse at the midline
|
|
• at 6 weeks, the frontal bone is defective and mostly composed of a cartilaginous membrane
|
|
• at 6 weeks, malleal defects are observed
• however, the incus and stapes are morphologically normal
|
|
• at 6 weeks, the manubrium is smaller than normal
|
|
• at 6 weeks, the body of the malleus is smaller than normal
|
|
• at 6 weeks, malleal defects are observed
• however, the incus and stapes are morphologically normal
|
|
• at 6 weeks, the manubrium is smaller than normal
|
|
• at 6 weeks, the body of the malleus is smaller than normal
|
|
• the coronal suture adjacent to the frontal bone has a curvilinear appearance and fails to fuse at the midline
|
|
• at 6 weeks, the frontal bone is defective and mostly composed of a cartilaginous membrane
|
|
• at 6 weeks, malleal defects are observed
• however, the incus and stapes are morphologically normal
|
|
• at 6 weeks, the manubrium is smaller than normal
|
|
• at 6 weeks, the body of the malleus is smaller than normal
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• in lymph node, parotid salivary gland, submandibular gland, and lacrimal gland
|
|
• in lymph node, parotid salivary gland, submandibular gland, and lacrimal gland
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• abnormal lymphatic vessels fail to extend into distal mesentery unlike in wild-type mice
• between E15.5 and E16.5, lymphatic vessels are almost completely lost unlike in wild-type mice
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• at E9.5, mice exhibit fewer progenitor cells migration into the outflow tract compared with control mice
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• Gnrh+ neurons in the medial preoptic area and posterior hypothalamus
|
|
• in the anterior olfactory nucleus
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• at E15.5 the collecting ducts are dilated and branch points are less evident
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• the number of cardiac neural crest cells reaching the outflow tract is moderately reduced compared to in wild-type mice
|
|
• mice exhibit abnormal patterning of cardiac neural crest cells compared to in wild-type mice
|
|
• the number of cardiac neural crest cells reaching the outflow tract is moderately reduced compared to in wild-type mice
|
|
• mice exhibit abnormal patterning of cardiac neural crest cells compared to in wild-type mice
|
|
• the number of cardiac neural crest cells reaching the outflow tract is moderately reduced compared to in wild-type mice
|
|
• mice exhibit abnormal patterning of cardiac neural crest cells compared to in wild-type mice
|
|
• mice exhibit abnormal patterning of cardiac neural crest cells compared to in wild-type mice
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• in primary podocyte cell cultures from doxycycline-treated mice
|
|
• in doxycycline-treated mice
|
|
• within the first 3 weeks following treatment with a high dose (50 ug/g) of doxycycline
• however, a lower doxycycline dose (15 ug/g) that produces FSGS does not affect lethality
|
|
• within the first 3 weeks following treatment with a high dose (50 ug/g) of doxycycline
• however, a lower doxycycline dose (15 ug/g) that produces FSGS does not affect lethality
|
|
• in doxycycline-treated mice
|
|
• with vacuolization after 10 days in mice treated with doxycycline
|
|
• reduced density in mice treated with doxycycline
|
|
• from 3 weeks of age, doxycycline-treated mice exhibit focal segmental glomerulosclerosis (FSGS) with adhesions, segmental accumulation of matrix, capillary hyalinosis, loss of capillaries, and declining glomerular numbers through 13 weeks unlike control mice
• however, mice do not develop FSGS when doxycycline is administered antenatally or at 10 and 11 days after birth or when mice are treated with a low dose of doxycycline (1.5 ug/g)
|
|
• in doxycycline-treated mice
|
Mouse Models of Human Disease |
DO ID | OMIM ID(s) | Ref(s) | |
| focal segmental glomerulosclerosis | DOID:1312 |
OMIM:PS603278 |
J:285673 | |
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
| N |
• doxycycline-treated mice do not exhibit focal segmental glomerulosclerosis
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• after tamoxifen treatment and a single injection of diphtheria toxin (DT), polyps contain many Dclk1-positive apoptotic tumor cells and are severely injured or collapsed with Dclk1-negative polyps not displaying DT-induced apoptosis
|
| N |
• after tamoxifen treatment and multiple diphtheria toxin injections to ablate Dclk1-positive cells, these cells are absent from the normal intestine with no significant damage to organ architecture observed in the intestine or stomach
|
| N |
• after tamoxifen treatment and multiple diphtheria toxin injections to ablate Dclk1-positive cells, no significant damage in organ architecture is observed in the pancreas or gallbladder
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• transgenic cre positive animals are obtained with low frequency from crosses with Gt(ROSA)26Sortm1Sor heterozygotes, suggesting that Tg(Cck-cre)CKres carriers may have reduced survival
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• mice die at P1
|
| N |
• despite loss of crypt basal columnar cells in diphtheria-treated E15 mice, intestinal epithelium homeostasis is normal
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• proliferation of parietal epithelial cells, not podocytes, is observed; proliferating cells are lacZ-negative, whereas podocytes express beta-galactosidase
|
|
• vacuolar degeneration of parietal epithelial cells is observed after LMB2 treatment
• proliferation of parietal epithelial cells, not podocytes, is also seen; proliferating cells are lacZ-negative, whereas podocytes express beta-galactosidase
|
|
• vacuolar degeneration of podocytes is observed after LMB2 treatment; podocytes are identified by lacZ staining
• podocytes are lost temporally after LMB2 treatment, correlating with progression of sclerosis
|
|
• hyalinosis is seen after LMB2 treatment
|
|
• mesangiolysis is seen after LMB2 treatment
|
|
• after treatment with the immunotoxin LMB2, transgenic animal rapidly develop glomerulosclerosis
• 18%, 23%, and 60% of glomeruli show segmental or global sclerosis at 10, 14 or 21 days after treatment, respectively
|
|
• proliferation of parietal epithelial cells, not podocytes, is observed; proliferating cells are lacZ-negative, whereas podocytes express beta-galactosidase
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• mice exhibit abnormal distribution of Reck+ cells compared with control mice
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• mice exhibit normal behavior, fertility, inner ear morphology and auditory brainstem responses to click stimuli
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• shortened outflow tracts
|
|
• cardiac outflow tracts of E11.5 embryos show no evidence of conotruncal septation
|
|
• fewer neural crest cells are seen in post-otic and circumpharyngeal streams of E10.5 embryos
|
|
• the depth of cardiac outflow tract penetration by neural crest cells is reduced and elongation of the outflow tract apparatus is truncated in E10.5 embryos, resulting in shortened outflow tracts
|
|
• fewer neural crest cells are seen in post-otic and circumpharyngeal streams of E10.5 embryos
|
|
• the depth of cardiac outflow tract penetration by neural crest cells is reduced and elongation of the outflow tract apparatus is truncated in E10.5 embryos, resulting in shortened outflow tracts
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• in the developing head region at E9.5
|
|
• decrease in the proportion of reporter expressing cells in the cranial region at E10.5 a some embryos
|
|
• in the developing head region at E9.5
|
|
• decrease in the proportion of reporter expressing cells in the cranial region at E10.5 a some embryos
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• muscleless diaphragms
• however, pleuroperitoneal fold-derived muscle connective tissue is present and mice do not develop diaphragmatic hernias
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
| N |
• males display normal fertility and no defects in spermatogenesis
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
| N |
• tamoxifen-treated mutants have ventricular conduction system (VCS) cellular fate maps indistinguishable from Tbx5-sufficient animals indicating that defects in conditional animals do not result from loss of VCS cells
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
| N |
• doxycycline-treated mice do not exhibit focal segmental glomerulosclerosis
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• mice exhibit beta to alpha cell transdifferentiation
|
|
• mice exhibit beta to alpha cell transdifferentiation
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
| N |
• at E10.5, E14.5 and E18.5, cardiac neural crest cell development is normal
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• specification of the definitive endoderm is disrupted
|
|
• visceral endoderm fails to displace proximally at E7.5
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• in some mice 7 months after tamoxifen treatment
|
|
• 7 months after tamoxifen treatment
|
|
• 7 months after tamoxifen treatment
|
|
• in some mice 7 months after tamoxifen treatment
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• anterior to posterior cell fate transformation is detected at 10 days post coitum, resulting in anterior forebrain reduction
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• anterior to posterior cell fate transformation is detected at 10 days post coitum, resulting in anterior forebrain reduction
• alterations are more severe than observed in corresponding Hesx1tm2Jpmb compound mutants
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• in the superficial dorsal horn, there are significantly fewer ( about 50%) lacZ-marked neurons compared to controls
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• mice are viable and express LacZ in cells where cre is expressed
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• mice are viable and express LacZ in cells where cre is expressed
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• in inter-follicular epidermis of tamoxifen-treated mice
|
|
• in inter-follicular epidermis of tamoxifen-treated mice
|
|
• in inter-follicular epidermis of tamoxifen-treated mice
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• by E8.5, homozygotes appear to resorb or degenerate and lack distinct features; no mutants are detected after E8.5
|
|
• mutants are unable to show even the earliest signs of gastrulation
|
|
• homozygotes appear normal in size and morphology at the early egg cylinder stage (E6.0), but fail to develop beyond this stage
|
|
• at E6.5 and E7.5, homozygotes exhibit growth retardation relative to wild-type embryos
|
|
• up to E6.0, mutant embryos appear normal and contain embryonic and extraembryonic structures and proamniotic cavities; however, by E6.5, the simple egg cylinder fails to elongate
• homozygotes show a rapid decline of proliferative activity and elevated cell death in the epiblast at the time of egg cylinder elongation; in contrast, proliferation occurs normally prior to E6.0
|
|
• mutant embryos fail to form a histologically recognizable mesoderm at gastrulation; they fail to form mesodermal cells or express mesodermal markers
|
|
• mutant embryos contain abnormal pyknotic cells and fail to form a primitive streak
|
|
• by E6.5, mutant extraembryonic regions appear to be underdeveloped relative to wild-type; a cavitated extraembryonic region fails to form
|
|
• mutant ectoplacental cones are proportionately correct in size but degenerate after E6.5
|
|
• visceral and parietal endoderm layers are present at E6.5 and E7.5, but appear developmentally delayed and fail to form the flattened endodermal cell phenotype in the embryonic region
|
|
• visceral and parietal endoderm layers are present at E6.5 and E7.5, but appear developmentally delayed and fail to form the flattened endodermal cell phenotype in the embryonic region
|
|
• at E6.5 and E7.5, homozygotes exhibit growth retardation relative to wild-type embryos
|
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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