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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Tg(GFAP-cre)#Gtm
transgene insertion #, David H Gutmann
MGI:3057344
Summary 12 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
cn1
Smarcb1tm2Sho/Smarcb1tm2Sho
Trp53tm1Brn/Trp53+
Tg(GFAP-cre)#Gtm/0
involves: 129P2/OlaHsd * 129S1/Sv * C57BL/6 * CBA MGI:5771804
cn2
Smarcb1tm2Sho/Smarcb1tm2Sho
Trp53tm1Brn/Trp53tm1Brn
Tg(GFAP-cre)#Gtm/0
involves: 129P2/OlaHsd * 129S1/Sv * C57BL/6 * CBA MGI:5771805
cn3
Smarcb1tm2Sho/Smarcb1+
Trp53tm1Brn/Trp53tm1Brn
Tg(GFAP-cre)#Gtm/0
involves: 129P2/OlaHsd * 129S1/Sv * C57BL/6 * CBA MGI:5771803
cn4
Smarcb1tm2Sho/Smarcb1+
Trp53tm1Brn/Trp53+
Tg(GFAP-cre)#Gtm/0
involves: 129P2/OlaHsd * 129S1/Sv * C57BL/6 * CBA MGI:5771802
cn5
Itgavtm2Hyn/Itgavtm2.1Hyn
Tg(GFAP-cre)#Gtm/0
involves: 129P2/OlaHsd * C57BL/6 * CBA MGI:5306155
cn6
Smarcb1tm2Sho/Smarcb1tm2Sho
Tg(GFAP-cre)#Gtm/0
involves: 129S1/Sv * C57BL/6 * CBA MGI:5771801
cn7
Tsc1tm1Djk/Tsc1tm1Djk
Tg(GFAP-cre)#Gtm/0
involves: 129S4/SvJae * C57BL/6 * CBA MGI:5292549
cn8
Gt(ROSA)26Sortm2(tTA,CMV*1-KIAA1549/BRAF,-EGFP)Gtm/Gt(ROSA)26Sor+
Tg(GFAP-cre)#Gtm/0
involves: 129S6/SvEvTac * C57BL/6 * CBA MGI:5543816
cn9
Nf1tm1Par/Nf1tm1Fcr
Tg(GFAP-cre)#Gtm/0
involves: 129S/SvEv * 129S1/Sv * 129X1/SvJ * C57BL/6 * CBA MGI:4838320
cn10
Nf1tm1Fcr/Nf1+
Tg(GFAP-cre)#Gtm/0
involves: 129S/SvEv * 129S4/SvJae * C57BL/6 * CBA MGI:5292552
cn11
Nf1tm1Fcr/Nf1+
Tsc1tm1Djk/Tsc1tm1Djk
Tg(GFAP-cre)#Gtm/0
involves: 129S/SvEv * 129S4/SvJae * C57BL/6 * CBA MGI:5292550
cn12
Gt(ROSA)26Sortm1(tTA,CMV*1-Rheb,-EGFP)Gtm/Gt(ROSA)26Sor+
Tg(GFAP-cre)#Gtm/0
involves: C57BL/6 * CBA MGI:5292547


Genotype
MGI:5771804
cn1
Allelic
Composition
Smarcb1tm2Sho/Smarcb1tm2Sho
Trp53tm1Brn/Trp53+
Tg(GFAP-cre)#Gtm/0
Genetic
Background
involves: 129P2/OlaHsd * 129S1/Sv * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Smarcb1tm2Sho mutation (0 available); any Smarcb1 mutation (14 available)
Tg(GFAP-cre)#Gtm mutation (0 available)
Trp53tm1Brn mutation (7 available); any Trp53 mutation (153 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• lesions in the white matter of the corpus callosum and cingulum

neoplasm
N
• no neoplastic growth is seen in the brain




Genotype
MGI:5771805
cn2
Allelic
Composition
Smarcb1tm2Sho/Smarcb1tm2Sho
Trp53tm1Brn/Trp53tm1Brn
Tg(GFAP-cre)#Gtm/0
Genetic
Background
involves: 129P2/OlaHsd * 129S1/Sv * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Smarcb1tm2Sho mutation (0 available); any Smarcb1 mutation (14 available)
Tg(GFAP-cre)#Gtm mutation (0 available)
Trp53tm1Brn mutation (7 available); any Trp53 mutation (153 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
behavior/neurological
• severe scratching behavior
• motor coordination problems become evident from around 3 weeks of age
• abnormal posture of the hind limbs
• mice exhibit tumbling repeatedly during attempted locomotion; mice frequently fall over and repeatedly lift and replace the same paw in various positions during each stride
• severe ataxia
• mice exhibit intermittent episodes of tail extension and dystonic posturing of the body, frequently in response to handling
• many mice appear lethargic with hind limb paralysis
• mice exhibit a non-uniform gait, with uneven stride length and width, dragging of the hindpaws and an inability to keep the hindquarters upr
• uneven stride length
• many mice appear lethargic with hind limb paralysis
• mice exhibit clear seizures or intermittent electrographic seizures associated either with forelimb clonus, evolving into body jerking, and wild running or arrest of activity during the ictal EEG discharges

cellular
• altered granule neuron migration, with some granule neurons failing to migrate out of the external germinal layer, others remaining trapped in the molecular layer
• altered cerebellar granule neuron migration is already seen at 3 weeks of age

growth/size/body
• body weight is reduced by about 40%

mortality/aging
• mice require water gel for survival

muscle
• mice exhibit intermittent episodes of tail extension and dystonic posturing of the body, frequently in response to handling

neoplasm
• mice develop brain tumors starting at around 1 month of age
• mice that die suddenly exhibit presence of high-grade, aggressive tumors that infiltrate and obliterate the surrounding cerebellar folia
• tumors appear to arise from the cerebellum
• tumors show hallmarks of atypical teratoid/rhabdoid tumor of the central nervous system

nervous system
• mice exhibit clear seizures or intermittent electrographic seizures associated either with forelimb clonus, evolving into body jerking, and wild running or arrest of activity during the ictal EEG discharges
• altered granule neuron migration, with some granule neurons failing to migrate out of the external germinal layer, others remaining trapped in the molecular layer
• altered cerebellar granule neuron migration is already seen at 3 weeks of age
• mice develop brain tumors starting at around 1 month of age
• mice that die suddenly exhibit presence of high-grade, aggressive tumors that infiltrate and obliterate the surrounding cerebellar folia
• tumors appear to arise from the cerebellum
• tumors show hallmarks of atypical teratoid/rhabdoid tumor of the central nervous system
• defects in white matter with complete loss of tissue in regions of white matter over time
• white matter fiber tracks are reduced
• loss of white matter is already seen at 3 weeks of age
• defects in the corpus callosum
• lesions in the corpus callosum are already seen at 3 weeks of age
• defects in the hippocampus
• reduced cerebral cortex is already seen at 3 weeks of age
• defects in the cytoarchitecture of the cerebellum
• progressive loss of cells and neuronal projections in the cerebellum
• the boundary between the internal granule layer and the molecular layer remains diffuse
• loss of oligodendrocytes with age
• high level of gliosis in the fiber tracks and in the molecular layer and in the remnants of the external germinal layer

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
central nervous system cancer DOID:3620 J:226786




Genotype
MGI:5771803
cn3
Allelic
Composition
Smarcb1tm2Sho/Smarcb1+
Trp53tm1Brn/Trp53tm1Brn
Tg(GFAP-cre)#Gtm/0
Genetic
Background
involves: 129P2/OlaHsd * 129S1/Sv * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Smarcb1tm2Sho mutation (0 available); any Smarcb1 mutation (14 available)
Tg(GFAP-cre)#Gtm mutation (0 available)
Trp53tm1Brn mutation (7 available); any Trp53 mutation (153 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
behavior/neurological
• excessive scratching behavior resulting in dermatitis around the neck, earlobes, and the flank region




Genotype
MGI:5771802
cn4
Allelic
Composition
Smarcb1tm2Sho/Smarcb1+
Trp53tm1Brn/Trp53+
Tg(GFAP-cre)#Gtm/0
Genetic
Background
involves: 129P2/OlaHsd * 129S1/Sv * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Smarcb1tm2Sho mutation (0 available); any Smarcb1 mutation (14 available)
Tg(GFAP-cre)#Gtm mutation (0 available)
Trp53tm1Brn mutation (7 available); any Trp53 mutation (153 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
behavior/neurological
• excessive scratching behavior resulting in dermatitis around the neck, earlobes, and the flank region




Genotype
MGI:5306155
cn5
Allelic
Composition
Itgavtm2Hyn/Itgavtm2.1Hyn
Tg(GFAP-cre)#Gtm/0
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Itgavtm2.1Hyn mutation (0 available); any Itgav mutation (32 available)
Itgavtm2Hyn mutation (0 available); any Itgav mutation (32 available)
Tg(GFAP-cre)#Gtm mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• at E18 and P5, mice exhibit microhemorrhage in the cerebellum, mid-brain, and cerebral cortex unlike in control mice
• at E18 and P5, mice exhibit microhemorrhage in the cerebellum unlike in control mice
• at E18 and P5, mice exhibit microhemorrhage in the cerebral cortex unlike in control mice
• between P7 and P14, mice exhibit progressive reduction in cerebral microhemorrhage
• however, adult mice exhibit no hemorrhage or edema in the brain

nervous system
• at E18 and P5, mice exhibit microhemorrhage in the cerebellum, mid-brain, and cerebral cortex unlike in control mice
• at E18 and P5, mice exhibit microhemorrhage in the cerebellum unlike in control mice
• at E18 and P5, mice exhibit microhemorrhage in the cerebral cortex unlike in control mice
• between P7 and P14, mice exhibit progressive reduction in cerebral microhemorrhage
• however, adult mice exhibit no hemorrhage or edema in the brain




Genotype
MGI:5771801
cn6
Allelic
Composition
Smarcb1tm2Sho/Smarcb1tm2Sho
Tg(GFAP-cre)#Gtm/0
Genetic
Background
involves: 129S1/Sv * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Smarcb1tm2Sho mutation (0 available); any Smarcb1 mutation (14 available)
Tg(GFAP-cre)#Gtm mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• variable, mild defect in granule neuron migration
• brain lesions that are prominent in the white matter of the corpus callosum with vacuolization, spongy changes, cystic-like breakdown and destruction of tissue
• extent of damage is variable and progresses with age
• posterior portion of the corpus callosum is more affected than the anterior portion
• disorganization of the Purkinje cell layer
• loss of axons
• loss of myelin

cellular
• variable, mild defect in granule neuron migration

neoplasm
N
• mice do not develop brain tumors up to more than 1 year of age




Genotype
MGI:5292549
cn7
Allelic
Composition
Tsc1tm1Djk/Tsc1tm1Djk
Tg(GFAP-cre)#Gtm/0
Genetic
Background
involves: 129S4/SvJae * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(GFAP-cre)#Gtm mutation (0 available)
Tsc1tm1Djk mutation (1 available); any Tsc1 mutation (47 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mice die by 6 to 10 weeks of age

nervous system
• by 6 to 10 weeks of age

behavior/neurological
• by 6 to 10 weeks of age




Genotype
MGI:5543816
cn8
Allelic
Composition
Gt(ROSA)26Sortm2(tTA,CMV*1-KIAA1549/BRAF,-EGFP)Gtm/Gt(ROSA)26Sor+
Tg(GFAP-cre)#Gtm/0
Genetic
Background
involves: 129S6/SvEvTac * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm2(tTA,CMV*1-KIAA1549/BRAF,-EGFP)Gtm mutation (0 available); any Gt(ROSA)26Sor mutation (380 available)
Tg(GFAP-cre)#Gtm mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
N
• mice exhibit normal GFAP+ and S100B+ astrocytes cell numbers




Genotype
MGI:4838320
cn9
Allelic
Composition
Nf1tm1Par/Nf1tm1Fcr
Tg(GFAP-cre)#Gtm/0
Genetic
Background
involves: 129S/SvEv * 129S1/Sv * 129X1/SvJ * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Nf1tm1Fcr mutation (3 available); any Nf1 mutation (92 available)
Nf1tm1Par mutation (4 available); any Nf1 mutation (92 available)
Tg(GFAP-cre)#Gtm mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
hematopoietic system
• at 9 months of age, mutants have significantly more microglia than controls; microglia are in the optic gliomas

immune system
• at 9 months of age, mutants have significantly more microglia than controls; microglia are in the optic gliomas

nervous system
• at 9 months of age, mutants have significantly more microglia than controls; microglia are in the optic gliomas
• mice develop optic gliomas in the optic chiasm/nerves
• optic gliomas appear as gross thickenings and enlargements of the pre-chiasmic nerve at 9 months of age
• irregularly shaped and thickened astrocytes are seen in the pre-chiasmatic optic nerves
• retinal ganglion cell loss in the middle and peripheral region
• optic gliomas form in the pre-chiasmatic optic nerve/optic chiasm, with increased vascularization to the area, abnormally shaped and thickened astrocytes, increase in microglia, and axonal and myelin degeneration
• mice exhibit abnormal optic nerve axon organization
• the optic chiasm/nerves at 9 months of age appear as gross fusiform enlargements that result in optic gliomas
• increase in vascularization in the pre-chiasmatic optic nerve and optic chiasm (and in the optic glioma)
• axonal and myelin degeneration are seen in the optic nerve
• increase in neoplastic astrocyte proliferation in the optic glioma
• disruption of the myelin is seen in the optic nerve, including degeneration and hypermyelination
• hypermyelination is seen in the optic nerve

neoplasm
• mice develop optic gliomas in the optic chiasm/nerves
• optic gliomas appear as gross thickenings and enlargements of the pre-chiasmic nerve at 9 months of age

vision/eye
• retinal ganglion cell loss in the middle and peripheral region
• optic gliomas form in the pre-chiasmatic optic nerve/optic chiasm, with increased vascularization to the area, abnormally shaped and thickened astrocytes, increase in microglia, and axonal and myelin degeneration
• mice exhibit abnormal optic nerve axon organization
• the optic chiasm/nerves at 9 months of age appear as gross fusiform enlargements that result in optic gliomas
• increase in vascularization in the pre-chiasmatic optic nerve and optic chiasm (and in the optic glioma)

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
neurofibromatosis DOID:8712 OMIM:101000
OMIM:162200
OMIM:162210
OMIM:162260
OMIM:162270
J:165209




Genotype
MGI:5292552
cn10
Allelic
Composition
Nf1tm1Fcr/Nf1+
Tg(GFAP-cre)#Gtm/0
Genetic
Background
involves: 129S/SvEv * 129S4/SvJae * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Nf1tm1Fcr mutation (3 available); any Nf1 mutation (92 available)
Tg(GFAP-cre)#Gtm mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype

Nf1tm1Fcr/Nf1+ Tg(GFAP-cre)#Gtm/0 mice develop prechiasmatic optic nerve and chiasmal gliomas

nervous system
• cell proliferation in the optic nerve is increased compared to in wild-type mice
• optic gliomas
• kinking of the prechiasmatic optic nerves

neoplasm
• optic gliomas

vision/eye
• kinking of the prechiasmatic optic nerves

cellular
• cell proliferation in the optic nerve is increased compared to in wild-type mice




Genotype
MGI:5292550
cn11
Allelic
Composition
Nf1tm1Fcr/Nf1+
Tsc1tm1Djk/Tsc1tm1Djk
Tg(GFAP-cre)#Gtm/0
Genetic
Background
involves: 129S/SvEv * 129S4/SvJae * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Nf1tm1Fcr mutation (3 available); any Nf1 mutation (92 available)
Tg(GFAP-cre)#Gtm mutation (0 available)
Tsc1tm1Djk mutation (1 available); any Tsc1 mutation (47 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• most mice die before 3 months of age

neoplasm
N
• mice do not develop gliomas




Genotype
MGI:5292547
cn12
Allelic
Composition
Gt(ROSA)26Sortm1(tTA,CMV*1-Rheb,-EGFP)Gtm/Gt(ROSA)26Sor+
Tg(GFAP-cre)#Gtm/0
Genetic
Background
involves: C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(tTA,CMV*1-Rheb,-EGFP)Gtm mutation (0 available); any Gt(ROSA)26Sor mutation (380 available)
Tg(GFAP-cre)#Gtm mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
N
• mice exhibit normal brain weight
• mice do not develop seizures
• astrocytes exhibit increased mTor signaling-dependent proliferation compared to in control cells

growth/size/body
N
• mice exhibit normal body weight





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last database update
08/15/2017
MGI 6.10
The Jackson Laboratory