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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Tg(GFAP-cre)25Mes
transgene insertion 25, Albee Messing
MGI:2179048
Summary 59 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
cn1
Hk2tm1.1Uku/Hk2tm1.1Uku
Tg(GFAP-cre)25Mes/0
B6.Cg-Hk2tm1.1Uku Tg(GFAP-cre)25Mes MGI:5571382
cn2
Mrtfatm1Eno/Mrtfatm1Eno
Mrtfbtm2.1Eno/Mrtfbtm2.1Eno
Tg(GFAP-cre)25Mes/0
involves: 129 * 129S/SvEv * C57BL/6 * FVB/N MGI:4818692
cn3
Pdcd10tm1Wami/Pdcd10tm1Wami
Tg(GFAP-cre)25Mes/0
involves: 129 * C57BL/6 * FVB/N MGI:5002697
cn4
Eportm1Hwu/Eportm1Hwu
Tg(GFAP-cre)25Mes/?
involves: 129 * C57BL/6 * FVB/N MGI:3613565
cn5
Gt(ROSA)26Sortm1(RICTOR)Jger/Gt(ROSA)26Sortm1(RICTOR)Jger
Tg(GFAP-cre)25Mes/0
involves: 129 * FVB/N MGI:5472015
cn6
Knl1tm1c(EUCOMM)Hmgu/Knl1tm1c(EUCOMM)Hmgu
Trp53tm1Brn/Trp53tm1Brn
Tg(GFAP-cre)25Mes/0
involves: 129P2/OlaHsd * 129S4/SvJaeSor * C57BL/6N * FVB/N MGI:6358254
cn7
Ptentm1Rdp/Pten+
Trp53tm1Brn/Trp53tm1Brn
Tg(GFAP-cre)25Mes/0
involves: 129P2/OlaHsd * 129S6/SvEvTac * C57BL/6 * FVB/N MGI:3831280
cn8
Gt(ROSA)26Sortm1(Smo/EYFP)Amc/Gt(ROSA)26Sor+
Hk2tm1.1Uku/Hk2tm1.1Uku
Tg(GFAP-cre)25Mes/0
involves: 129P2/OlaHsd * 129X1/SvJ * C57BL/6 * FVB/N MGI:5571383
cn9
Gt(ROSA)26Sortm1(Smo/EYFP)Amc/Gt(ROSA)26Sor+
Hk2tm1.1Uku/Hk2+
Tg(GFAP-cre)25Mes/0
involves: 129P2/OlaHsd * 129X1/SvJ * C57BL/6 * FVB/N MGI:5571384
cn10
Mib1tm2Kong/Mib1tm2Kong
Tg(GFAP-cre)25Mes/0
involves: 129P2/OlaHsd * C57BL/6 * FVB/N MGI:3804817
cn11
Trp53tm1Brn/Trp53tm1Brn
Tg(GFAP-cre)25Mes/0
involves: 129P2/OlaHsd * C57BL/6 * FVB/N MGI:3831281
cn12
Glultm3Whla/Glultm1Whla
Tg(GFAP-cre)25Mes/0
involves: 129P2/OlaHsd * FVB/N MGI:4462796
cn13
Glultm3Whla/Glultm3Whla
Tg(GFAP-cre)25Mes/0
involves: 129P2/OlaHsd * FVB/N MGI:4462797
cn14
Phgdhtm1.2Shfu/Phgdhtm1.2Shfu
Tg(GFAP-cre)25Mes/0
involves: 129P2/OlaHsd * FVB/N MGI:4881761
cn15
Cdc42tm1.1Rac/Cdc42tm1.1Rac
Tg(GFAP-cre)25Mes/0
involves: 129P2/OlaHsd * FVB/N MGI:5495325
cn16
Nf1tm1Par/Nf1+
Ptentm1Hwu/Pten+
Trp53tm1Tyj/Trp53+
Tg(GFAP-cre)25Mes/0
involves: 129S1/Sv * 129S2/SvPas * 129S4/SvJae * 129X1/SvJ * FVB/N MGI:4840094
cn17
Nf1tm1Par/Nf1+
Trp53tm1Tyj/Trp53+
Tg(GFAP-cre)25Mes/0
involves: 129S1/Sv * 129S2/SvPas * 129X1/SvJ * FVB/N MGI:4840090
cn18
Nf1tm1Par/Nf1+
Ptentm1Hwu/Pten+
Trp53tm1Elee/Trp53+
Tg(GFAP-cre)25Mes/0
involves: 129S1/Sv * 129S4/SvJae * 129X1/SvJ * FVB/N MGI:4840096
cn19
Nf1tm1Par/Nf1+
Trp53tm1Elee/Trp53+
Tg(GFAP-cre)25Mes/0
involves: 129S1/Sv * 129S4/SvJae * 129X1/SvJ * FVB/N MGI:4840095
cn20
Gt(ROSA)26Sortm1(RICTOR)Jger/Gt(ROSA)26Sortm1(RICTOR)Jger
Tg(GFAP-cre)25Mes/0
Tg(GFAP-EGFR*,-lacZ)#Agu/0
involves: 129S1/Sv * 129X1/SvJ * FVB/N MGI:5472016
cn21
Dag1tm1Kcam/Dag1tm2Kcam
Tg(GFAP-cre)25Mes/0
involves: 129S1/Sv * 129X1/SvJ * FVB/N MGI:2684282
cn22
Mapk1tm1Gela/Mapk1tm1Gela
Tg(GFAP-cre)25Mes/0
involves: 129S1/Sv * 129X1/SvJ * FVB/N MGI:3805515
cn23
Dag1tm2Kcam/Dag1tm2Kcam
Tg(GFAP-cre)25Mes/0
involves: 129S1/Sv * 129X1/SvJ * FVB/N MGI:2684281
cn24
Ntf3tm1Esm/Ntf3tm1Esm
Tg(GFAP-cre)25Mes/0
involves: 129S1/Sv * FVB/N MGI:4436771
cn25
Trp53tm1Elee/Trp53tm1Tyj
Tg(GFAP-cre)25Mes/0
involves: 129S2/SvPas * 129S4/SvJae * FVB/N MGI:3849178
cn26
Kmt2atm1.1Erns/Kmt2atm1.1Erns
Tg(GFAP-cre)25Mes/0
involves: 129S2/SvPas * FVB/N MGI:3839880
cn27
Olig2tm1Qrlu/Olig2tm1Qrlu
Tg(GFAP-cre)25Mes/?
involves: 129S4/SvJae * C57BL/6J * FVB/N MGI:3615302
cn28
Ptentm1Hwu/Ptentm1Hwu
Tg(GFAP-cre)25Mes/0
involves: 129S4/SvJae * FVB/N MGI:4830362
cn29
Trp53tm1Elee/Trp53tm1Elee
Tg(GFAP-cre)25Mes/0
involves: 129S4/SvJae * FVB/N MGI:3849177
cn30
Pomt2tm1.1Hhu/Pomt2tm1.1Hhu
Tg(GFAP-cre)25Mes/0
involves: 129S4/SvJaeSor * 129S6/SvEvTac * C57BL/6J * FVB/N MGI:5302861
cn31
Knl1tm1c(EUCOMM)Hmgu/Knl1tm1c(EUCOMM)Hmgu
Tg(GFAP-cre)25Mes/0
involves: 129S4/SvJaeSor * C57BL/6N * FVB/N MGI:6358252
cn32
Cul3tm1Jdsr/Cul3tm1Jdsr
Tg(GFAP-cre)25Mes/0
involves: 129S4/SvJaeSor * FVB/N MGI:6449669
cn33
Cul3tm1Jdsr/Cul3+
Tg(GFAP-cre)25Mes/0
involves: 129S4/SvJaeSor * FVB/N MGI:6449671
cn34
Nsdhltm1.1Hrm/Y
Tg(GFAP-cre)25Mes/0
involves: 129S6/SvEvTac * C57BL/6J * FVB/N MGI:5896534
cn35
Nf1tm1Fcr/Nf1tm1Fcr
Trp53tm1Elee/Trp53tm1Elee
Tg(GFAP-cre)25Mes/0
involves: 129S/SvEv * 129S4/SvJae * FVB/N MGI:3849179
cn36
Mef2atm1.1Limm/Mef2atm1.1Limm
Mef2ctm2Eno/Mef2ctm2Eno
Mef2dtm3Eno/Mef2dtm3Eno
Tg(GFAP-cre)25Mes/0
involves: 129S/SvEv * C57BL/6 * FVB/N MGI:5560657
cn37
Mrtfbtm2.1Eno/Mrtfbtm2.1Eno
Tg(GFAP-cre)25Mes/0
involves: 129S/SvEv * C57BL/6 * FVB/N MGI:4818691
cn38
Mef2atm1.1Limm/Mef2atm1.1Limm
Tg(GFAP-cre)25Mes/0
involves: 129S/SvEv * C57BL/6 * FVB/N MGI:5560660
cn39
Mef2atm1.1Limm/Mef2atm1.1Limm
Mef2dtm3Eno/Mef2dtm3Eno
Tg(GFAP-cre)25Mes/0
involves: 129S/SvEv * C57BL/6 * FVB/N MGI:5560659
cn40
Lgi1tm2.1Jkc/Lgi1tm2.1Jkc
Tg(GFAP-cre)25Mes/0
involves: 129/Sv * C57BL/6 * FVB/N MGI:6275806
cn41
Ptch1tm1Bjw/Ptch1tm1Bjw
Tg(GFAP-cre)25Mes/0
involves: 129T2/SvEms * FVB/N MGI:5286072
cn42
Fgfr1tm1Upir/Fgfr1tm1Upir
Fgfr2tm1Dor/Fgfr2tm1Dor
Tg(GFAP-cre)25Mes/0
involves: 129X1/SvJ * FVB/N MGI:3641106
cn43
Fgfr2tm1Dor/Fgfr2tm1Dor
Tg(GFAP-cre)25Mes/0
involves: 129X1/SvJ * FVB/N MGI:3641105
cn44
Gt(ROSA)26Sortm1(Smo/EYFP)Amc/Gt(ROSA)26Sortm1(Smo/EYFP)Amc
Tg(GFAP-cre)25Mes/0
involves: 129X1/SvJ * FVB/N MGI:3810317
cn45
Ephx2tm1.1Arte/Ephx2tm1.1Arte
Tg(GFAP-cre)25Mes/0
involves: C57BL/6 * FVB/N MGI:5609321
cn46
Hip1tm5.1(HIP1)Tsr/Hip1tm5.1(HIP1)Tsr
Tg(GFAP-cre)25Mes/0
involves: C57BL/6 * FVB/N MGI:6719557
cn47
Bicd2tm1Hgrd/Bicd2tm1Hgrd
Tg(GFAP-cre)25Mes/0
involves: C57BL/6 * FVB/N MGI:5810136
cn48
Drd2tm1Smoc/Drd2tm1Smoc
Tg(GFAP-cre)25Mes/0
involves: C57BL/6 * FVB/N MGI:5499900
cn49
Trpv4tm1c(KOMP)Wtsi/Trpv4tm1c(KOMP)Wtsi
Tg(GFAP-cre)25Mes/0
involves: C57BL/6J * C57BL/6N * FVB/N MGI:6256831
cn50
Aqp4tm1.1Geno/Aqp4tm1.1Geno
Tg(GFAP-cre)25Mes/0
involves: C57BL/6J * FVB/N MGI:5297540
cn51
S1pr1tm1Jch/S1pr1tm1Jch
Tg(GFAP-cre)25Mes/?
involves: C57BL/6J * FVB/N MGI:4939155
cn52
Ren1tm1.1Sig/Ren1tm1.1Sig
Tg(GFAP-cre)25Mes/0
involves: C57BL/6J * FVB/N MGI:4939886
cn53
Marveld1tm1.1Liy/Marveld1tm1.1Liy
Tg(GFAP-cre)25Mes/0
involves: C57BL/6J * FVB/N MGI:6377096
cn54
Ric8atm1.1Zhua/Ric8atm1.1Zhua
Tg(GFAP-cre)25Mes/0
involves: FVB/N MGI:5467513
cn55
Dio2tm1Acb/Dio2tm1Acb
Tg(GFAP-cre)25Mes/0
involves: FVB/N MGI:5513868
cn56
Fgfr1tm1Upir/Fgfr1tm1Upir
Tg(GFAP-cre)25Mes/0
involves: FVB/N MGI:3641103
cn57
Lrp2tm1Tew/Lrp2tm1Tew
Tg(GFAP-cre)25Mes/0
involves: FVB/N MGI:6199477
cn58
Ntrk2tm1Jom/Ntrk2tm1Jom
Tg(GFAP-cre)25Mes/0
involves: FVB/N MGI:3612962
cn59
Bdnftm1Limm/Bdnftm1Limm
Tg(GFAP-cre)25Mes/0
involves: FVB/N MGI:3770149


Genotype
MGI:5571382
cn1
Allelic
Composition
Hk2tm1.1Uku/Hk2tm1.1Uku
Tg(GFAP-cre)25Mes/0
Genetic
Background
B6.Cg-Hk2tm1.1Uku Tg(GFAP-cre)25Mes
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Hk2tm1.1Uku mutation (1 available); any Hk2 mutation (42 available)
Tg(GFAP-cre)25Mes mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• cerebellar granule neuron progenitors fail to migrate over the Purkinje cell layer
• at P7, cerebellar granule neuron progenitors exhibit reduced proliferation in response to Shh compared with wild-type cells
• focal disorganization of the external granule cell layer
• regions of focal thinning or thickening, abnormal migration and increased vascularization at P7
• regions of focal thinning or thickening at P7

cellular
• cerebellar granule neuron progenitors fail to migrate over the Purkinje cell layer
• at P7, cerebellar granule neuron progenitors exhibit reduced proliferation in response to Shh compared with wild-type cells




Genotype
MGI:4818692
cn2
Allelic
Composition
Mrtfatm1Eno/Mrtfatm1Eno
Mrtfbtm2.1Eno/Mrtfbtm2.1Eno
Tg(GFAP-cre)25Mes/0
Genetic
Background
involves: 129 * 129S/SvEv * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Mrtfatm1Eno mutation (0 available); any Mrtfa mutation (25 available)
Mrtfbtm2.1Eno mutation (0 available); any Mrtfb mutation (56 available)
Tg(GFAP-cre)25Mes mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mice die between P16 and P21

nervous system
• in the striatum
• neurons exhibit defective neurite outgrowth compared with wild-type neurons
• neurons fail to migrate along the rostral migratory stream unlike in wild-type mice
• mice exhibit a smaller striatum than wild-type mice
• the hippocampus is compressed unlike in wild-type mice
• hippocampal neuronal projections are decreased compared to in wild-type mice
• olfactory bulbs contain fewer neurons than in wild-type mice
• neurons fail to migrate along the rostral migratory stream unlike in wild-type mice
• mice exhibit an expansion of the subventricular zone compared with wild-type mice
• however, expansion is not do to increased cell proliferation

cellular
• in the striatum
• neurons exhibit defective neurite outgrowth compared with wild-type neurons
• mouse embryonic fibroblasts fail to migrate to the wound site in an in vitro scratch test unlike wild-type cells
• neurons fail to migrate along the rostral migratory stream unlike in wild-type mice

growth/size/body




Genotype
MGI:5002697
cn3
Allelic
Composition
Pdcd10tm1Wami/Pdcd10tm1Wami
Tg(GFAP-cre)25Mes/0
Genetic
Background
involves: 129 * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Pdcd10tm1Wami mutation (0 available); any Pdcd10 mutation (17 available)
Tg(GFAP-cre)25Mes mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mice do not survive beyond 12 months of age
• 80% of rate die by 4 weeks

nervous system
• abnormal cytoarchitecture
• brain capillaries are dilated and less organized and dense than in control mice
• between 3 weeks and 12 months, two-thirds of mice develop cerebrovascular lesions resembling cavernomas unlike in control mice
• at 2 months
• starting in early postnatal stages
• astrocyte proliferation is increased compared to in control cells
• astrocytes exhibit resistance to cycloheximide-induced apoptosis compared with control cells
• retinal astrocyte spreading is decreased compared to in control mice

cardiovascular system
• brain capillaries are dilated and less organized and dense than in control mice
• between 3 weeks and 12 months, two-thirds of mice develop cerebrovascular lesions resembling cavernomas unlike in control mice
• endothelial cell migration is delayed compared to in control mice
• brain capillaries

neoplasm
• between 3 weeks and 12 months, two-thirds of mice develop cerebrovascular lesions resembling cavernomas unlike in control mice
• mice develop cavernomas in the spinal cord unlike wild-type mice

behavior/neurological
• unsteady

growth/size/body

cellular
• endothelial cell migration is delayed compared to in control mice

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
cerebral cavernous malformation 3 DOID:0060671 OMIM:603285
J:170480




Genotype
MGI:3613565
cn4
Allelic
Composition
Eportm1Hwu/Eportm1Hwu
Tg(GFAP-cre)25Mes/?
Genetic
Background
involves: 129 * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Eportm1Hwu mutation (0 available); any Epor mutation (18 available)
Tg(GFAP-cre)25Mes mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• subventricular zone decreased in volume and with fewer cells although the overall brain architecture of the cortex, olfactory bulbs and cerebellum is normal
• reduced cell proliferation at age 15 days with still greater reduction at 6 months of age
• infarct size from stroke not affected, contrary to expectations due to the neuroprotective effects of exogenous erythropoietin




Genotype
MGI:5472015
cn5
Allelic
Composition
Gt(ROSA)26Sortm1(RICTOR)Jger/Gt(ROSA)26Sortm1(RICTOR)Jger
Tg(GFAP-cre)25Mes/0
Genetic
Background
involves: 129 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(RICTOR)Jger mutation (0 available); any Gt(ROSA)26Sor mutation (758 available)
Tg(GFAP-cre)25Mes mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype

Gliomas in Gt(ROSA)26Sortm1(RICTOR)Jger/Gt(ROSA)26Sortm1(RICTOR)Jger Tg(GFAP-cre)25Mes/0 mice

mortality/aging
• most mice succumb to gliomas by 22 weeks

neoplasm
• intratumoral hemorrhage
• bilateral, multifocal infiltrating glioma in the amygdalohippocampal region or surrounding cortex in close proximity to the subventricular zone
• infiltrating gliomas exhibit oligodendroglial-like features with the typical fried egg appearance

nervous system
• bilateral, multifocal infiltrating glioma in the amygdalohippocampal region or surrounding cortex in close proximity to the subventricular zone
• infiltrating gliomas exhibit oligodendroglial-like features with the typical fried egg appearance
• 2-fold increase in thickness

cardiovascular system
• intratumoral hemorrhage




Genotype
MGI:6358254
cn6
Allelic
Composition
Knl1tm1c(EUCOMM)Hmgu/Knl1tm1c(EUCOMM)Hmgu
Trp53tm1Brn/Trp53tm1Brn
Tg(GFAP-cre)25Mes/0
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJaeSor * C57BL/6N * FVB/N
Cell Lines HEPD0665_2_E05
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Knl1tm1c(EUCOMM)Hmgu mutation (0 available); any Knl1 mutation (65 available)
Tg(GFAP-cre)25Mes mutation (2 available)
Trp53tm1Brn mutation (17 available); any Trp53 mutation (205 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging

nervous system
N
• neuron loss is rescued by conditional knock-out of Trp53
• partially rescued by conditional knock-out of Trp53

cellular
• partial rescue of apoptosis and DNA damage by conditional knock-out of Trp53

growth/size/body
• partially rescued by conditional knock-out of Trp53




Genotype
MGI:3831280
cn7
Allelic
Composition
Ptentm1Rdp/Pten+
Trp53tm1Brn/Trp53tm1Brn
Tg(GFAP-cre)25Mes/0
Genetic
Background
involves: 129P2/OlaHsd * 129S6/SvEvTac * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ptentm1Rdp mutation (0 available); any Pten mutation (78 available)
Tg(GFAP-cre)25Mes mutation (2 available)
Trp53tm1Brn mutation (17 available); any Trp53 mutation (205 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
behavior/neurological
• in 73% of mice at 15 to 40 weeks of age
• in 73% of mice at 15 to 40 weeks of age
• in 73% of mice at 15 to 40 weeks of age

neoplasm
• 73% of mice develop malignant gliomas consisting of anaplastic astrocytomas (in 66% of mice with tumors) and glioblastomas (in 34% of mice with tumors)
• 34% of mice with tumors develop glioblastomas
• anaplastic astrocytomas (in 66% of mice with tumors)

nervous system
• in 73% of mice at 15 to 40 weeks of age
• 73% of mice develop malignant gliomas consisting of anaplastic astrocytomas (in 66% of mice with tumors) and glioblastomas (in 34% of mice with tumors)
• 34% of mice with tumors develop glioblastomas
• anaplastic astrocytomas (in 66% of mice with tumors)




Genotype
MGI:5571383
cn8
Allelic
Composition
Gt(ROSA)26Sortm1(Smo/EYFP)Amc/Gt(ROSA)26Sor+
Hk2tm1.1Uku/Hk2tm1.1Uku
Tg(GFAP-cre)25Mes/0
Genetic
Background
involves: 129P2/OlaHsd * 129X1/SvJ * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(Smo/EYFP)Amc mutation (1 available); any Gt(ROSA)26Sor mutation (758 available)
Hk2tm1.1Uku mutation (1 available); any Hk2 mutation (42 available)
Tg(GFAP-cre)25Mes mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• median survival is 31 days compared with mice with wild-type Hk2 that die by P20

neoplasm
• increased micro-vascularization
• compared to in mice with wild-type Hk2
• all mice develop tumors with reduced growth and at increased latency compared to in mice with wild-type Hk2
• all mice develop tumors with increased latency compared to in mice with wild-type Hk2

nervous system
• reduced cerebellar granule neuron progenitors proliferation
• all mice develop tumors with reduced growth and at increased latency compared to in mice with wild-type Hk2

cellular
• reduced cerebellar granule neuron progenitors proliferation

cardiovascular system
• increased micro-vascularization




Genotype
MGI:5571384
cn9
Allelic
Composition
Gt(ROSA)26Sortm1(Smo/EYFP)Amc/Gt(ROSA)26Sor+
Hk2tm1.1Uku/Hk2+
Tg(GFAP-cre)25Mes/0
Genetic
Background
involves: 129P2/OlaHsd * 129X1/SvJ * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(Smo/EYFP)Amc mutation (1 available); any Gt(ROSA)26Sor mutation (758 available)
Hk2tm1.1Uku mutation (1 available); any Hk2 mutation (42 available)
Tg(GFAP-cre)25Mes mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system

mortality/aging
• mice die by P20

neoplasm




Genotype
MGI:3804817
cn10
Allelic
Composition
Mib1tm2Kong/Mib1tm2Kong
Tg(GFAP-cre)25Mes/0
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Mib1tm2Kong mutation (0 available); any Mib1 mutation (35 available)
Tg(GFAP-cre)25Mes mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mice die at 2 to 4 months of age

nervous system
• mice exhibit a delay in the migration of cells from the external granule layer to the internal granule layer
• at P9, the external granule cell layer contains more granule cells than in wild-type mice
• unlike in wild-type mice, granule cells are maintained at P17 but migrate to the internal granule cell layer by P21
• however, cell proliferation within the external granule layer is normal
• at P15, Bergmann glial cell processes are severely disorganized

growth/size/body

cellular
• mice exhibit a delay in the migration of cells from the external granule layer to the internal granule layer




Genotype
MGI:3831281
cn11
Allelic
Composition
Trp53tm1Brn/Trp53tm1Brn
Tg(GFAP-cre)25Mes/0
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(GFAP-cre)25Mes mutation (2 available)
Trp53tm1Brn mutation (17 available); any Trp53 mutation (205 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• 4 of 23 mice develop anaplastic astrocytomas

neoplasm
• 4 of 23 mice develop anaplastic astrocytomas




Genotype
MGI:4462796
cn12
Allelic
Composition
Glultm3Whla/Glultm1Whla
Tg(GFAP-cre)25Mes/0
Genetic
Background
involves: 129P2/OlaHsd * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Glultm1Whla mutation (0 available); any Glul mutation (28 available)
Glultm3Whla mutation (1 available); any Glul mutation (28 available)
Tg(GFAP-cre)25Mes mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• born in normal numbers
• none found at 6-8 days of age
• death at 2-3 days of age

behavior/neurological
• nursed immediately after birth but milk intake then declined

nervous system
• moderately elevated brain ammonia levels
• no gross brain malformations

homeostasis/metabolism
• decreased alanine in the cortex of the brain at two days of age
• decreased glutamine in the cortex of the brain at two days of age
• increased glycine in the cortex of the brain at two days of age
• moderately elevated brain ammonia levels
• blood glucose levels at 30% of controls at 2 days of age




Genotype
MGI:4462797
cn13
Allelic
Composition
Glultm3Whla/Glultm3Whla
Tg(GFAP-cre)25Mes/0
Genetic
Background
involves: 129P2/OlaHsd * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Glultm3Whla mutation (1 available); any Glul mutation (28 available)
Tg(GFAP-cre)25Mes mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• born in normal numbers
• none found at 6-8 days of age
• death at 2-3 days of age

behavior/neurological
• nursed immediately after birth but milk intake then declined

homeostasis/metabolism
• decreased glutamine and alanine in the cortex of the brain at two days of age
• decreased glutamine in the cortex of the brain at two days of age
• increased glycine in the cortex of the brain at two days of age
• moderately elevated brain ammonia levels
• blood glucose levels at 30% of controls at 2 days of age

nervous system
• moderately elevated brain ammonia levels
• no gross brain malformations




Genotype
MGI:4881761
cn14
Allelic
Composition
Phgdhtm1.2Shfu/Phgdhtm1.2Shfu
Tg(GFAP-cre)25Mes/0
Genetic
Background
involves: 129P2/OlaHsd * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Phgdhtm1.2Shfu mutation (1 available); any Phgdh mutation (27 available)
Tg(GFAP-cre)25Mes mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• at 6 weeks but not at P0

homeostasis/metabolism
• arginine levels in the cerebral cortex are decreased compared to in control mice
• arginine levels in the hippocampus are increased compared to in control mice
• serum glycine concentration is subtly increased compared to in control mice
• cystathionine levels in the cerebral cortex and hippocampus are decreased compared to in control mice
• glutamic acid levels in the hippocampus are decreased compared to in control mice
• glutamine levels in the hippocampus are increased compared to in control mice
• free glycine levels in the cerebral cortex are decreased compared to in control mice
• phenylalanine levels in the cerebral cortex are decreased compared to in control mice
• phenylalanine levels in the hippocampus are increased compared to in control mice
• free L- and D-serine levels in the cerebral cortex and hippocampus are decreased compared to in control mice
• L-serine or D-serine injection results in a greater increase in L-serine and D-serine content than in similarly treated control mice
• threonine levels in the hippocampus are decreased compared to in control mice

growth/size/body
• at P42 but not at P0




Genotype
MGI:5495325
cn15
Allelic
Composition
Cdc42tm1.1Rac/Cdc42tm1.1Rac
Tg(GFAP-cre)25Mes/0
Genetic
Background
involves: 129P2/OlaHsd * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cdc42tm1.1Rac mutation (0 available); any Cdc42 mutation (42 available)
Tg(GFAP-cre)25Mes mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• more than half of mice die before 3 months of age due to severe hydrocephalus

nervous system
• severe
• ependymal cells are detached from the lateral and third ventricle
• ependymal cells are detached from the lateral and third ventricle

craniofacial
• in most mice at 4 weeks

skeleton
• in most mice at 4 weeks

cellular




Genotype
MGI:4840094
cn16
Allelic
Composition
Nf1tm1Par/Nf1+
Ptentm1Hwu/Pten+
Trp53tm1Tyj/Trp53+
Tg(GFAP-cre)25Mes/0
Genetic
Background
involves: 129S1/Sv * 129S2/SvPas * 129S4/SvJae * 129X1/SvJ * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Nf1tm1Par mutation (4 available); any Nf1 mutation (111 available)
Ptentm1Hwu mutation (16 available); any Pten mutation (78 available)
Tg(GFAP-cre)25Mes mutation (2 available)
Trp53tm1Tyj mutation (12 available); any Trp53 mutation (205 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• most die as early as 10 weeks of age, and usually within a week of showing signs of morbidity

behavior/neurological
• exaggerated startle response
• ataxic gait
• generalized motor seizures

nervous system
• generalized motor seizures
• gliomas from asymptomatic mutants are primarily classified as grade 3 astocytomas
• 5-fold higher growth rate of astrocytomas compared with tumors from transgenic mice heterozygous for Nf1tm1Par and Trp53tm1Tyj and hemizygous for Tg(GFAP-cre)25Mes

neoplasm
• gliomas from asymptomatic mutants are primarily classified as grade 3 astocytomas
• 5-fold higher growth rate of astrocytomas compared with tumors from transgenic mice heterozygous for Nf1tm1Par and Trp53tm1Tyj and hemizygous for Tg(GFAP-cre)25Mes

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
malignant astrocytoma DOID:3069 J:134611




Genotype
MGI:4840090
cn17
Allelic
Composition
Nf1tm1Par/Nf1+
Trp53tm1Tyj/Trp53+
Tg(GFAP-cre)25Mes/0
Genetic
Background
involves: 129S1/Sv * 129S2/SvPas * 129X1/SvJ * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Nf1tm1Par mutation (4 available); any Nf1 mutation (111 available)
Tg(GFAP-cre)25Mes mutation (2 available)
Trp53tm1Tyj mutation (12 available); any Trp53 mutation (205 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• complete penetrance of malignant astrocytomas
• gliomas from asymptomatic mutants are primarily classified as grade 2 astocytomas
• neurospheres from mutant astrocytomas exhibit loss of heterozygosity at both Nf1 and Trp53 loci

mortality/aging
• mutants survive up to 8 weeks beyond initial appearance of symptoms

neoplasm
• complete penetrance of malignant astrocytomas
• gliomas from asymptomatic mutants are primarily classified as grade 2 astocytomas
• neurospheres from mutant astrocytomas exhibit loss of heterozygosity at both Nf1 and Trp53 loci

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
malignant astrocytoma DOID:3069 J:134611




Genotype
MGI:4840096
cn18
Allelic
Composition
Nf1tm1Par/Nf1+
Ptentm1Hwu/Pten+
Trp53tm1Elee/Trp53+
Tg(GFAP-cre)25Mes/0
Genetic
Background
involves: 129S1/Sv * 129S4/SvJae * 129X1/SvJ * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Nf1tm1Par mutation (4 available); any Nf1 mutation (111 available)
Ptentm1Hwu mutation (16 available); any Pten mutation (78 available)
Tg(GFAP-cre)25Mes mutation (2 available)
Trp53tm1Elee mutation (0 available); any Trp53 mutation (205 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• most die as early as 10 weeks of age, and usually within a week of showing signs of morbidity

behavior/neurological
• exaggerated startle response
• ataxic gait
• generalized motor seizures

nervous system
• generalized motor seizures
• mutants develop astrocytomas
• neurospheres from mutant astrocytomas exhibit loss of heterozygosity at both Nf1 and Trp53 loci

neoplasm
• mutants develop astrocytomas
• neurospheres from mutant astrocytomas exhibit loss of heterozygosity at both Nf1 and Trp53 loci




Genotype
MGI:4840095
cn19
Allelic
Composition
Nf1tm1Par/Nf1+
Trp53tm1Elee/Trp53+
Tg(GFAP-cre)25Mes/0
Genetic
Background
involves: 129S1/Sv * 129S4/SvJae * 129X1/SvJ * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Nf1tm1Par mutation (4 available); any Nf1 mutation (111 available)
Tg(GFAP-cre)25Mes mutation (2 available)
Trp53tm1Elee mutation (0 available); any Trp53 mutation (205 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mutants survive up to 8 weeks beyond initial appearance of symptoms

behavior/neurological
• exaggerated startle response
• ataxic gait
• generalized motor seizures

nervous system
• generalized motor seizures
• mutants develop astrocytomas
• neurospheres from mutant astrocytomas exhibit loss of heterozygosity at both Nf1 and Trp53 loci

neoplasm
• mutants develop astrocytomas
• neurospheres from mutant astrocytomas exhibit loss of heterozygosity at both Nf1 and Trp53 loci

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
malignant astrocytoma DOID:3069 J:134611




Genotype
MGI:5472016
cn20
Allelic
Composition
Gt(ROSA)26Sortm1(RICTOR)Jger/Gt(ROSA)26Sortm1(RICTOR)Jger
Tg(GFAP-cre)25Mes/0
Tg(GFAP-EGFR*,-lacZ)#Agu/0
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(RICTOR)Jger mutation (0 available); any Gt(ROSA)26Sor mutation (758 available)
Tg(GFAP-cre)25Mes mutation (2 available)
Tg(GFAP-EGFR*,-lacZ)#Agu mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype

Increased grade of oligodendroglioma in Gt(ROSA)26Sortm1(RICTOR)Jger/Gt(ROSA)26Sortm1(RICTOR)Jger Tg(GFAP-EGFR*,-lacZ)#Agu/0 Tg(GFAP-cre)25Mes/0 mice

mortality/aging
• all mice succumb to gliomas by 18 weeks

neoplasm
• mice exhibit accelerated glioma development compared with Gt(ROSA)26Sortm1(RICTOR)Jger/Gt(ROSA)26Sortm1(RICTOR)Jger Tg(GFAP-cre)25Mes mice
• mixed astrocytic-oligodendroglial tumors
• mixed astrocytic-oligodendroglial tumors
• mice exhibit accelerated glioma development compared with Gt(ROSA)26Sortm1(RICTOR)Jger/Gt(ROSA)26Sortm1(RICTOR)Jger Tg(GFAP-cre)25Mes mice

nervous system
• mice exhibit accelerated glioma development compared with Gt(ROSA)26Sortm1(RICTOR)Jger/Gt(ROSA)26Sortm1(RICTOR)Jger Tg(GFAP-cre)25Mes mice
• mixed astrocytic-oligodendroglial tumors
• mixed astrocytic-oligodendroglial tumors
• 3-fold increase in thickness




Genotype
MGI:2684282
cn21
Allelic
Composition
Dag1tm1Kcam/Dag1tm2Kcam
Tg(GFAP-cre)25Mes/0
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Dag1tm1Kcam mutation (1 available); any Dag1 mutation (98 available)
Dag1tm2Kcam mutation (2 available); any Dag1 mutation (98 available)
Tg(GFAP-cre)25Mes mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• cerebral, cerebellar and brain stem neuronal migration abnormalities

cellular
• cerebral, cerebellar and brain stem neuronal migration abnormalities

growth/size/body

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
lissencephaly DOID:0050453 OMIM:PS607432
J:86901




Genotype
MGI:3805515
cn22
Allelic
Composition
Mapk1tm1Gela/Mapk1tm1Gela
Tg(GFAP-cre)25Mes/0
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Mapk1tm1Gela mutation (1 available); any Mapk1 mutation (34 available)
Tg(GFAP-cre)25Mes mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
behavior/neurological
• long-term memory for contextual conditioning is significantly impaired compared to wild-type controls
• overtraining does not rescue defect as mice continue to display less freezing behavior than wild-type littermates
• long-term memory for cued conditioning is significantly impaired compared to wild-type controls
• overtraining does not rescue defect as mice continue to display less freezing behavior than wild-type littermates

nervous system
• cellular density appears greater throughout cortex, but laminar organization is normal
• at P10 mice show a 10% reduction in neuron number in cerebral cortex, with a 40% increase in non-neuronal, presumptive glial cells
• neuron number in layer VI and cortical preplate is reduced by 35%at P2
• in layer V, there are only 50% as many neurons as in wild-type at P2
• layers II-IV show a 30% decrease in neurons at P2
• dramatic increase in astrocyte number is observed throughout cortex and subventricular zone
• astrocyte metabolism and viability are similar to wild-type; neuronal apoptosis and differentiation are similar to controls
• cortical thickness is significantly reduced throughout the dorsal telencephalon relative to wild-type at P2

cellular




Genotype
MGI:2684281
cn23
Allelic
Composition
Dag1tm2Kcam/Dag1tm2Kcam
Tg(GFAP-cre)25Mes/0
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Dag1tm2Kcam mutation (2 available); any Dag1 mutation (98 available)
Tg(GFAP-cre)25Mes mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• cerebral, cerebellar and brain stem neuronal migration abnormalities
• fusion of the cerebral interhemispheric fissure and adjacent cerebellar folia
• malformations resembling polymicrogyria
• granule cells are observed in the subrarachnoid space during postnatal cerebellar development indicating aberrant migration of granule cells
• about 20% increase in brain size
• some mutants show minor dispersion of neuronal cell bodies in the CA1 region
• some mutants show focal irregularities of the dentate granule cell layer in the hippocampus
• cerebral cortical surfaces show widespread discontinuities of the glia limitans (pial surface basal lamina) accompanied by glial neuronal heterotopia within the leptomeninges
• multifocal disarray of neuronal layering in the cerebral cortex
• cerebellar cortical surfaces show widespread discontinuities of the glia limitans (pial surface basal lamina) accompanied by glial neuronal heterotopia within the leptomeninges
• GFAP-immunoreactive astrocytes are prominent in the cerebral cortex, indicating gliosis
• the normally open subarachnoid space is filled with heterotopic astrocytic and neuronal processes
• induction of long-term potentiation (LTP) by high-frequency stimulation is blunted in hippocampal slices, however baseline neurotransmission is unaffected and presynaptic neurotransmitter release is not affected

vision/eye
• significantly reduced positive scotopic threshold response
• significantly increased negative scotopic threshold response
• the b-wave responses are severely attenuated

cellular
• cerebral, cerebellar and brain stem neuronal migration abnormalities

growth/size/body

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
lissencephaly DOID:0050453 OMIM:PS607432
J:86901




Genotype
MGI:4436771
cn24
Allelic
Composition
Ntf3tm1Esm/Ntf3tm1Esm
Tg(GFAP-cre)25Mes/0
Genetic
Background
involves: 129S1/Sv * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ntf3tm1Esm mutation (0 available); any Ntf3 mutation (17 available)
Tg(GFAP-cre)25Mes mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• loss of subcortical tract results in a reduction in axonal bundles in subcortical white matter

vision/eye
• impaired visual function indicated by the visual cliff avoidance test: mutants often cross the cliff edge without hesitation and show no preference for either side of the box




Genotype
MGI:3849178
cn25
Allelic
Composition
Trp53tm1Elee/Trp53tm1Tyj
Tg(GFAP-cre)25Mes/0
Genetic
Background
involves: 129S2/SvPas * 129S4/SvJae * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(GFAP-cre)25Mes mutation (2 available)
Trp53tm1Elee mutation (0 available); any Trp53 mutation (205 available)
Trp53tm1Tyj mutation (12 available); any Trp53 mutation (205 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• all mice die prior to 500 days

behavior/neurological
• 85% of mice
• 85% of mice
• 85% of mice
• 85% of mice

neoplasm
• 90% of mice develop medulloblastomas
• mice develop tumors outside of the central nervous system consisting of soft-tissue sarcomas
• 90% of mice develop malignant gliomas with astrocytic characteristics
• 40% of high-grade astrocytic gliomas exhibit necrosis, pseudopalisading tumors cells, high degree of nuclear atypia, and microvascular proliferation similar to human glioblastoma multiforme
• tumors are relatively heterogeneous histological and in lineage marker expression

nervous system
N
• at 2 months of age, brain cells in the subventricular zone and progenitor cells exhibit normal growth rates
• 85% of mice
• 90% of mice develop medulloblastomas
• 90% of mice develop malignant gliomas with astrocytic characteristics
• 40% of high-grade astrocytic gliomas exhibit necrosis, pseudopalisading tumors cells, high degree of nuclear atypia, and microvascular proliferation similar to human glioblastoma multiforme
• tumors are relatively heterogeneous histological and in lineage marker expression
• in mice with neurological defects

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
glioblastoma DOID:3068 J:149662




Genotype
MGI:3839880
cn26
Allelic
Composition
Kmt2atm1.1Erns/Kmt2atm1.1Erns
Tg(GFAP-cre)25Mes/0
Genetic
Background
involves: 129S2/SvPas * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Kmt2atm1.1Erns mutation (0 available); any Kmt2a mutation (80 available)
Tg(GFAP-cre)25Mes mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mice die between P25 and P30

nervous system
• cultured subventricular cells produce fewer neuronal cells while remaining gliogenic unlike wild-type cells
• however, cultured subventricular cells exhibit normal proliferation and apoptosis
• neuroblast chain migration in mice and from subventricular zone explants is severely disorganized, and migration is reduced 40% compared to wild-type cells
• all regions of the brain that undergo postnatal neurogenesis including the cerebellar granule cell layer, hippocampal dentate gyrus, and olfactory bulb are reduced in size compared to in wild-type mice
• however, the ependymal layer and oligodendrocytes develop normally
• reduced in size with reduced neurons
• with reduced neurons
• with reduced neurons
• the expanded subventricular zone contains 3- to 4-fold fewer proliferating neuroblasts compared to in wild-type mice
• after P7, neuroblasts accumulate in the subventricular zone due to impaired migration unlike in wild-type mice
• the subventricular zone contains more cells positive for an astrocyte-specific marker than in wild-type mice
• the subventricular zone and other brain regions contains more cells positive for an astrocyte-specific marker than in wild-type mice
• the subventricular zone contains 3- to 4-fold fewer proliferating neuroblasts compared to in wild-type mice
• under differentiation condition, cultured subventricular zone cells produce more than 20-fold fewer Tuj1+ (marking neuron precursor cells) compared similarly treated wild-type cells

behavior/neurological

growth/size/body

cellular
• cultured subventricular cells produce fewer neuronal cells while remaining gliogenic unlike wild-type cells
• however, cultured subventricular cells exhibit normal proliferation and apoptosis
• neuroblast chain migration in mice and from subventricular zone explants is severely disorganized, and migration is reduced 40% compared to wild-type cells




Genotype
MGI:3615302
cn27
Allelic
Composition
Olig2tm1Qrlu/Olig2tm1Qrlu
Tg(GFAP-cre)25Mes/?
Genetic
Background
involves: 129S4/SvJae * C57BL/6J * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Olig2tm1Qrlu mutation (0 available); any Olig2 mutation (36 available)
Tg(GFAP-cre)25Mes mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
behavior/neurological
• abnormal limb clasping reflex
• beginning at 2 weeks of age
• beginning at 2 weeks of age

nervous system
• severe reduction in numbers of myelinated axons and myelin sheaths are thinner
• development arrested in dorsal cortex before formation of cells capable of forming myelin




Genotype
MGI:4830362
cn28
Allelic
Composition
Ptentm1Hwu/Ptentm1Hwu
Tg(GFAP-cre)25Mes/0
Genetic
Background
involves: 129S4/SvJae * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ptentm1Hwu mutation (16 available); any Pten mutation (78 available)
Tg(GFAP-cre)25Mes mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• death occurs around P21

nervous system
• cerebella layering defects
• before P3, cerebella are enlarged but the external granule layer (EGL) and cerebellar lobules are normal and Purkinje cell position is normal
• however, after P6, mutants show a marked cerebellar enlargement and lack internal granule layer and folia
• loss of foliation after P6
• Purkinje layer defect is first seen at P4-P6 and by P9, numerous Purkinje neurons are randomly scattered
• disruption of Bergmann glial layering
• premature differentiation of Bergmann glia leading to extensive layering defects
• some Bergmann cell bodies are randomly distributed at P7 and lose their contacts to the pial surface and are positioned deep within the internal granule layer region
• Purkinje cell layer is normal at P3 but there are many ectopic Purkinje cells by P9
• lack of an organized internal granule layer (IGL) at P6
• severe granule neuron layering defects
• mutants exhibit granule neuron migration defects, with granule neurons failing to migrate to the internal granule layer and accumulating in the molecular layer (ML)
• granule neurons are resistant to low potassium-induced cell death under serum deprivation conditions

cellular
• premature differentiation of Bergmann glia leading to extensive layering defects

growth/size/body




Genotype
MGI:3849177
cn29
Allelic
Composition
Trp53tm1Elee/Trp53tm1Elee
Tg(GFAP-cre)25Mes/0
Genetic
Background
involves: 129S4/SvJae * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(GFAP-cre)25Mes mutation (2 available)
Trp53tm1Elee mutation (0 available); any Trp53 mutation (205 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• all mice die prior to 400 days

behavior/neurological
• 84% of mice
• 84% of mice
• 84% of mice
• 84% of mice

neoplasm
• 90% of mice develop medulloblastomas
• mice develop tumors outside of the central nervous system consisting of soft-tissue sarcomas
• 90% of mice develop malignant gliomas with astrocytic characteristics
• 40% of high-grade astrocytic gliomas exhibit necrosis, pseudopalisading tumors cells, high degree of nuclear atypia, and microvascular proliferation similar to human glioblastoma multiforme
• tumors are relatively heterogeneous histological and in lineage marker expression

nervous system
N
• at 2 months of age, brain cells in the subventricular zone and progenitor cells exhibit normal growth rates
• 84% of mice
• 90% of mice develop medulloblastomas
• 90% of mice develop malignant gliomas with astrocytic characteristics
• 40% of high-grade astrocytic gliomas exhibit necrosis, pseudopalisading tumors cells, high degree of nuclear atypia, and microvascular proliferation similar to human glioblastoma multiforme
• tumors are relatively heterogeneous histological and in lineage marker expression
• in mice with neurological defects




Genotype
MGI:5302861
cn30
Allelic
Composition
Pomt2tm1.1Hhu/Pomt2tm1.1Hhu
Tg(GFAP-cre)25Mes/0
Genetic
Background
involves: 129S4/SvJaeSor * 129S6/SvEvTac * C57BL/6J * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Pomt2tm1.1Hhu mutation (1 available); any Pomt2 mutation (26 available)
Tg(GFAP-cre)25Mes mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• some granule cells fail to migrate in the cerebellum
• however, forebrain architecture is normal
• adult mice exhibit breaches in the pial basement membrane and the glia limitans in limited areas at the midline between the cerebral hemispheres compared to in wild-type mice

cellular
• some granule cells fail to migrate in the cerebellum
• however, forebrain architecture is normal
• adult mice exhibit breaches in the pial basement membrane and the glia limitans in limited areas at the midline between the cerebral hemispheres compared to in wild-type mice




Genotype
MGI:6358252
cn31
Allelic
Composition
Knl1tm1c(EUCOMM)Hmgu/Knl1tm1c(EUCOMM)Hmgu
Tg(GFAP-cre)25Mes/0
Genetic
Background
involves: 129S4/SvJaeSor * C57BL/6N * FVB/N
Cell Lines HEPD0665_2_E05
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Knl1tm1c(EUCOMM)Hmgu mutation (0 available); any Knl1 mutation (65 available)
Tg(GFAP-cre)25Mes mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging

nervous system
• neural progenitor cells prematurely exhibit the cell cycle and become migratory
• mis-segregated chromosomes with DNA bridges located at the cleavage furrow
• however, karyotypes are normal
• at E15.5 and E16.5 with some precursor cells located outside the ventricular zone and subventricular zone
• POU3F2-expressing L2-5 neurons
• CUX1-expressing L2-4 neurons
• due to increased apoptosis
• however, deep layer neuron numbers are normal

cellular
• mis-segregated chromosomes with DNA bridges located at the cleavage furrow
• however, karyotypes are normal
• in the cortex at E15.5, abundant in the germinal zones and intermediate zone
• marginally by E17.5
• associated with increased DNA damage determined by gammaH2AX staining
• however, apoptotic cells are largely absent from the cortical plate
• neural progenitor cells prematurely exhibit the cell cycle and become migratory

growth/size/body
• less severe than in mice with the conditional activated by Emx1tm1(cre)Krj

homeostasis/metabolism

immune system
• mis-segregated chromosomes with DNA bridges located at the cleavage furrow
• however, karyotypes are normal

hematopoietic system
• mis-segregated chromosomes with DNA bridges located at the cleavage furrow
• however, karyotypes are normal




Genotype
MGI:6449669
cn32
Allelic
Composition
Cul3tm1Jdsr/Cul3tm1Jdsr
Tg(GFAP-cre)25Mes/0
Genetic
Background
involves: 129S4/SvJaeSor * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cul3tm1Jdsr mutation (1 available); any Cul3 mutation (42 available)
Tg(GFAP-cre)25Mes mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• deformed hippocampus

mortality/aging
• mice die before age P17

growth/size/body




Genotype
MGI:6449671
cn33
Allelic
Composition
Cul3tm1Jdsr/Cul3+
Tg(GFAP-cre)25Mes/0
Genetic
Background
involves: 129S4/SvJaeSor * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cul3tm1Jdsr mutation (1 available); any Cul3 mutation (42 available)
Tg(GFAP-cre)25Mes mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
behavior/neurological
N
• normal latency to fall in rotarod test
• normal distance traveled in open field test
• normal number of arm entries and spontaneous alterations in Y-maze test
• normal time and number of grooming episodes
• fewer entries into and time spent in open arms in elevated plus maze test
• normal total distance travelled and time spent in closed arms in elevated plus maze test
• less time spent in center in open field test
• normal distance traveled in open field test
• reduced social preference index when introduced to novel mouse and novel inanimate object in three-chamber test
• reduced social preference index when introduced to novel mouse and known mouse in three-chamber test

nervous system
N
• normal cerebral cortex, corpus callosum and hippocampus morphology and brain weight
• normal latency to localize buried food pellets in olfactory sensing test
• normal neuron morphology in CA1 and CA3 hippocampal regions and in cerebral neocortex layers at age P60
• normal length and complexity of apical and basal dendrites of hippocampal CA1 neurons at age P60
• normal resting membrane potential (RMP) in hippocampal CA1 pyramidal neurons at age P60
• normal number of inhibitory synapses in hippocampal CA1 pyramidal neurons at age P15
• increased number of spines on apical dendrites of hippocampal CA1 neurons at age P15 and P60
• increased AP frequency in response to injected currents in hippocampal CA1 pyramidal neurons at age P60
• higher rate of successful responses and synaptic efficacy to minimal stimulation in hippocampal CA1 pyramidal neurons at age P60
• increased EPSC/IPSC ratio in hippocampal CA1 pyramidal neurons at age P60
• normal synaptic potency to minimal stimulation in hippocampal CA1 pyramidal neurons at age P60
• increased mEPSC frequency in hippocampal CA1 pyramidal neurons at age P15 and P60
• normal mEPSC amplitude in hippocampal CA1 pyramidal neurons at age P15 and P60
• increased mIPSC frequency in hippocampal CA1 pyramidal neurons at age P60
• normal mIPSC amplitude in hippocampal CA1 pyramidal neurons at age P60
• reduced paired-pulse ratio in hippocampal CA1 pyramidal neurons at age P60

mortality/aging
N
• viable and normal lifespan

growth/size/body
N
• normal body size

reproductive system




Genotype
MGI:5896534
cn34
Allelic
Composition
Nsdhltm1.1Hrm/Y
Tg(GFAP-cre)25Mes/0
Genetic
Background
involves: 129S6/SvEvTac * C57BL/6J * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Nsdhltm1.1Hrm mutation (0 available); any Nsdhl mutation (7 available)
Tg(GFAP-cre)25Mes mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• die between P12-P20

behavior/neurological
• by P8 to P10

nervous system
• thinner with fewer granule cell precursors at P5 and becoming progressively worse with age
• at P8 only a single layer of granule cell precursors is present in severely affected mice
• appears disorganized with fewer hippocampal neurons
• fewer neurons present in the dentate gyrus at P0
• fewer hippocampal neurons at P0 especially in the dentate gyrus
• reduced numbers and organization of granule neurons at P7
• at P7
• increase in pycnotic nuclei in the outer layer
• fewer, shorter cells that appear disorganized
• reduced numbers and organization of granule neurons at P7
• decreased cholesterol levels and increased levels of sterol intermediates in granule cell precursors at P3, P5, and P7
• cultured granule cell precursors produce fewer and thinner neurite extensions
• cell morphology is improved with the addition of cholesterol to the culture medium
• cerebellar Purkinje cells fail to form extensive dendritic trees unlike wild-type controls
• dendritic trees eventually degenerate
• progressively reduced proliferation of granule cell precursors in cerebella starting at P5
• increase in apoptosis of granule cell precursors in cerebella beginning at P7
• cultured granule cell precurors show reduced proliferation that is largely restored with the addition of cholesterol to the culture medium




Genotype
MGI:3849179
cn35
Allelic
Composition
Nf1tm1Fcr/Nf1tm1Fcr
Trp53tm1Elee/Trp53tm1Elee
Tg(GFAP-cre)25Mes/0
Genetic
Background
involves: 129S/SvEv * 129S4/SvJae * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Nf1tm1Fcr mutation (3 available); any Nf1 mutation (111 available)
Tg(GFAP-cre)25Mes mutation (2 available)
Trp53tm1Elee mutation (0 available); any Trp53 mutation (205 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• 70% of gliomas exhibit necrosis, a feature of human glioblastoma multiforme
• tumors are relatively homogeneous histological and in lineage marker expression

mortality/aging
• all mice die prior to 200 days

neoplasm
• 70% of gliomas exhibit necrosis, a feature of human glioblastoma multiforme
• tumors are relatively homogeneous histological and in lineage marker expression
• all mice develop astrocytic gliomas with shorter latency than observed in Trp53tm1Elee/Trp53tm1Tyj Tg(GFAP-cre)25Mes or Trp53tm1Elee/ Trp53tm1Elee Tg(GFAP-cre)25Mes mice

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
glioblastoma DOID:3068 J:149662




Genotype
MGI:5560657
cn36
Allelic
Composition
Mef2atm1.1Limm/Mef2atm1.1Limm
Mef2ctm2Eno/Mef2ctm2Eno
Mef2dtm3Eno/Mef2dtm3Eno
Tg(GFAP-cre)25Mes/0
Genetic
Background
involves: 129S/SvEv * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Mef2atm1.1Limm mutation (0 available); any Mef2a mutation (31 available)
Mef2ctm2Eno mutation (0 available); any Mef2c mutation (22 available)
Mef2dtm3Eno mutation (0 available); any Mef2d mutation (59 available)
Tg(GFAP-cre)25Mes mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• partial lethality by 5 weeks

nervous system
N
• mice exhibit normal numbers of spines per length of dendrite in pyramidal neurons
• mice exhibit decreased input-output curve compared with wild-type mice
• however, long term potentiation is normal

growth/size/body

cellular




Genotype
MGI:4818691
cn37
Allelic
Composition
Mrtfbtm2.1Eno/Mrtfbtm2.1Eno
Tg(GFAP-cre)25Mes/0
Genetic
Background
involves: 129S/SvEv * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Mrtfbtm2.1Eno mutation (0 available); any Mrtfb mutation (56 available)
Tg(GFAP-cre)25Mes mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
normal phenotype
• mice are normal




Genotype
MGI:5560660
cn38
Allelic
Composition
Mef2atm1.1Limm/Mef2atm1.1Limm
Tg(GFAP-cre)25Mes/0
Genetic
Background
involves: 129S/SvEv * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Mef2atm1.1Limm mutation (0 available); any Mef2a mutation (31 available)
Tg(GFAP-cre)25Mes mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
behavior/neurological
N
• mice exhibit normal behavior




Genotype
MGI:5560659
cn39
Allelic
Composition
Mef2atm1.1Limm/Mef2atm1.1Limm
Mef2dtm3Eno/Mef2dtm3Eno
Tg(GFAP-cre)25Mes/0
Genetic
Background
involves: 129S/SvEv * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Mef2atm1.1Limm mutation (0 available); any Mef2a mutation (31 available)
Mef2dtm3Eno mutation (0 available); any Mef2d mutation (59 available)
Tg(GFAP-cre)25Mes mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
behavior/neurological
N
• mice exhibit normal learning and memory in context- and cue-dependent fear conditioning tests, normal anxiety-related behaviors and pain sensitivity
• on a rotarod

nervous system
N
• mice exhibit normal synapse number and basal synaptic transmission




Genotype
MGI:6275806
cn40
Allelic
Composition
Lgi1tm2.1Jkc/Lgi1tm2.1Jkc
Tg(GFAP-cre)25Mes/0
Genetic
Background
involves: 129/Sv * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Lgi1tm2.1Jkc mutation (1 available); any Lgi1 mutation (24 available)
Tg(GFAP-cre)25Mes mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
N
• mice do not develop seizures, cortical dysplasia or hypercellularity in the outer cortical layers




Genotype
MGI:5286072
cn41
Allelic
Composition
Ptch1tm1Bjw/Ptch1tm1Bjw
Tg(GFAP-cre)25Mes/0
Genetic
Background
involves: 129T2/SvEms * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ptch1tm1Bjw mutation (2 available); any Ptch1 mutation (88 available)
Tg(GFAP-cre)25Mes mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• by 4 weeks, mice become severely ill and must be sacrificed

nervous system
• expanded at E16.5
• thick and disorganized, at birth
• rhombic lip expansion at E16.5
• cerebellar cells exhibit increased neurospheres compared with wild-type mice

neoplasm

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
medulloblastoma DOID:0050902 OMIM:155255
J:139573




Genotype
MGI:3641106
cn42
Allelic
Composition
Fgfr1tm1Upir/Fgfr1tm1Upir
Fgfr2tm1Dor/Fgfr2tm1Dor
Tg(GFAP-cre)25Mes/0
Genetic
Background
involves: 129X1/SvJ * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Fgfr1tm1Upir mutation (0 available); any Fgfr1 mutation (207 available)
Fgfr2tm1Dor mutation (2 available); any Fgfr2 mutation (65 available)
Tg(GFAP-cre)25Mes mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• numbers of astrocytes reaching the cortex is significantly reduced compared to controls at P7




Genotype
MGI:3641105
cn43
Allelic
Composition
Fgfr2tm1Dor/Fgfr2tm1Dor
Tg(GFAP-cre)25Mes/0
Genetic
Background
involves: 129X1/SvJ * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Fgfr2tm1Dor mutation (2 available); any Fgfr2 mutation (65 available)
Tg(GFAP-cre)25Mes mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• mice show a subtle reduction in cortical size compared to control mice
• numbers of astrocytes reaching the cortex is significantly reduced compared to controls at P7; greatest loss (60%) is in the upper cortical layers with 22% loss in the subcortical white matter
• there is an intermediate reduction (39%) in astrocte density was seen in the inferior cortical layers




Genotype
MGI:3810317
cn44
Allelic
Composition
Gt(ROSA)26Sortm1(Smo/EYFP)Amc/Gt(ROSA)26Sortm1(Smo/EYFP)Amc
Tg(GFAP-cre)25Mes/0
Genetic
Background
involves: 129X1/SvJ * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(Smo/EYFP)Amc mutation (1 available); any Gt(ROSA)26Sor mutation (758 available)
Tg(GFAP-cre)25Mes mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• mice develop diffuse medulloblastoma tumors and have a mean survival of 57 days

mortality/aging
• mice survive 57 days

neoplasm
• mice develop diffuse medulloblastoma tumors and have a mean survival of 57 days

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
medulloblastoma DOID:0050902 OMIM:155255
J:139574




Genotype
MGI:5609321
cn45
Allelic
Composition
Ephx2tm1.1Arte/Ephx2tm1.1Arte
Tg(GFAP-cre)25Mes/0
Genetic
Background
involves: C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ephx2tm1.1Arte mutation (0 available); any Ephx2 mutation (23 available)
Tg(GFAP-cre)25Mes mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• in the retina the upper capillary layer is less dense and characterized by fewer branching points in central areas and at the leading edge
• however, unlike in germ line deleted mice, no delay in radial extension of the vascular plexus is seen

vision/eye
• in the retina the upper capillary layer is less dense and characterized by fewer branching points in central areas and at the leading edge
• however, unlike in germ line deleted mice, no delay in radial extension of the vascular plexus is seen




Genotype
MGI:6719557
cn46
Allelic
Composition
Hip1tm5.1(HIP1)Tsr/Hip1tm5.1(HIP1)Tsr
Tg(GFAP-cre)25Mes/0
Genetic
Background
involves: C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Hip1tm5.1(HIP1)Tsr mutation (1 available); any Hip1 mutation (53 available)
Tg(GFAP-cre)25Mes mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
skeleton
• unexpectedly, mice exhibit severe kypholordosis at 6 months of age, indicating that brain-specific expression of human HIP1 does not rescue the spinal phenotype




Genotype
MGI:5810136
cn47
Allelic
Composition
Bicd2tm1Hgrd/Bicd2tm1Hgrd
Tg(GFAP-cre)25Mes/0
Genetic
Background
involves: C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Bicd2tm1Hgrd mutation (0 available); any Bicd2 mutation (23 available)
Tg(GFAP-cre)25Mes mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype

Disrupted laminar organization of the cortex in Bicd2tm1Hgrd/Bicd2tm1Hgrd Tg(GFAP-cre)25Mes/0 mice

mortality/aging
• mice with hydrocephalus die by 3-4 weeks of age
• mice without hydrocephalus survive to >8 weeks

nervous system
• FoxP2, a marker normally present in deep corticofugal layer V and VI pyramidal neurons, is abnormally distributed in superficial lamina, consistent with impaired radial migration
• corticofugal axonal trajectories (labelled with anti-neurofilament M antibody) arise in superficial instead of deep cortical layers
• mice exhibit the same cerebellar granule cell migration defects observed in Bicd2tm1.1Hgrd homozygotes
• some mice develop less severe hydrocephalus than that observed in Bicd2tm1.1Hgrd mice
• others do not develop hydrocephalus
• mice exhibit a thin corpus callosum
• mice exhibit a thin capsula externa
• mice without hydrocephalus exhibit disrupted laminar organization in the hippocampus
• at P20, the hippocampus pyramidal cell layer appears disorganized in the CA1 region
• mice without hydrocephalus exhibit disrupted laminar organization in the cerebral cortex
• FoxP2, a marker normally present in deep corticofugal layer V and VI pyramidal neurons, is abnormally distributed in superficial lamina
• laminar organization of NeuN+ cells is absent
• mice without hydrocephalus exhibit disrupted laminar organization in the cerebellar cortex
• mice do not develop an internal granule cell layer

cellular
• FoxP2, a marker normally present in deep corticofugal layer V and VI pyramidal neurons, is abnormally distributed in superficial lamina, consistent with impaired radial migration
• corticofugal axonal trajectories (labelled with anti-neurofilament M antibody) arise in superficial instead of deep cortical layers
• mice exhibit the same cerebellar granule cell migration defects observed in Bicd2tm1.1Hgrd homozygotes




Genotype
MGI:5499900
cn48
Allelic
Composition
Drd2tm1Smoc/Drd2tm1Smoc
Tg(GFAP-cre)25Mes/0
Genetic
Background
involves: C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Drd2tm1Smoc mutation (0 available); any Drd2 mutation (63 available)
Tg(GFAP-cre)25Mes mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
N
• MPTP treated mice exhibit normal astrocyte proliferation in the substantia nigra
• mice exhibit normal development of dopaminergic neurons in the ventral tagmental area
• in the substantia nigra
• mild increase in the production of pro-inflammatory mediator RNAs




Genotype
MGI:6256831
cn49
Allelic
Composition
Trpv4tm1c(KOMP)Wtsi/Trpv4tm1c(KOMP)Wtsi
Tg(GFAP-cre)25Mes/0
Genetic
Background
involves: C57BL/6J * C57BL/6N * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(GFAP-cre)25Mes mutation (2 available)
Trpv4tm1c(KOMP)Wtsi mutation (1 available); any Trpv4 mutation (41 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism
• after region-specific injection of hyaluronic acid to induce acute retinal detachment (RD), Mueller cells exhibit 50% less cell death and fail to exhibit significant mechanical stimuli-evoked current or inward current and HC067047 did not have an inhibitory effect unlike in wild-type Mueller cells
• however, retina subjected to RD exhibit normal gliosis and increased proliferation




Genotype
MGI:5297540
cn50
Allelic
Composition
Aqp4tm1.1Geno/Aqp4tm1.1Geno
Tg(GFAP-cre)25Mes/0
Genetic
Background
involves: C57BL/6J * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Aqp4tm1.1Geno mutation (0 available); any Aqp4 mutation (32 available)
Tg(GFAP-cre)25Mes mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• after water injection, mice exhibit decreased water uptake compared with similarly treated wild-type mice
• basal brain water content is increased compared to in wild-type mice
• however, the blood-brain barrier is intake in a Evans dye transfer assay

nervous system
• after water injection, mice exhibit decreased water uptake compared with similarly treated wild-type mice
• basal brain water content is increased compared to in wild-type mice
• however, the blood-brain barrier is intake in a Evans dye transfer assay




Genotype
MGI:4939155
cn51
Allelic
Composition
S1pr1tm1Jch/S1pr1tm1Jch
Tg(GFAP-cre)25Mes/?
Genetic
Background
involves: C57BL/6J * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
S1pr1tm1Jch mutation (0 available); any S1pr1 mutation (20 available)
Tg(GFAP-cre)25Mes mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
immune system
• Experimental Autoimmune Encephalitis induced by Myelin Oligodendrocyte Glycoprotein is attenuated but otherwise similar to contrtols

nervous system
• does not develop in Experimental Autoimmune Encephalitis
• reduced axonal damage in Experimental Autoimmune Encephalitis
• reduced in Experimental Autoimmune Encephalitis




Genotype
MGI:4939886
cn52
Allelic
Composition
Ren1tm1.1Sig/Ren1tm1.1Sig
Tg(GFAP-cre)25Mes/0
Genetic
Background
involves: C57BL/6J * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ren1tm1.1Sig mutation (0 available); any Ren1 mutation (28 available)
Tg(GFAP-cre)25Mes mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
N
• mice exhibit normal survival unlike Ren1tm1.2Sig homozygotes

renal/urinary system
N
• mice exhibit normal renal morphology and function

cardiovascular system
N
• mice exhibit normal blood pressure

homeostasis/metabolism
N
• mice exhibit normal metabolism




Genotype
MGI:6377096
cn53
Allelic
Composition
Marveld1tm1.1Liy/Marveld1tm1.1Liy
Tg(GFAP-cre)25Mes/0
Genetic
Background
involves: C57BL/6J * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Marveld1tm1.1Liy mutation (0 available); any Marveld1 mutation (13 available)
Tg(GFAP-cre)25Mes mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• granule cells accumulate on the molecular layer
• irregular at 6 days of age
• apical dendritic arbors are abnormal and unable to anchor in the basement membrane
• absence of strong glial fibers in mice at 6 days of age

cellular
• granule cells accumulate on the molecular layer




Genotype
MGI:5467513
cn54
Allelic
Composition
Ric8atm1.1Zhua/Ric8atm1.1Zhua
Tg(GFAP-cre)25Mes/0
Genetic
Background
involves: FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ric8atm1.1Zhua mutation (0 available); any Ric8a mutation (23 available)
Tg(GFAP-cre)25Mes mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• impaired migration from the external to internal granule layer
• severely disorganized
• no basement membrane separates neighboring lobules in the cerebellum and remains on the surface
• however, granule cell precursors are normal
• no basement membrane separates neighboring lobules
• however, folial pattern is more or less normal
• Bergmann glial scaffolds surrounding he primary and secondary fissures are severely disorganized
• the Bergmann glial scaffolds surrounding other fissures is severely reduced in fiber density compared to in wild-type mice
• severely reduced Bergmann glia-basement membrane interaction compared to in wild-type mice
• however, the Bergmann glial scaffolds surrounding other fissures is still associated with basement membrane
• scattered over a wide area in the cerebellum and frequently intermingled with ectopic granule cells
• most obvious in lobules surrounding the primary and secondary fissures
• throughout the molecular layer and external granule layer (EGL) surrounding the primary and secondary fissures
• in the EGL, but not the molecular layer, surrounding other lobules
• primary and secondary fissures
• no basement membrane separates neighboring lobules
• however, folial pattern is more or less normal
• expanded volume from P0 to P4

behavior/neurological

cellular
• impaired migration from the external to internal granule layer
• no basement membrane separates neighboring lobules in the cerebellum and remains on the surface




Genotype
MGI:5513868
cn55
Allelic
Composition
Dio2tm1Acb/Dio2tm1Acb
Tg(GFAP-cre)25Mes/0
Genetic
Background
involves: FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Dio2tm1Acb mutation (0 available); any Dio2 mutation (13 available)
Tg(GFAP-cre)25Mes mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
skeleton

endocrine/exocrine glands
N
• mice exhibit normal hypothalamic-pituitary-thyroid axis (HPT), HPT sensitivity and thyroid economy




Genotype
MGI:3641103
cn56
Allelic
Composition
Fgfr1tm1Upir/Fgfr1tm1Upir
Tg(GFAP-cre)25Mes/0
Genetic
Background
involves: FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Fgfr1tm1Upir mutation (0 available); any Fgfr1 mutation (207 available)
Tg(GFAP-cre)25Mes mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• in mutants, midline cells do not migrate from the ventricular zone to the subpial region of the dorsomedial pallium
• average midline width of the dorsal commissures is markedly smaller compared to controls; anterior and posterior are significantly more affected than the middle
• in 83% of mice, there is a complete loss of callosal axons from the motor and somatosensory cortex at birth
• there is a loss of hippocampal commissural axons in neonatal mice
• idusium griseum astroglia are absent in the anterior regions of mutants
• processes emerging from the glial wedge and ventricular zone remain attached at the ventricular zone and the pia and very few astrocytes are observed in between the glial wedge and the idusium griseum
• numbers of astrocytes reaching the cortex are significantly reduced compared to controls

cellular
• in mutants, midline cells do not migrate from the ventricular zone to the subpial region of the dorsomedial pallium




Genotype
MGI:6199477
cn57
Allelic
Composition
Lrp2tm1Tew/Lrp2tm1Tew
Tg(GFAP-cre)25Mes/0
Genetic
Background
involves: FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Lrp2tm1Tew mutation (0 available); any Lrp2 mutation (155 available)
Tg(GFAP-cre)25Mes mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
vision/eye
N
• mice exhibit normal retinal differentiation and eye formation




Genotype
MGI:3612962
cn58
Allelic
Composition
Ntrk2tm1Jom/Ntrk2tm1Jom
Tg(GFAP-cre)25Mes/0
Genetic
Background
involves: FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ntrk2tm1Jom mutation (0 available); any Ntrk2 mutation (54 available)
Tg(GFAP-cre)25Mes mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
N
• no defects in barrel cortex formation




Genotype
MGI:3770149
cn59
Allelic
Composition
Bdnftm1Limm/Bdnftm1Limm
Tg(GFAP-cre)25Mes/0
Genetic
Background
involves: FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Bdnftm1Limm mutation (0 available); any Bdnf mutation (32 available)
Tg(GFAP-cre)25Mes mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
behavior/neurological
• female, but not male, mice exhibit more immobility when placed in swim test than wild-type female mice
• male, but not female, mice exhibit increased locomotor activity compared to same sex wild-type mice





Contributing Projects:
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
05/10/2022
MGI 6.19
The Jackson Laboratory