Analysis Tools|
Allele Symbol Allele Name Allele ID |
Pax7+ wild type MGI:2431553 |
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| Summary |
25 genotypes
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Data Sources
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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 |
| N |
• diphtheria toxin-treated mice retain multipotent fibroblastic/adipogenic mesenchymal progenitors
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• diphtheria toxin-treated mice exhibit modest cellular interstitial infiltration (primarily macrophagic) in muscles unlike in similarly treated wild-type mice
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• in diphtheria-treated muscles, even following diphtheria toxin depletion
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• mice treated with diphtheria and cardiotoxin exhibit impaired muscle regeneration with massive tissue infiltration, loss of myofibres and failure to reconstitute skeletal muscle tissue structure and mass compared with similarly treated wild-type mice
• following treatment and depletion of diphtheria toxin, cardiotoxin-treated mice exhibit impaired muscle regeneration with inflammation and fat infiltration unlike wild-type mice
• diphtheria toxin treated mice subjected to an exercise routine exhibit a dramatic loss of myofibers, inflammation, fat infiltration, and loss of muscle mass unlike similarly treated wild-type mice
• transplantation of satellite cells expressing Tg(Pax7-EGFP)#Tajb fails to rescue muscle regeneration in diphtheria toxin-treated mice
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• diphtheria toxin-treated mice exhibit modest cellular interstitial infiltration (primarily macrophagic) in muscles unlike in similarly treated wild-type mice
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• in tamoxifen treated mice at 3 and 7 days after cardiotoxin induced muscle damage mice show a significant decrease in the number of regenerating myofibers and persistence of necrotic fibers
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
| N |
• at E15.5, rhythmic activity in the pre-Botzinger complex is preserved
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• earlier tumor onset, from 32 to 65 days of age
• bortezomib treated mice have better survival
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• earlier tumor onset, from 32 to 65 days of age
• bortezomib treated mice have better survival
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• reduction in myogenic precursor marker Pax7 peptide level and 50% reduction in Pax7+ myogenic precursor cells in E16.5 embryos
• significantly reduced levels of committed myoblast markers MyoD and myogenin peptide levels and 60% reduction in MyoD+ myoblasts in E16.5 embryos
• 7x increased MyHC-slow peptide levels in E16.5 embryos
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| N |
• normal apoptosis in E16.5 embryos
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• 83-84% of satellite cells are ablated in the right tibialis anterior muscle after 5 doses of tamoxifen and 5days after muscle damage induced by BaCl2 injection
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• reduced fibroblast expansion by 52% 5 days after muscle injury in tamoxifen treated mice
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• 89% reduction in regenerating myofibers 5 days after muscle injury in tamoxifen treated mice
• muscle regeneration dramatically impaired 28 days after injury
• right tibialis anterior muscle entirely fibrotic at 28 days and uninjured left tibialis anterior is reduced by 38%
• similar result when damage induced with cardiotoxin, no recovery after 56 days
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
| N |
• adult mice treated with tamoxifen show complete abrogation of the increased number of Pax7+ muscle stem cells (satellite cells) seen in homozygous 2310065F04Riktm1.1Boet mice
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
| N |
• mice are viable and do not show any apparent developmental abnormalities and have regular numbers of Pax7+ muscle stem cells (satellite cells)
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
| N |
• the increased body weight seen in homozygous 2310065F04Riktm1.1Boet mice is normalized
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| N |
• mice show complete abrogation of the increased number of Pax7+ muscle stem cells (satellite cells) and of the increased EdU-labeled quiescent muscle stem cells, the increased tibialis anterior muscle weight, and the muscle hypertrophy and increased myonuclei numbers in fibers that are seen in homozygous 2310065F04Riktm1.1Boet mice
• mice do not show the general myofiber hypertrophy that is seen in homozygous 2310065F04Riktm1.1Boet mice 4 weeks after cardiotoxin-induced muscle damage
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• although born at the expected Mendelian ratio, all homozygous pups die within a few hours after birth; no live pups older than 1 day are recovered
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• pulmonary alveoli fail to open in newborn pups
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• however, some residual sarcomeres are still present in skeletal muscles
• at P1, TEM analysis showed severe disruption of the sarcomeric structures in both the diaphragm and hindlimb muscles
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• at P1, pups show defective sarcomeres in striated muscles; skeletal muscles of P1 pups show an obvious increase in protein levels of non-muscle myosin IIs (MYH9 and MYH10)
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• because of breathing difficulties few mutants survive beyond 3.5 months of age
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• agenesis of the rostral premaxilla is seen
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• hypoplasia of the lacrimal bone is seen
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• a narrowed nose is seen
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• the nasal turbinates are underdeveloped
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• agenesis of the rostral premaxilla is seen
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• hypoplasia of the lacrimal bone is seen
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• a narrowed nose is seen
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• the nasal turbinates are underdeveloped
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• at 3 weeks of age mutants weigh less than one-third of wild-type littermates
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• severe growth retardation is seen by 3 weeks of age
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• myofiber diameter is reduced
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• muscle mass is reduced
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• the number of satellite cells is reduced
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• myofiber density is increased
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• a narrowed nose is seen
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• the nasal turbinates are underdeveloped
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• agenesis of the rostral premaxilla is seen
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• hypoplasia of the lacrimal bone is seen
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• the nasal turbinates are underdeveloped
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• live embryos at E18.5 but no live progeny
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• severe craniofacial deformation
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• muscle progenitor cells fail to differentiate ex vitro
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• following CTX-induced muscle injury, tamoxifen-treated mice exhibit decreased myofiber density with increased necrotic tissues and inflammatory cell infiltration compared with control mice
• however, mice exhibit regeneration of smaller caliber myofibers
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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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• muscle progenitor cells fail to differentiate ex vitro
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• following CTX-induced muscle injury, tamoxifen-treated mice exhibit decreased myofiber density with increased necrotic tissues and inflammatory cell infiltration compared with control mice
• however, mice exhibit regeneration of smaller caliber myofibers
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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N |
• 9-week-old tamoxifen-treated females implanted with a biodegradable pellet containing 10 mg dihydrotestostorone (DHT) to induce muscle hypertrophy show a similar increase in tibialis anterior, quadriceps, and gastrocnemius muscle mass as wild-type mice
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• 9 of 30 double heterozygous mice become ataxic starting around 88-100 days of age
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• all ataxic mice have rapidly growing tumors in the cerebellum
• high nuclear to cytoplasm ratio in tumor cells
• tumors invade the subarachnoid space
• evidence of leptomeningeal metastasis
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• all ataxic mice have rapidly growing tumors in the cerebellum
• high nuclear to cytoplasm ratio in tumor cells
• tumors invade the subarachnoid space
• evidence of leptomeningeal metastasis
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• satellite cells isolated from 8 month tamoxifen-treated mice exhibit premature senescence unlike control cells
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• tamoxifen-treated mice subjected to cardiotoxin-induced muscle injury exhibit smaller and poorly organized regenerating myofibers compared with control mice
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• satellite cells or cardiotoxin-injured tibialis anterior muscles isolated from 8 month tamoxifen-treated mice exhibit premature senescence unlike control cells
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• cardiotoxin-injured tibialis anterior muscles isolated from 8 month tamoxifen-treated mice exhibit premature senescence unlike control cells
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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 |
Perturbed myogenic differentiation of Six1tm2.1Mair/Six1tm2.1Mair Pax7tm1(cre/ERT2)Gaka/Pax7+ satellite cell descendants ex vivo
| N |
• normal muscle tissue weights or histology up to a year after tamoxifen treatment
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• in tamoxifen-treated mice subjected to a single cardiotoxin injury
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• satellite cells from tamoxifen-treated mice exhibit reduced ability to differentiate of satellite cell descendants ex vivo and increased self-renewal capacity in vivo compared with control cells
• ex vivo satellite cells from tamoxifen-treated mice exhibit increased self-renewal compared with control cells
• however, satellite cells exhibit normal quiescence, activation and proliferation and polarity of division
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• satellite cells from tamoxifen-treated mice form smaller myotubes containing fewer nuclei ex vivo compared with control cells
• regenerating muscle from tamoxifen-treated mice subjected to a single cardiotoxin injury exhibit smaller newly formed myofibers with fewer nuclei, numerous lagged fibers of small caliber, reduced cell size and necrotic myofibers compared with controls
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• decrease in the number of myogenin positive cells in cultured satellite cells from tamoxifen treated mice indicating a defect in myoblast differentiation
• when induced to differentiate for 3 days satellite cells for fewer myotubes and have reduced fusion and differentiation indices
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• following CTX-induced muscle injury muscles in tamoxifen treated mice show smaller regenerated myofiber cross-section area
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• decrease in the number of myogenin positive cells in cultured satellite cells from tamoxifen treated mice indicating a defect in myoblast differentiation
• when induced to differentiate for 3 days satellite cells for fewer myotubes and have reduced fusion and differentiation indices
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• when mice older than 6 weeks are given systemic tamoxifen treatment by intraperitoneal delivery, mice develop multiple tumors (avg. 3.9 per mouse) with 100% penetrance within 1-2 months; median tumor-free survival is 44 days
• tumors develop at various locations, including clinically relevant sites including the orbit
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• tamoxifen treated mice develop tumors displaying a histological spectrum ranging from undifferentiated pleomorphic sarcoma (UPS) to rhabdomyosarcoma (RMS)
• tumors mimic embryonic RMS, pleomorphic RMS, or myogenic or nonmyogenic UPS
• sarcomas can appear in the body wall (37%), the extremities (31%), head and neck (23%), with some being subcutaneous (9%)
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• mice develop mainly embryonal rhabdomyosarcoma, with 92% of tumors being embryonal rhabdomyosarcoma
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• 100% of mice develop sarcoma
• 8% of tumors are undifferentiated pleomorphic sarcoma
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• mice develop mainly embryonal rhabdomyosarcoma, with 92% of tumors being embryonal rhabdomyosarcoma
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• mice treated with diphtheria toxin and cardiotoxin exhibit an almost total loss of GFP+ satellite cells
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• mice treated with diphtheria and cardiotoxin exhibit impaired muscle regeneration compared with similarly treated wild-type mice
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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 01/13/2026 MGI 6.24 |
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