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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Tg(GFAP-tTA)67Pop
transgene insertion 67, Brian Popko
MGI:4355880
Summary 3 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
cx1
Tg(GFAP-tTA)67Pop/0
Tg(tetO-Ifng)184Pop/0
B6.Cg-Tg(GFAP-tTA)67Pop Tg(tetO-Ifng)184Pop MGI:4355901
cx2
Tg(GFAP-tTA)67Pop/0
Tg(tetO-Ifng)184Pop/0
involves: 129S/SvEv * C57BL/6 * DBA/2 MGI:4355902
cx3
Stat1tm1Rds/Stat1tm1Rds
Tg(GFAP-tTA)67Pop/0
Tg(tetO-Ifng)184Pop/0
involves: 129S/SvEv * C57BL/6 * DBA/2 MGI:4355903


Genotype
MGI:4355901
cx1
Allelic
Composition
Tg(GFAP-tTA)67Pop/0
Tg(tetO-Ifng)184Pop/0
Genetic
Background
B6.Cg-Tg(GFAP-tTA)67Pop Tg(tetO-Ifng)184Pop
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(GFAP-tTA)67Pop mutation (0 available)
Tg(tetO-Ifng)184Pop mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
N
• if double transgenic pups receive doxycycline through gestation and postnatally, or through gestation but treatment stops at birth, animals appear healthy with no histologic lesions
• if pregnant mice do not receive doxycycline (dox) during gestation, >80% of pups die in the neonatal period; double transgenic animals are never recovered
• all ataxic mice (when dox treatment is stopped at E16) die at 3-4 weeks from a progressive neurological syndrome

growth/size/body
• if double transgenic pups receive doxycycline until E16, about 80% start to show growth retardation in the second postnatal week

tumorigenesis
• necropsy of animals dying at 3-4 weeks shows infiltrative lesions of cerebellar hemispheres composed of tumor cells (mitotically active, primitive-appearing cells with hyperchromatic nuclei and little cytoplasm)
• when affected mice start to receive dox again at P16, tumors show less necrosis and apoptosis than untreated mutants
• pups which received doxycline to birth with cessation at P0 have normal cerebellar architecture and do not show tumor formation or migration abnormalities of granule cell precursors

behavior/neurological
• if double transgenic pups receive doxycycline until E16, about 80% develop tremor around P12
• if double transgenic pups receive doxycycline until E16, about 80% develop ataxia around P12

nervous system
• tumor cells are observed primarily in the molecular layer and external granule layer, but also frequently invading the deep cerebellar white matter and brainstem structures
• at P12, mice which received doxycycline until E16 display lesions confined to the EGL which shows a diffuse hyperplasia throughout the cerebellar hemispheres
• at P16, affected animals show marked proliferation of the EGL with diffuse infiltration of the molecular layer, consistent with malignant tumor formation; in contrast, control animals exhibit complete regression of the EGL
• necropsy of animals dying at 3-4 weeks shows infiltrative lesions of cerebellar hemispheres composed of tumor cells (mitotically active, primitive-appearing cells with hyperchromatic nuclei and little cytoplasm)
• when affected mice start to receive dox again at P16, tumors show less necrosis and apoptosis than untreated mutants
• pups which received doxycline to birth with cessation at P0 have normal cerebellar architecture and do not show tumor formation or migration abnormalities of granule cell precursors

Mouse Models of Human Disease
OMIM ID Ref(s)
Medulloblastoma; MDB 155255 J:94092




Genotype
MGI:4355902
cx2
Allelic
Composition
Tg(GFAP-tTA)67Pop/0
Tg(tetO-Ifng)184Pop/0
Genetic
Background
involves: 129S/SvEv * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(GFAP-tTA)67Pop mutation (0 available)
Tg(tetO-Ifng)184Pop mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• when doxycycline treatment is stopped at E 16, around 90% of double mutants develop medulloblastoma and die by P21

tumorigenesis
• when doxycycline treatment is stopped at E 16, around 90% of double mutants develop medulloblastoma and die by P21

Mouse Models of Human Disease
OMIM ID Ref(s)
Medulloblastoma; MDB 155255 J:94092




Genotype
MGI:4355903
cx3
Allelic
Composition
Stat1tm1Rds/Stat1tm1Rds
Tg(GFAP-tTA)67Pop/0
Tg(tetO-Ifng)184Pop/0
Genetic
Background
involves: 129S/SvEv * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Stat1tm1Rds mutation (2 available); any Stat1 mutation (24 available)
Tg(GFAP-tTA)67Pop mutation (0 available)
Tg(tetO-Ifng)184Pop mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
N
• if doxycycline treatment is stopped at E16, pups display a milder phenotype and survive at least until 8 weeks of age
• no double transgenic pups are recovered if dams did not receive any doxycycline treatment

behavior/neurological
• if doxycycline treatment is stopped at E16, pups display minor ataxia at 2 weeks
• if doxycycline treatment is stopped at E16, pups display minor ataxia at 2 weeks

tumorigenesis
N
• if doxycycline treatment is stopped at E16, no tumors are observed in cerebella of adult mice





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last database update
04/19/2016
MGI 6.03
The Jackson Laboratory