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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Foxg1tm1(cre)Skm
targeted mutation 1, Susan K McConnell
MGI:1932522
Summary 50 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
hm1
Foxg1tm1(cre)Skm/Foxg1tm1(cre)Skm 129(Cg)-Foxg1tm1(cre)Skm/J MGI:3581545
ht2
Foxg1tm1(cre)Skm/Foxg1+ 129(Cg)-Foxg1tm1(cre)Skm/J MGI:3580339
ht3
Foxg1tm1(cre)Skm/Foxg1+ B6.129P2-Foxg1tm1(cre)Skm MGI:3767188
ht4
Foxg1tm1(cre)Skm/Foxg1+ involves: 129P2/OlaHsd * C57BL/6J MGI:5806112
ht5
Foxg1tm1(cre)Skm/Foxg1+ involves: C57BL/6 * CBA MGI:3767191
cn6
Bmp4tm1Blh/Bmp4tm4Blh
Foxg1tm1(cre)Skm/Foxg1+
involves: 129 * Black Swiss * C57BL/6 * SJL MGI:3805980
cn7
Notch1tm1Grid/Notch1tm2Rko
Foxg1tm1(cre)Skm/Foxg1+
involves: 129 * C57BL/6J * Swiss Webster MGI:3776429
cn8
Chd7tm1.1Dmm/Chd7+
Foxg1tm1(cre)Skm/Foxg1+
involves: 129 * C57BL/6 * Swiss Webster MGI:4835273
cn9
Chd7Gt(S20-7E1)Sor/Chd7tm1.1Dmm
Foxg1tm1(cre)Skm/Foxg1+
involves: 129 * C57BL/6 * Swiss Webster MGI:4835272
cn10
Fgf8tm1.3Mrt/Fgf8tm1.4Mrt
Foxg1tm1(cre)Skm/Foxg1+
involves: 129P2/OlaHsd MGI:3654831
cn11
Fgf8tm1.1Mrt/Fgf8tm1.4Mrt
Foxg1tm1(cre)Skm/Foxg1+
involves: 129P2/OlaHsd MGI:3654834
cn12
Aifm1tm2Pngr/Y
Foxg1tm1(cre)Skm/Foxg1+
involves: 129P2/OlaHsd MGI:3687280
cn13
Gt(ROSA)26Sortm1(RARA*)Soc/Gt(ROSA)26Sortm1(RARA*)Soc
Foxg1tm1(cre)Skm/Foxg1+
involves: 129P2/OlaHsd MGI:3795697
cn14
Cdc42tm1Yizh/Cdc42tm1Yizh
Foxg1tm1(cre)Skm/Foxg1+
involves: 129P2/OlaHsd MGI:3693870
cn15
Rhoatm1Yuyo/Rhoatm1Yuyo
Foxg1tm1(cre)Skm/Foxg1+
involves: 129P2/OlaHsd MGI:5004979
cn16
Pbx1tm1Koss/Pbx1tm1Koss
Pbx3tm1Mlc/Pbx3+
Foxg1tm1(cre)Skm/Foxg1+
involves: 129P2/OlaHsd MGI:5305924
cn17
Fgf8tm1.2Mrt/Fgf8tm1.3Mrt
Foxg1tm1(cre)Skm/Foxg1+
involves: 129P2/OlaHsd MGI:3720595
cn18
Celsr3tm1Agof/Celsr3tm2Agof
Foxg1tm1(cre)Skm/Foxg1+
involves: 129P2/OlaHsd MGI:3795739
cn19
Ntf3tm1Esm/Ntf3tm1Esm
Foxg1tm1(cre)Skm/Foxg1+
involves: 129P2/OlaHsd * 129S1/Sv MGI:2653845
cn20
Jag1tm1Grid/Jag1tm2Grid
Foxg1tm1(cre)Skm/Foxg1+
involves: 129P2/OlaHsd * 129S1/Sv MGI:3693201
cn21
Apaf1Gt(IRESBetageo)XIX18Pgr/Apaf1Gt(IRESBetageo)XIX18Pgr
Aifm1tm2Pngr/Y
Foxg1tm1(cre)Skm/Foxg1+
involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ MGI:3687281
cn22
Gt(ROSA)26Sortm1Red/Gt(ROSA)26Sor+
Foxg1tm1(cre)Skm/Foxg1+
involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ MGI:5508374
cn23
Igs1tm11(CAG-Bgeo,-Edn2)Nat/Igs1+
Foxg1tm1(cre)Skm/Foxg1+
involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ * C57BL/6 MGI:5544092
cn24
Slc12a2tm1.1Jheb/Slc12a2tm1.1Jheb
Foxg1tm1(cre)Skm/Foxg1+
involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ * C57BL/6 MGI:5538347
cn25
Notch2tm3Grid/Notch2tm3Grid
Foxg1tm1(cre)Skm/Foxg1+
involves: 129P2/OlaHsd * 129S1/Sv * C57BL/6 MGI:4361706
cn26
Olig2tm1Qrlu/Olig2tm1Qrlu
Foxg1tm1(cre)Skm/Foxg1+
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 MGI:3615303
cn27
Mafbtm1.1Good/Mafbtm1Jeng
Foxg1tm1(cre)Skm/Foxg1+
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * SJL MGI:5581686
cn28
Lmo4tm1Gan/Lmo4tm2.1Gan
Foxg1tm1(cre)Skm/Foxg1+
involves: 129P2/OlaHsd * 129S4/SvJaeSor * 129S6/SvEvTac * C57BL/6J MGI:4421423
cn29
Chd7tm1.1Dmm/Chd7tm1.1Dmm
Foxg1tm1(cre)Skm/Foxg1+
involves: 129P2/OlaHsd * 129S6/SvEvTac MGI:5807348
cn30
Bmp4tm3Blh/Bmp4tm3Blh
Foxg1tm1(cre)Skm/Foxg1+
involves: 129P2/OlaHsd * 129S6/SvEvTac MGI:2661104
cn31
Bmp4tm3Blh/Bmp4+
Foxg1tm1(cre)Skm/Foxg1+
involves: 129P2/OlaHsd * 129S6/SvEvTac MGI:3811334
cn32
Pbx1tm1Mlc/Pbx1+
Wnt9btm1Amc/Wnt9btm1Amc
Foxg1tm1(cre)Skm/Foxg1+
involves: 129P2/OlaHsd * 129S6/SvEvTac * 129X1/SvJ MGI:5305933
cn33
Actbtm1.1Erv/Actbtm1.1Erv
Foxg1tm1(cre)Skm/Foxg1+
involves: 129P2/OlaHsd * 129S6/SvEvTac * C57BL/6 * FVB/N MGI:4882049
cn34
Lmo4tm2.1Gan/Lmo4tm2.1Gan
Foxg1tm1(cre)Skm/Foxg1+
involves: 129P2/OlaHsd * 129S6/SvEvTac * C57BL/6J MGI:4421425
cn35
Bmp2tm1Brd/Bmp2tm1.1Mis
Foxg1tm1(cre)Skm/Foxg1+
involves: 129P2/OlaHsd * 129S7/SvEvBrd * C57BL/6J MGI:4430833
cn36
Pbx1tm1Koss/Pbx1tm1Koss
Pbx2tm1Mlc/Pbx2+
Foxg1tm1(cre)Skm/Foxg1+
involves: 129P2/OlaHsd * 129S/Sv MGI:5305855
cn37
Pbx1tm1Koss/Pbx1tm1Koss
Pbx2tm1Mlc/Pbx2tm1Mlc
Foxg1tm1(cre)Skm/Foxg1+
involves: 129P2/OlaHsd * 129S/Sv MGI:5305923
cn38
Wnt9btm1Amc/Wnt9btm1Amc
Foxg1tm1(cre)Skm/Foxg1+
involves: 129P2/OlaHsd * 129X1/SvJ MGI:5305932
cn39
Sp8tm2.1Aman/Sp8tm2.1Aman
Foxg1tm1(cre)Skm/Foxg1+
involves: 129P2/OlaHsd * C57BL/6 MGI:4455199
cn40
Atrxtm1Rjg/Y
Foxg1tm1(cre)Skm/Foxg1+
involves: 129P2/OlaHsd * C57BL/6 * FVB/N MGI:3530074
cn41
Dll1tm1Mjo/Dll1tm1Mjo
Foxg1tm1(cre)Skm/Foxg1+
involves: 129P2/OlaHsd * C57BL/6J MGI:3624333
cn42
Gt(ROSA)26Sortm1(Tbx1/GFP)Bem/Gt(ROSA)26Sor+
Foxg1tm1(cre)Skm/Foxg1+
involves: 129P2/OlaHsd * C57BL/6 * SJL MGI:5551750
cn43
Fgfr1tm1Upir/Fgfr1tm1Upir
Foxg1tm1(cre)Skm/Foxg1+
involves: 129P2/OlaHsd * ICR MGI:3702999
cn44
Fgfr1tm1Upir/Fgfr1tm1.1Upir
Foxg1tm1(cre)Skm/Foxg1+
involves: 129P2/OlaHsd * ICR MGI:3702998
cn45
Six3tm3Gco/Six3tm3Gco
Foxg1tm1(cre)Skm/Foxg1+
involves: 129S1/Sv * C57BL/6 MGI:3814903
cn46
Top2btm2Jcw/Top2btm2.1Jcw
Foxg1tm1(cre)Skm/Foxg1+
involves: 129S4/SvJae * 129S6/SvEvTac * 129X1/SvJ MGI:3521928
cn47
Bsndtm1Tjj/Bsndtm1Tjj
Foxg1tm1(cre)Skm/Foxg1+
involves: 129/Sv * 129P2/OlaHsd * 129X1/SvJ * C57BL/6 MGI:3826853
cn48
Tbx1tm2.1Bem/Tbx1tm2.2Bem
Foxg1tm1(cre)Skm/Foxg1+
involves: 129/Sv * C57BL/6 * SJL * Swiss Webster MGI:3619802
cn49
Jag1tm1Jlew/Jag1tm1Jlew
Foxg1tm1(cre)Skm/Foxg1+
involves: C57BL/6J MGI:3624332
cx50
Smarca1tm1.1Pick/Y
Foxg1tm1(cre)Skm/Foxg1+
involves: 129P2/OlaHsd * 129S4/SvJae * CD-1 MGI:5427352


Genotype
MGI:3581545
hm1
Allelic
Composition
Foxg1tm1(cre)Skm/Foxg1tm1(cre)Skm
Genetic
Background
129(Cg)-Foxg1tm1(cre)Skm/J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Foxg1tm1(cre)Skm mutation (2 available); any Foxg1 mutation (12 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• homozygous mice die perinatally




Genotype
MGI:3580339
ht2
Allelic
Composition
Foxg1tm1(cre)Skm/Foxg1+
Genetic
Background
129(Cg)-Foxg1tm1(cre)Skm/J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Foxg1tm1(cre)Skm mutation (2 available); any Foxg1 mutation (12 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
normal phenotype
• heterozygous mutant mice are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities




Genotype
MGI:3767188
ht3
Allelic
Composition
Foxg1tm1(cre)Skm/Foxg1+
Genetic
Background
B6.129P2-Foxg1tm1(cre)Skm
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Foxg1tm1(cre)Skm mutation (2 available); any Foxg1 mutation (12 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• volume of prosencephalon is reduced by 23%
• in adult, volume of thalamus is reduced by 21.6%, however at postnatal day 4, volume is not reduced
• total number of cells is reduced in levels 1 and 2 of the ventrobasal complex
• volume of striatum is reduced by 29.7%
• length of the medio-lateral and midline anterior-posterior axes of the cerebral hemispheres is reduced
• reduction in dimensions of cerebral hemispheres is observed by postnatal day 4
• area of cortical sheet is reduced at postnatal day 8 and in adult brain
• volume of hippocampus is reduced by 18.6%
• volume of cerebral cortex is reduced by 40.7%
• radial domain of cerebral cortex is substantially disrupted, especially in supragranular layers
• thickness of supragranular layer is reduced by 41.4% although granular and infragranular layers are not reduced
• numbers of large and medium sized neurons are reduced in superficial layers of cortex
• Background Sensitivity: thinning is observed only in C57BL/6 background, not in mixed C57BL/6 and CBA background




Genotype
MGI:5806112
ht4
Allelic
Composition
Foxg1tm1(cre)Skm/Foxg1+
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Foxg1tm1(cre)Skm mutation (2 available); any Foxg1 mutation (12 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
vision/eye
• visually evoked potential amplitudes at low spatial frequency are strongly diminished
• however, no changes in general organization, architecture and pattern or lamination of retina are seen
• cortical visual acuity is reduced at P30

nervous system
• decrease in spine density, but not spine length, in the basal dendrites of pyramidal cells (layer 2/3) in visual cortices
• the visual cortex is thinner, with specific layer II-III and layer IV reduction
• increase in interneuron density and a reduction of parvalbumin-positive cell density in layers II-III and VI of the visual cortex

Mouse Models of Human Disease
OMIM ID Ref(s)
Rett Syndrome, Congenital Variant 613454 J:235875




Genotype
MGI:3767191
ht5
Allelic
Composition
Foxg1tm1(cre)Skm/Foxg1+
Genetic
Background
involves: C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Foxg1tm1(cre)Skm mutation (2 available); any Foxg1 mutation (12 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• Background Sensitivity: reduction in dimensions of cerebral hemispheres is observed by postnatal day 4, however, on the mixed background the substantial reductions reported in the C57BL/6J forebrain are not observed




Genotype
MGI:3805980
cn6
Allelic
Composition
Bmp4tm1Blh/Bmp4tm4Blh
Foxg1tm1(cre)Skm/Foxg1+
Genetic
Background
involves: 129 * Black Swiss * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Bmp4tm1Blh mutation (2 available); any Bmp4 mutation (10 available)
Bmp4tm4Blh mutation (0 available); any Bmp4 mutation (10 available)
Foxg1tm1(cre)Skm mutation (2 available); any Foxg1 mutation (12 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
hearing/vestibular/ear
• cochlear ducts show variability in length
• less severely affected embryos display truncation of lateral canals
• not discernible in most severely affected embryos at E13.5
• not discernible in most severely affected embryos at E13.5
• malformed in most severely affected embryos at E13.5
• malformed in most severely affected embryos at E13.5
• intact endolymphatic duct only is evident in dorsal region of inner ear




Genotype
MGI:3776429
cn7
Allelic
Composition
Notch1tm1Grid/Notch1tm2Rko
Foxg1tm1(cre)Skm/Foxg1+
Genetic
Background
involves: 129 * C57BL/6J * Swiss Webster
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Foxg1tm1(cre)Skm mutation (2 available); any Foxg1 mutation (12 available)
Notch1tm1Grid mutation (0 available); any Notch1 mutation (61 available)
Notch1tm2Rko mutation (2 available); any Notch1 mutation (61 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
hearing/vestibular/ear
• increases in inner hair cell number are more than in Dll1tm1Gos/Dll1tm2Gos Jag2tm1Grid/Jag2tm1Grid mice
• decreases in inner hair cell number are slightly than in Dll1tm1Gos/Dll1tm2Gos Jag2tm1Grid/Jag2tm1Grid mice or Dll1tm1Gos Jag2tm1Grid homozygotes

nervous system
• increases in inner hair cell number are more than in Dll1tm1Gos/Dll1tm2Gos Jag2tm1Grid/Jag2tm1Grid mice




Genotype
MGI:4835273
cn8
Allelic
Composition
Chd7tm1.1Dmm/Chd7+
Foxg1tm1(cre)Skm/Foxg1+
Genetic
Background
involves: 129 * C57BL/6 * Swiss Webster
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Chd7tm1.1Dmm mutation (0 available); any Chd7 mutation (71 available)
Foxg1tm1(cre)Skm mutation (2 available); any Foxg1 mutation (12 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
hearing/vestibular/ear
• decrease in the number of proliferating cells in the otic epithelium at E10.5
• truncated or hypoplastic

nervous system
• decrease in the number of proliferating cells at E9.5 but not at E10.5




Genotype
MGI:4835272
cn9
Allelic
Composition
Chd7Gt(S20-7E1)Sor/Chd7tm1.1Dmm
Foxg1tm1(cre)Skm/Foxg1+
Genetic
Background
involves: 129 * C57BL/6 * Swiss Webster
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Chd7Gt(S20-7E1)Sor mutation (0 available); any Chd7 mutation (71 available)
Chd7tm1.1Dmm mutation (0 available); any Chd7 mutation (71 available)
Foxg1tm1(cre)Skm mutation (2 available); any Foxg1 mutation (12 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• die within 1 day of birth with no obvious milk in the stomach

hearing/vestibular/ear
• reductions in cellular proliferation at E10.5 in both the otic epithelium and the vestibulocochlear ganglion
• severe defects in cochlear structures
• severely hypoplastic
• undercoiled with abnormal twisting at the apex
• severe defects in vestibular structures
• hypoplastic

nervous system
• reductions in cellular proliferation at E10.5 in both the otic epithelium and the vestibulocochlear ganglion
• about 1.5 fold smaller at E10.5-E12.5 compared to heterozygous and wild-type controls
• reduction in cellular proliferation at E10.5 in the vestibulocochlear ganglion
• severe reduction in the number of neuroblasts in the otic epithelium and vestibulocochlear ganglion at E9.5, E10.5 and E11.5

craniofacial
• at E12.5

vision/eye
• medially displaced eyes at E12.5

behavior/neurological
• die within 1 day of birth with no obvious milk in the stomach

cellular
• reductions in cellular proliferation at E10.5 in both the otic epithelium and the vestibulocochlear ganglion

growth/size/body
• at E12.5




Genotype
MGI:3654831
cn10
Allelic
Composition
Fgf8tm1.3Mrt/Fgf8tm1.4Mrt
Foxg1tm1(cre)Skm/Foxg1+
Genetic
Background
involves: 129P2/OlaHsd
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Fgf8tm1.3Mrt mutation (1 available); any Fgf8 mutation (10 available)
Fgf8tm1.4Mrt mutation (0 available); any Fgf8 mutation (10 available)
Foxg1tm1(cre)Skm mutation (2 available); any Foxg1 mutation (12 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• apoptosis in the telencephalon is increased in a qualitatively similar manner to the Fgf8 conditional KOs, but is more severe

cellular
• apoptosis in the telencephalon is increased in a qualitatively similar manner to the Fgf8 conditional KOs, but is more severe




Genotype
MGI:3654834
cn11
Allelic
Composition
Fgf8tm1.1Mrt/Fgf8tm1.4Mrt
Foxg1tm1(cre)Skm/Foxg1+
Genetic
Background
involves: 129P2/OlaHsd
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Fgf8tm1.1Mrt mutation (1 available); any Fgf8 mutation (10 available)
Fgf8tm1.4Mrt mutation (0 available); any Fgf8 mutation (10 available)
Foxg1tm1(cre)Skm mutation (2 available); any Foxg1 mutation (12 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• apoptosis in the telencephalon is increased in a qualitatively similar manner to the Fgf8 conditional KOs, but is more severe

cellular
• apoptosis in the telencephalon is increased in a qualitatively similar manner to the Fgf8 conditional KOs, but is more severe




Genotype
MGI:3687280
cn12
Allelic
Composition
Aifm1tm2Pngr/Y
Foxg1tm1(cre)Skm/Foxg1+
Genetic
Background
involves: 129P2/OlaHsd
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Aifm1tm2Pngr mutation (0 available); any Aifm1 mutation (6 available)
Foxg1tm1(cre)Skm mutation (2 available); any Foxg1 mutation (12 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging

cellular
• mitochondria in cultured neurites are short and fragmented
• while morphology is restored by expression of anchored Pdcd8, mitochondrial length is increased compared to controls; cristae in mutant neurons are dilated and disorganized vs wild-type; cross-sectional distance of mitochondrial cristae is ~2.5-fold wider than wild-type; expression of anchored Pdcd8 reduces intercristae distance from 20 to 17 microns
• cultured neurons transfected with a mitochondrially-anchored Pdcd8 show similar survival to wild-type neurons expressing GFP
• after camptothecin treatment, neurons show increased survival vs wild-type over the first 12 hours (~45% loss vs ~55% in wild-type)
• there is a marked increase in cell death in postmitotic cell regions
• membrane potential is hyperpolarized relative to wild-type cells
• membrane potential hyperpolarization is restored to normal by expression of anchored Pdcd8
• ATP production and oxygen consumption in cultured mutant neurons is restored by mitochondrially anchored Pdcd8
• mutant neurites have few mitochondria vs wild-type

homeostasis/metabolism
• expression of complex I respiratory chain complex is abrogated in mutants

nervous system
• cultured neurons transfected with a mitochondrially-anchored Pdcd8 show similar survival to wild-type neurons expressing GFP
• after camptothecin treatment, neurons show increased survival vs wild-type over the first 12 hours (~45% loss vs ~55% in wild-type)
• there is a marked increase in cell death in postmitotic cell regions
• cortical thickness is reduced, mostly at the cortical plate (CP) and intermediate zone (IZ) and to lesser extent the subventricular zone (SVZ)




Genotype
MGI:3795697
cn13
Allelic
Composition
Gt(ROSA)26Sortm1(RARA*)Soc/Gt(ROSA)26Sortm1(RARA*)Soc
Foxg1tm1(cre)Skm/Foxg1+
Genetic
Background
involves: 129P2/OlaHsd
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Foxg1tm1(cre)Skm mutation (2 available); any Foxg1 mutation (12 available)
Gt(ROSA)26Sortm1(RARA*)Soc mutation (0 available); any Gt(ROSA)26Sor mutation (343 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• at E10.5, mice exhibit a 15% decrease in cell proliferation in the dorsal telencephalic progenitors due to slowed cell cycle progression compared to in control mice
• at E10.5, apoptosis is increased 5-fold in the pallium and 4-fold in the subpallium compared to in control mice
• Nkx2.1+ progenitor cells in the medial ganglionic eminence are mispecified




Genotype
MGI:3693870
cn14
Allelic
Composition
Cdc42tm1Yizh/Cdc42tm1Yizh
Foxg1tm1(cre)Skm/Foxg1+
Genetic
Background
involves: 129P2/OlaHsd
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cdc42tm1Yizh mutation (1 available); any Cdc42 mutation (37 available)
Foxg1tm1(cre)Skm mutation (2 available); any Foxg1 mutation (12 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• numbers of homozygotes starts to decline after E13.5

nervous system
• mutant embryos display a much thicker neuroepithelium (NE) wall, and a lack of telencephalic vesicle enlargement in the developing forebrain at E10.5
• roof plate has thinner NE wall and lacked invagination of dorsal telencephalon
• apical-basal polarity of NE of developing forebrain is disrupted
• at E12.5, telencephalon remains single chambered and clear distinction between cortical plate and ganglionic eminences is absent
• in E11.5 mutants, neural progenitors and postmitotic neurons are intermingled throughout NE but in wild-type brain, progenitors are mainly confined to ventricular surface of forebrain and postmitotic neurons are found along apical-basal NE axis
• roof plate lacks invagination of dorsal telencephalon at E12.5
• between E9.5-12.5, mutants do not exhibit enlargement of telencephalic vesicles in contrast to wild-type embryos

vision/eye
• in E9.5-12.5 mutants, eye development is delayed compared to wild-type

embryo
• mutant embryos display a much thicker neuroepithelium (NE) wall, and a lack of telencephalic vesicle enlargement in the developing forebrain at E10.5
• roof plate has thinner NE wall and lacked invagination of dorsal telencephalon
• apical-basal polarity of NE of developing forebrain is disrupted




Genotype
MGI:5004979
cn15
Allelic
Composition
Rhoatm1Yuyo/Rhoatm1Yuyo
Foxg1tm1(cre)Skm/Foxg1+
Genetic
Background
involves: 129P2/OlaHsd
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Foxg1tm1(cre)Skm mutation (2 available); any Foxg1 mutation (12 available)
Rhoatm1Yuyo mutation (0 available); any Rhoa mutation (87 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• the apical/ventricular surface is disorganized
• increasing incidence of exencephaly from E13.5 to E14.5
• exencephalic mass consists of greatly expanded neural progenitors
• exencephalic mass consists of greatly expanded neural progenitors




Genotype
MGI:5305924
cn16
Allelic
Composition
Pbx1tm1Koss/Pbx1tm1Koss
Pbx3tm1Mlc/Pbx3+
Foxg1tm1(cre)Skm/Foxg1+
Genetic
Background
involves: 129P2/OlaHsd
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Foxg1tm1(cre)Skm mutation (2 available); any Foxg1 mutation (12 available)
Pbx1tm1Koss mutation (0 available); any Pbx1 mutation (24 available)
Pbx3tm1Mlc mutation (0 available); any Pbx3 mutation (22 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
craniofacial
• cleft lip and/or palate
• cleft lip and/or palate

digestive/alimentary system
• cleft lip and/or palate

growth/size/body
• cleft lip and/or palate
• cleft lip and/or palate




Genotype
MGI:3720595
cn17
Allelic
Composition
Fgf8tm1.2Mrt/Fgf8tm1.3Mrt
Foxg1tm1(cre)Skm/Foxg1+
Genetic
Background
involves: 129P2/OlaHsd
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Fgf8tm1.2Mrt mutation (0 available); any Fgf8 mutation (10 available)
Fgf8tm1.3Mrt mutation (1 available); any Fgf8 mutation (10 available)
Foxg1tm1(cre)Skm mutation (2 available); any Foxg1 mutation (12 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mutant mice die at birth due to defects in forebrain development

nervous system
• at birth, mutants exhibit lethal defects in forebrain development
• however, overall development of the inner ear and cochlea appeared normal

hearing/vestibular/ear
• at E18.5, IHCs and OHCs appear to be in direct contact with each other in some cochlear sections
• at E18.5, mutant mice show a significant reduction in the size and number of pillar cells (PCs) relative to control mice
• at E18.5, the distance between the lateral edge of the IHC and the medial edge of the first row OHC (a measure of the degree of PC development) is significantly decreased along the length of the cochlea
• at E18.5, PCs with weak or no lumenal projections are noted along the entire cochlear length with no region-specific variations
• at E18.5, pillar cells are missing or underdeveloped
• at E18.5, lumenal surface of the organ of Corti shows disruption of pillar cell growth and close approximation of IHCs to OHCs
• however, the overall structure of the epithelium and putative developing pillar cells are normal up to E15

cellular
• at E18.5, the distance between the lateral edge of the IHC and the medial edge of the first row OHC (a measure of the degree of PC development) is significantly decreased along the length of the cochlea
• at E18.5, PCs with weak or no lumenal projections are noted along the entire cochlear length with no region-specific variations




Genotype
MGI:3795739
cn18
Allelic
Composition
Celsr3tm1Agof/Celsr3tm2Agof
Foxg1tm1(cre)Skm/Foxg1+
Genetic
Background
involves: 129P2/OlaHsd
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Celsr3tm1Agof mutation (0 available); any Celsr3 mutation (43 available)
Celsr3tm2Agof mutation (0 available); any Celsr3 mutation (43 available)
Foxg1tm1(cre)Skm mutation (2 available); any Foxg1 mutation (12 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• despite normal expression in the dorsal thalamus, the three components of the internal capsule (corticothalamic axons, thalamocortical axons and subcerebral projections) are abnormal
• unlike in control mice, no thalamic fibers turn towards the striatum
• however, corticothalamic axons grow towards the ventral telencephalon




Genotype
MGI:2653845
cn19
Allelic
Composition
Ntf3tm1Esm/Ntf3tm1Esm
Foxg1tm1(cre)Skm/Foxg1+
Genetic
Background
involves: 129P2/OlaHsd * 129S1/Sv
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Foxg1tm1(cre)Skm mutation (2 available); any Foxg1 mutation (12 available)
Ntf3tm1Esm mutation (0 available); any Ntf3 mutation (14 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
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

nervous system
• reduced thalamocortical synaptic interactions
• thalamthalamocortical projections are similar to controls at P0, but by P3, axonal bundles projecting from the thalamus through the cortical white matter are reducedcortical projections are similar to controls at P0, but by P3, thalamocortical projection is reduced
• reduction in the number of lateral geniculate nucleus projections to the visual cortex and anteroventral and laterodorsal nuclei projections to retrosplenial cortex




Genotype
MGI:3693201
cn20
Allelic
Composition
Jag1tm1Grid/Jag1tm2Grid
Foxg1tm1(cre)Skm/Foxg1+
Genetic
Background
involves: 129P2/OlaHsd * 129S1/Sv
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Foxg1tm1(cre)Skm mutation (2 available); any Foxg1 mutation (12 available)
Jag1tm1Grid mutation (1 available); any Jag1 mutation (35 available)
Jag1tm2Grid mutation (1 available); any Jag1 mutation (35 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mutants survive through E18.5

hearing/vestibular/ear
N
• at E15.5, inner ear structures not associated with sensory formation such as endolymphatic duct and sac, and crus are not affected
• formation of prosensory domain is disrupted by E18.5
• severe hair cell patterning defects are observed at E18.5
• no clear formation of rows or distinction between inner and outer hair cells is observed in midbasal regions of the organ of Corti; hair cells form in patches
• at E16.5, patterns look similar to those at E18.5 with patches of hair cells in midbasal regions and absent hair cells in very basal regions
• in middle portion of cochlea, patterning of inner and sparse outer hair cells is abnormal
• in apical turn of cochlea, there are only two rows instead of four rows of hair cells
• no hair cell formation is observed in basal turns of cochlea; at E18.5, hair cells and supporting cells are absent in very basal region of cochlea
• no outer hair cells or supporting Deiter's cells are present in apex of cochlea
• at E18.5, tunnel of Corti is not apparent
• semicircular canals are mostly absent, with only a small portion of lateral semicircular canal present at E15.5
• cristae and ampullae are missing or severely disrupted by E14.5 in homozygotes
• at E15.5, only a small portion of the anterior canal is present in homozygotes
• at E15.5, semicircular canals are largely absent
• structure is extremely small, with few differentiating hair cells; severe disruption of differentiation of utricular macula is observed
• observed at E13.5
• at E13.5, saccule appears misshapen
• at E18.5, saccule and macula are relatively normal, but entire saccular structure is shaped differently compared to controls

nervous system
• severe hair cell patterning defects are observed at E18.5
• no clear formation of rows or distinction between inner and outer hair cells is observed in midbasal regions of the organ of Corti; hair cells form in patches
• at E16.5, patterns look similar to those at E18.5 with patches of hair cells in midbasal regions and absent hair cells in very basal regions
• in middle portion of cochlea, patterning of inner and sparse outer hair cells is abnormal
• in apical turn of cochlea, there are only two rows instead of four rows of hair cells
• no hair cell formation is observed in basal turns of cochlea; at E18.5, hair cells and supporting cells are absent in very basal region of cochlea
• no outer hair cells or supporting Deiter's cells are present in apex of cochlea




Genotype
MGI:3687281
cn21
Allelic
Composition
Apaf1Gt(IRESBetageo)XIX18Pgr/Apaf1Gt(IRESBetageo)XIX18Pgr
Aifm1tm2Pngr/Y
Foxg1tm1(cre)Skm/Foxg1+
Genetic
Background
involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Aifm1tm2Pngr mutation (0 available); any Aifm1 mutation (6 available)
Apaf1Gt(IRESBetageo)XIX18Pgr mutation (1 available); any Apaf1 mutation (41 available)
Foxg1tm1(cre)Skm mutation (2 available); any Foxg1 mutation (12 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cellular
• neurons show increased survival vs wild-type after camptothecin treatment
• neurons cultured in pyruvate supplemented media show increased survival after camptothecin treatment
• expression of anchored Pdcd8 does not provide further protection from death to neurons
• cultured neurons show increased apoptosis reconstituted with wild-type Pdcd8 compared to control; mutant neurons expressing Pdcd8 with a nuclear exclusion sequence show cell death equivalent to control neurons expressing GFP
• cultured neurons can maintain oxygen consumption after camptothecin treatment if anchored Pdcd8 is expressed

nervous system
• neurons show increased survival vs wild-type after camptothecin treatment
• neurons cultured in pyruvate supplemented media show increased survival after camptothecin treatment
• expression of anchored Pdcd8 does not provide further protection from death to neurons
• cultured neurons show increased apoptosis reconstituted with wild-type Pdcd8 compared to control; mutant neurons expressing Pdcd8 with a nuclear exclusion sequence show cell death equivalent to control neurons expressing GFP
• cortex is thickened compared to Pdcd8 conditional embryos




Genotype
MGI:5508374
cn22
Allelic
Composition
Gt(ROSA)26Sortm1Red/Gt(ROSA)26Sor+
Foxg1tm1(cre)Skm/Foxg1+
Genetic
Background
involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Foxg1tm1(cre)Skm mutation (2 available); any Foxg1 mutation (12 available)
Gt(ROSA)26Sortm1Red mutation (0 available); any Gt(ROSA)26Sor mutation (343 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• fewer cortical neurons expressing Satb2
• however, the number of Foxp1 and total neuron numbers are normal




Genotype
MGI:5544092
cn23
Allelic
Composition
Igs1tm11(CAG-Bgeo,-Edn2)Nat/Igs1+
Foxg1tm1(cre)Skm/Foxg1+
Genetic
Background
involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Foxg1tm1(cre)Skm mutation (2 available); any Foxg1 mutation (12 available)
Igs1tm11(CAG-Bgeo,-Edn2)Nat mutation (1 available); any Igs1 mutation (10 available)
phenotype observed in females
phenotype observed in males
N normal phenotype

Absence of vascular defects in the brains of embryonic day 18 Igs1tm11(CAG-Bgeo,-Edn2)Nat/Igs1+ Foxg1tm1(cre)Skm/Foxg1+

mortality/aging
• early postnatal lethality

craniofacial

vision/eye

digestive/alimentary system

growth/size/body




Genotype
MGI:5538347
cn24
Allelic
Composition
Slc12a2tm1.1Jheb/Slc12a2tm1.1Jheb
Foxg1tm1(cre)Skm/Foxg1+
Genetic
Background
involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Foxg1tm1(cre)Skm mutation (2 available); any Foxg1 mutation (12 available)
Slc12a2tm1.1Jheb mutation (0 available); any Slc12a2 mutation (23 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
behavior/neurological

hearing/vestibular/ear
• collapse of the membranes of the vestibular compartments
• cristae degeneration




Genotype
MGI:4361706
cn25
Allelic
Composition
Notch2tm3Grid/Notch2tm3Grid
Foxg1tm1(cre)Skm/Foxg1+
Genetic
Background
involves: 129P2/OlaHsd * 129S1/Sv * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Foxg1tm1(cre)Skm mutation (2 available); any Foxg1 mutation (12 available)
Notch2tm3Grid mutation (1 available); any Notch2 mutation (40 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• nearly two-thirds do not survive to adulthood
• born in approximately Mendelian ratios (21%)

growth/size/body
• disrupted relatively uniform spacing of sustentacular nuclei
• some areas significantly disrupted and thinner, other areas appear relatively normal
• smaller and more irregularly shaped sustentacular nuclei
• gaps and a reduction in the number of dendritic tufts at the apical surface
• no apparent weight difference at P0
• weigh 27% less than controls at 2.5 week old
• weigh 47% less than controls at 8-19 week old

nervous system
• significantly smaller pituitary in size
• increased olfactory neuronal progenitors in the neuronal and apical layer in adults mutants
• disorganized olfactory sensory neurons
• does not occur during early postnatal life (P0-2.5weeks), but increase as the animal ages
• increased TUNEL-positive cells in the neuronal layer of the olfactory epithelium
• lower Glutathione S-transferase activity in mutant olfactory epithelia
• increased TUNEL-positive cells in the neuronal layer of the olfactory epithelium
• does not occur during early postnatal life (P0-2.5weeks), but increase as the animal ages

taste/olfaction
• disrupted relatively uniform spacing of sustentacular nuclei
• some areas significantly disrupted and thinner, other areas appear relatively normal
• smaller and more irregularly shaped sustentacular nuclei
• gaps and a reduction in the number of dendritic tufts at the apical surface

cellular
• increased TUNEL-positive cells in the apical layer of the olfactory epithelium (0.3 cells/mm vs. 0/mm)
• increased TUNEL-positive cells in the neuronal layer of the olfactory epithelium
• does not occur during early postnatal life (P0-2.5weeks), but increase as the animal ages

endocrine/exocrine glands
• significantly smaller pituitary in size

respiratory system
• disrupted relatively uniform spacing of sustentacular nuclei
• some areas significantly disrupted and thinner, other areas appear relatively normal
• smaller and more irregularly shaped sustentacular nuclei
• gaps and a reduction in the number of dendritic tufts at the apical surface

craniofacial
• disrupted relatively uniform spacing of sustentacular nuclei
• some areas significantly disrupted and thinner, other areas appear relatively normal
• smaller and more irregularly shaped sustentacular nuclei
• gaps and a reduction in the number of dendritic tufts at the apical surface




Genotype
MGI:3615303
cn26
Allelic
Composition
Olig2tm1Qrlu/Olig2tm1Qrlu
Foxg1tm1(cre)Skm/Foxg1+
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Foxg1tm1(cre)Skm mutation (2 available); any Foxg1 mutation (12 available)
Olig2tm1Qrlu mutation (0 available); any Olig2 mutation (29 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• no myelination in dorsal cortex while myelination in ventral cortex is normal




Genotype
MGI:5581686
cn27
Allelic
Composition
Mafbtm1.1Good/Mafbtm1Jeng
Foxg1tm1(cre)Skm/Foxg1+
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Foxg1tm1(cre)Skm mutation (2 available); any Foxg1 mutation (12 available)
Mafbtm1.1Good mutation (0 available); any Mafb mutation (10 available)
Mafbtm1Jeng mutation (0 available); any Mafb mutation (10 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging

respiratory system
• central apnea

hearing/vestibular/ear
N
• inner ear develops normally

nervous system
N
• spiral ganglion neuron neurite organization is normal




Genotype
MGI:4421423
cn28
Allelic
Composition
Lmo4tm1Gan/Lmo4tm2.1Gan
Foxg1tm1(cre)Skm/Foxg1+
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJaeSor * 129S6/SvEvTac * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Foxg1tm1(cre)Skm mutation (2 available); any Foxg1 mutation (12 available)
Lmo4tm1Gan mutation (0 available); any Lmo4 mutation (4 available)
Lmo4tm2.1Gan mutation (0 available); any Lmo4 mutation (4 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
hearing/vestibular/ear
• at E15.5, mice exhibit vestibular defects observed in Lmo4tm1Gan homozygotes
• at E15.5, mice lack anterior and posterior ampullae unlike in wild-type mice




Genotype
MGI:5807348
cn29
Allelic
Composition
Chd7tm1.1Dmm/Chd7tm1.1Dmm
Foxg1tm1(cre)Skm/Foxg1+
Genetic
Background
involves: 129P2/OlaHsd * 129S6/SvEvTac
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Chd7tm1.1Dmm mutation (0 available); any Chd7 mutation (71 available)
Foxg1tm1(cre)Skm mutation (2 available); any Foxg1 mutation (12 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
vision/eye
• optic vesicle is present and appears normal at E9.5, however no progression toward formation of optic cup or lens structures is seen even as late as E12.5
• optic vesicle is present and appears normal at E9.5, however no progression toward formation of optic cup or lens structures is seen even as late as E12.5




Genotype
MGI:2661104
cn30
Allelic
Composition
Bmp4tm3Blh/Bmp4tm3Blh
Foxg1tm1(cre)Skm/Foxg1+
Genetic
Background
involves: 129P2/OlaHsd * 129S6/SvEvTac
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Bmp4tm3Blh mutation (0 available); any Bmp4 mutation (10 available)
Foxg1tm1(cre)Skm mutation (2 available); any Foxg1 mutation (12 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• all die between E12.5 and E14.5
• only necrotic embryos are found at E14.5

craniofacial
• recessed jaws
• recessed snout

vision/eye
• severely deficient

nervous system
N
• despite Cre-mediated deletion in the telencephalon, no defects in telencephalic patterning or development are detected

skeleton
• recessed jaws

growth/size/body
• recessed snout




Genotype
MGI:3811334
cn31
Allelic
Composition
Bmp4tm3Blh/Bmp4+
Foxg1tm1(cre)Skm/Foxg1+
Genetic
Background
involves: 129P2/OlaHsd * 129S6/SvEvTac
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Bmp4tm3Blh mutation (0 available); any Bmp4 mutation (10 available)
Foxg1tm1(cre)Skm mutation (2 available); any Foxg1 mutation (12 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• fewer mice survive to birth than expected




Genotype
MGI:5305933
cn32
Allelic
Composition
Pbx1tm1Mlc/Pbx1+
Wnt9btm1Amc/Wnt9btm1Amc
Foxg1tm1(cre)Skm/Foxg1+
Genetic
Background
involves: 129P2/OlaHsd * 129S6/SvEvTac * 129X1/SvJ
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Foxg1tm1(cre)Skm mutation (2 available); any Foxg1 mutation (12 available)
Pbx1tm1Mlc mutation (0 available); any Pbx1 mutation (24 available)
Wnt9btm1Amc mutation (0 available); any Wnt9b mutation (14 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
craniofacial
• bilateral in all mice

digestive/alimentary system

growth/size/body
• bilateral in all mice




Genotype
MGI:4882049
cn33
Allelic
Composition
Actbtm1.1Erv/Actbtm1.1Erv
Foxg1tm1(cre)Skm/Foxg1+
Genetic
Background
involves: 129P2/OlaHsd * 129S6/SvEvTac * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Actbtm1.1Erv mutation (0 available); any Actb mutation (23 available)
Foxg1tm1(cre)Skm mutation (2 available); any Foxg1 mutation (12 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mice seldom survive to adulthood

hearing/vestibular/ear
N
• stereocilia are apparently normal at 2 days of age
• stereocilia are still present at 21 days of age




Genotype
MGI:4421425
cn34
Allelic
Composition
Lmo4tm2.1Gan/Lmo4tm2.1Gan
Foxg1tm1(cre)Skm/Foxg1+
Genetic
Background
involves: 129P2/OlaHsd * 129S6/SvEvTac * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Foxg1tm1(cre)Skm mutation (2 available); any Foxg1 mutation (12 available)
Lmo4tm2.1Gan mutation (0 available); any Lmo4 mutation (4 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
hearing/vestibular/ear
• at E15.5, mice exhibit vestibular defects observed in Lmo4tm1Gan homozygotes
• at E15.5, mice lack anterior and posterior ampullae unlike in wild-type mice




Genotype
MGI:4430833
cn35
Allelic
Composition
Bmp2tm1Brd/Bmp2tm1.1Mis
Foxg1tm1(cre)Skm/Foxg1+
Genetic
Background
involves: 129P2/OlaHsd * 129S7/SvEvBrd * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Bmp2tm1.1Mis mutation (0 available); any Bmp2 mutation (8 available)
Bmp2tm1Brd mutation (0 available); any Bmp2 mutation (8 available)
Foxg1tm1(cre)Skm mutation (2 available); any Foxg1 mutation (12 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
hearing/vestibular/ear
N
• no obvious abnormalities in cochlea morphology is observed




Genotype
MGI:5305855
cn36
Allelic
Composition
Pbx1tm1Koss/Pbx1tm1Koss
Pbx2tm1Mlc/Pbx2+
Foxg1tm1(cre)Skm/Foxg1+
Genetic
Background
involves: 129P2/OlaHsd * 129S/Sv
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Foxg1tm1(cre)Skm mutation (2 available); any Foxg1 mutation (12 available)
Pbx1tm1Koss mutation (0 available); any Pbx1 mutation (24 available)
Pbx2tm1Mlc mutation (0 available); any Pbx2 mutation (5 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging

craniofacial
• abnormal maxillary palatal and palatine process
• the premaxillary process is absent
• bilateral

respiratory system

digestive/alimentary system
• abnormal maxillary palatal and palatine process

skeleton
• abnormal maxillary palatal and palatine process
• the premaxillary process is absent

growth/size/body
• abnormal maxillary palatal and palatine process
• bilateral




Genotype
MGI:5305923
cn37
Allelic
Composition
Pbx1tm1Koss/Pbx1tm1Koss
Pbx2tm1Mlc/Pbx2tm1Mlc
Foxg1tm1(cre)Skm/Foxg1+
Genetic
Background
involves: 129P2/OlaHsd * 129S/Sv
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Foxg1tm1(cre)Skm mutation (2 available); any Foxg1 mutation (12 available)
Pbx1tm1Koss mutation (0 available); any Pbx1 mutation (24 available)
Pbx2tm1Mlc mutation (0 available); any Pbx2 mutation (5 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
craniofacial
• bilateral

cellular
• in the nasal epithelial at E10.75

growth/size/body
• bilateral




Genotype
MGI:5305932
cn38
Allelic
Composition
Wnt9btm1Amc/Wnt9btm1Amc
Foxg1tm1(cre)Skm/Foxg1+
Genetic
Background
involves: 129P2/OlaHsd * 129X1/SvJ
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Foxg1tm1(cre)Skm mutation (2 available); any Foxg1 mutation (12 available)
Wnt9btm1Amc mutation (0 available); any Wnt9b mutation (14 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
craniofacial
• bilateral in all mice

digestive/alimentary system

growth/size/body
• bilateral in all mice




Genotype
MGI:4455199
cn39
Allelic
Composition
Sp8tm2.1Aman/Sp8tm2.1Aman
Foxg1tm1(cre)Skm/Foxg1+
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Foxg1tm1(cre)Skm mutation (2 available); any Foxg1 mutation (12 available)
Sp8tm2.1Aman mutation (0 available); any Sp8 mutation (17 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging

nervous system
• between E10.5 and E18.5, post-mitotic neurons and neuronal progenitors exhibit an increase in apoptosis in the forebrain compared to in wild-type mice
• at E18.5, fewer BrdU+ cells are found within the upper cortical layers of the subventricular zone while more are detected in the superficial positions in the cortical plate compared to in wild-type mice
• at E12.5 and E15.5, mice lack the septum at the rostral level unlike wild-type mice
• mice exhibit dysgenesis of the olfactory bulb and septum, including an almost complete absence of the midline, compared with wild-type mice
• corticofugal fiber tracts do not cross the midline and instead form probst bundles and, caudally, neuronal fibers form bundles between the internal and external capsules
• as determined by marker expression, dorsal ventral patterning of the medial telencephalon is altered compared to in wild-type mice
• as determined by marker expression, mice exhibit abnormal cortical arealization and thalamic innervation compared to in wild-type mice
• mice exhibit defective preplate splitting compared with wild-type mice
• as determined by marker expression, mice exhibit abnormal cortical arealization and thalamic innervation compared to in wild-type mice
• as determined by marker expression, lower cortical layers are not correctly specified and upper cortical layer neurons are reduced compared to in wild-type mice
• mice exhibit misspecification in specific cortical neuron subtypes (Cux1+, Lhx2+, Rorb+, and Etv1+)
• mice exhibit dysgenesis of the olfactory bulb and septum, including an almost complete absence of the midline, compared with wild-type mice
• mild rostral
• the lateral ventricles are fused because of the complete disgenesis of the midline unlike in wild-type mice
• aberrant bundles of Gap43+ fibers form within the internal capsule with some axons projecting ectopically towards the marginal zone and basal telencephalon unlike in wild-type mice
• basal ganglia consist of a single eminence with a barely discernable constriction between the lateral and medial ganglion eminence compared to in wild-type mice

craniofacial

cellular
• between E10.5 and E18.5, post-mitotic neurons and neuronal progenitors exhibit an increase in apoptosis in the forebrain compared to in wild-type mice
• at E18.5, fewer BrdU+ cells are found within the upper cortical layers of the subventricular zone while more are detected in the superficial positions in the cortical plate compared to in wild-type mice




Genotype
MGI:3530074
cn40
Allelic
Composition
Atrxtm1Rjg/Y
Foxg1tm1(cre)Skm/Foxg1+
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Atrxtm1Rjg mutation (0 available); any Atrx mutation (75 available)
Foxg1tm1(cre)Skm mutation (2 available); any Foxg1 mutation (12 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mutant males die within 24 - 48 hours of birth, with only 1 male surviving to 24 days of age

behavior/neurological
• mutant males lack milk in their stomachs
• mutant males do not suckle well

growth/size/body
• mutants are smaller at birth

nervous system
• the dentate gyrus is replaced by a mass of disorganized cells
• reduced numbers of CA1 and CA3 pyramidal neurons are seen
• the subiculum and hippocampus are reduced in size
• the frontal cortex is reduced in size especially in the caudal-medial cortex and cell density is decreased in the cortex as a result of increased cell death and not a change in proliferation
• cell numbers in the cortical plate are reduced by 20-30%
• cell loss is not seen at E13.5 but is significant at E15.5




Genotype
MGI:3624333
cn41
Allelic
Composition
Dll1tm1Mjo/Dll1tm1Mjo
Foxg1tm1(cre)Skm/Foxg1+
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Dll1tm1Mjo mutation (1 available); any Dll1 mutation (22 available)
Foxg1tm1(cre)Skm mutation (2 available); any Foxg1 mutation (12 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
hearing/vestibular/ear
• hair cells in Dll1 conditional knockouts differentiate prematurely and hair cells can be seen in the apex of the cochlea at E17.5, while none are visible in control littermates
• by E17.5 and the inner hair-cell row seems to have been duplicated in the apex
• in rhw middle and basal regions, there are increased numbers of inner hair cells
• in the apex, between 6 and 8 rows of outer hair cells have formed in the mutant by E17.5
• in rhw middle and basal regions, there is one extra row of outer hair cells
• at E17.5, there are fewer turns in the cochlea in the mutant compared to wild-type and in mutants the cochlea has a shorter length with an extreme broadening of the sensory patch at the apex
• the utricular macula is severely reduced or lost
• the saccular macula is severely reduced or lost

nervous system
• hair cells in Dll1 conditional knockouts differentiate prematurely and hair cells can be seen in the apex of the cochlea at E17.5, while none are visible in control littermates
• by E17.5 and the inner hair-cell row seems to have been duplicated in the apex
• in rhw middle and basal regions, there are increased numbers of inner hair cells
• in the apex, between 6 and 8 rows of outer hair cells have formed in the mutant by E17.5
• in rhw middle and basal regions, there is one extra row of outer hair cells




Genotype
MGI:5551750
cn42
Allelic
Composition
Gt(ROSA)26Sortm1(Tbx1/GFP)Bem/Gt(ROSA)26Sor+
Foxg1tm1(cre)Skm/Foxg1+
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Foxg1tm1(cre)Skm mutation (2 available); any Foxg1 mutation (12 available)
Gt(ROSA)26Sortm1(Tbx1/GFP)Bem mutation (1 available); any Gt(ROSA)26Sor mutation (343 available)
phenotype observed in females
phenotype observed in males
N normal phenotype

Thymic aplasia, nasal malformations, and eye, pharyngeal and ear defects in Gt(ROSA)26Sortm1(Tbx1/GFP)Bem/Gt(ROSA)26Sor+ Foxg1tm1(cre)Skm/Foxg1+ mice and microcephaly, ocular and ear defects in Gt(ROSA)26Sortm1(Tbx1/GFP)Bem/Gt(ROSA)26Sor+ Tg(Pax2-cre)1Akg/0 mice

mortality/aging

hearing/vestibular/ear
• hypoplastic to varying degrees, but enlarged in two instances
• enlarged at E14.5

nervous system
• abnormal size and misguided projections
• abnormal size and misguided projections
• abnormal size and misguided projections
• abnormal size and misguided projections

respiratory system

vision/eye

hematopoietic system
• thymic aplasia

craniofacial

taste/olfaction

immune system
• thymic aplasia

endocrine/exocrine glands
• thymic aplasia




Genotype
MGI:3702999
cn43
Allelic
Composition
Fgfr1tm1Upir/Fgfr1tm1Upir
Foxg1tm1(cre)Skm/Foxg1+
Genetic
Background
involves: 129P2/OlaHsd * ICR
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Fgfr1tm1Upir mutation (0 available); any Fgfr1 mutation (195 available)
Foxg1tm1(cre)Skm mutation (2 available); any Foxg1 mutation (12 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• phenotype is stated to be comparable to that of mice that are compound heterozygous for Fgfr1tm1.1Upir and Fgfr1tm1Upir and also heterozygous for Foxg1tm1(cre)Skm; however, no data are presented in J:78879

hearing/vestibular/ear




Genotype
MGI:3702998
cn44
Allelic
Composition
Fgfr1tm1Upir/Fgfr1tm1.1Upir
Foxg1tm1(cre)Skm/Foxg1+
Genetic
Background
involves: 129P2/OlaHsd * ICR
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Fgfr1tm1.1Upir mutation (0 available); any Fgfr1 mutation (195 available)
Fgfr1tm1Upir mutation (0 available); any Fgfr1 mutation (195 available)
Foxg1tm1(cre)Skm mutation (2 available); any Foxg1 mutation (12 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mutants die within 24 hrs after birth

hearing/vestibular/ear
• at birth, mutant cochleae are frequently slightly shorter than normal
• however, mutant otocysts appear morphologically normal at E10.5 and E11.5
• in addition, initiation of cochlear duct outgrowth from the otocyst is unaffected at E12.5
• at birth, the sensory epithelium of the upper cochlear half is arranged in small sensory patches that mainly consist of IHCs and pillar supporting cells, while the lower cochlear half is less severely affected
• in contrast, the vestibular sensory epithelium remains unchanged
• at around birth, the organ of Corti is severely disrupted due to impaired production of precursor cells between E12 and E15, as shown by BrdU labeling
• at E16.5, mutants display no molecular signs of HC specification or differentiation in the gap regions found between sensory patches; OHCs are more severely affected
• at E16.5, the remaining HCs in the sensory patches appear to undergo normal differentiation
• at E18.5, most cochlear sections are devoid of HCs and the greater epithelial ridge is abnormally thin, due to reduced precursor cell proliferation in the ventral wall of the cochlear duct between E12 and E15.5
• apparently, the remaining precursors of the organ of Corti preferentially differentiate into IHCs and pillar cells
• no differences in precursor cell proliferation rate are observed in the dorsal, non-sensory wall of the cochlear duct
• at P0, mutants show a 85% reduction in the total number of differentiating HCs relative to wild-type mice
• at birth, only very low numbers of OHCs are formed, and these are located in lower cochlear half
• at birth, the small sensory patches found in the upper cochlear half frequently show doublet IHCs instead of a single continuous IHC row
• at birth, the small sensory patches found in the upper cochlear half frequently show an accumulation of disorientated IHCs at the edges
• at birth, the sensory patches found in the upper cochlear half frequently show no signs of differentiation of supporting cells

nervous system
• at E16.5, mutants display no molecular signs of HC specification or differentiation in the gap regions found between sensory patches; OHCs are more severely affected
• at E16.5, the remaining HCs in the sensory patches appear to undergo normal differentiation
• at E18.5, most cochlear sections are devoid of HCs and the greater epithelial ridge is abnormally thin, due to reduced precursor cell proliferation in the ventral wall of the cochlear duct between E12 and E15.5
• apparently, the remaining precursors of the organ of Corti preferentially differentiate into IHCs and pillar cells
• no differences in precursor cell proliferation rate are observed in the dorsal, non-sensory wall of the cochlear duct
• at P0, mutants show a 85% reduction in the total number of differentiating HCs relative to wild-type mice
• at birth, only very low numbers of OHCs are formed, and these are located in lower cochlear half
• at birth, the small sensory patches found in the upper cochlear half frequently show doublet IHCs instead of a single continuous IHC row
• at birth, the small sensory patches found in the upper cochlear half frequently show an accumulation of disorientated IHCs at the edges




Genotype
MGI:3814903
cn45
Allelic
Composition
Six3tm3Gco/Six3tm3Gco
Foxg1tm1(cre)Skm/Foxg1+
Genetic
Background
involves: 129S1/Sv * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Foxg1tm1(cre)Skm mutation (2 available); any Foxg1 mutation (12 available)
Six3tm3Gco mutation (0 available); any Six3 mutation (5 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• many display a phenotype typical of holoprosencephaly
• anterior diencephalon is normal

Mouse Models of Human Disease
OMIM ID Ref(s)
Holoprosencephaly 2; HPE2 157170 J:140315




Genotype
MGI:3521928
cn46
Allelic
Composition
Top2btm2Jcw/Top2btm2.1Jcw
Foxg1tm1(cre)Skm/Foxg1+
Genetic
Background
involves: 129S4/SvJae * 129S6/SvEvTac * 129X1/SvJ
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Foxg1tm1(cre)Skm mutation (2 available); any Foxg1 mutation (12 available)
Top2btm2.1Jcw mutation (0 available); any Top2b mutation (45 available)
Top2btm2Jcw mutation (1 available); any Top2b mutation (45 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• died of respiratory failure within 30 min after birth, however decreased body size was not observed as in homozygous Top2b mutant mice

behavior/neurological
• lack the vigor of wild-type newborns, however show some body movements upon tactile stimulation

respiratory system
• collapsed lung alveoli in dead pups suggests respiratory failure

nervous system
• ill-defined granule cell layer in the hippocampus
• ill-defined pyramidal cell layer in the hippocampus
• less developed olfactory bulb




Genotype
MGI:3826853
cn47
Allelic
Composition
Bsndtm1Tjj/Bsndtm1Tjj
Foxg1tm1(cre)Skm/Foxg1+
Genetic
Background
involves: 129/Sv * 129P2/OlaHsd * 129X1/SvJ * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Bsndtm1Tjj mutation (0 available); any Bsnd mutation (9 available)
Foxg1tm1(cre)Skm mutation (2 available); any Foxg1 mutation (12 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mice fail to survive until adulthood

homeostasis/metabolism
• mice are moderately dehydrated

hearing/vestibular/ear




Genotype
MGI:3619802
cn48
Allelic
Composition
Tbx1tm2.1Bem/Tbx1tm2.2Bem
Foxg1tm1(cre)Skm/Foxg1+
Genetic
Background
involves: 129/Sv * C57BL/6 * SJL * Swiss Webster
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Foxg1tm1(cre)Skm mutation (2 available); any Foxg1 mutation (12 available)
Tbx1tm2.1Bem mutation (0 available); any Tbx1 mutation (15 available)
Tbx1tm2.2Bem mutation (0 available); any Tbx1 mutation (15 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mice do not survive beyond the neonatal period (J:105980)
• mutants die between E18.5 and E20.5 with multiple defects of the pharyngeal apparatus (J:109536)

homeostasis/metabolism
• at E17.5, mutants appear edematous

craniofacial
• at E17.5, mutants display severe malformations of craniofacial bone structures
• at E17.5, mutants display fused basisphenoid and basioccipital bones (J:109536)
• zygomatic arch is missing
• hyoid bone is hypoplastic
• mandible is shorter than in wild-type
• middle ear is absent (J:105980)
• at E15.5-E17.5, middle ear ossicles do not start the condensation process and thus fail to develop (J:109536)
• observed at E17.5 (J:105980)
• at E17.5, mutants exhibit cleft palate (J:109536)
• at E15.5-E17.5, the pinnae do not start the condensation process and thus fail to develop (J:109536)

hearing/vestibular/ear
• at E15.5-E17.5, the pinnae do not start the condensation process and thus fail to develop (J:109536)
• at E10.5 or later
• early otic vesicle development is normal; however, the structure is slightly hypoplastic by E10.5 and appears cystic at E17.5
• in contrast, periotic mesenchyme development appears normal
• at E17.5, mutants display a cystic endolymphatic duct
• at E17.5, the otic capsule is hypoplastic
• at E17.5, mutants show complete aplasia of inner ear sensory organs
• at E17.5, mutants exhibit severe hypoplasia of the inner ear, developing only a cystic OV and endolymphatic duct
• at E10.5, the pharyngeal endoderm fails to invaginate toward the surface endoderm to form the tubotympanic recess, resulting in disruption of middle ear development
• middle ear is absent (J:105980)
• at E15.5-E17.5, middle ear ossicles do not start the condensation process and thus fail to develop (J:109536)
• at E17.5, mutants lack tympanic rings (J:109536)

respiratory system
• pharynx in conditional null embryos is hypoplastic, lacking distal arches; the first pouch appears to be hypoplastic

skeleton
• at E17.5, mutants display severe malformations of craniofacial bone structures
• at E17.5, mutants display fused basisphenoid and basioccipital bones (J:109536)
• zygomatic arch is missing
• hyoid bone is hypoplastic
• mandible is shorter than in wild-type
• middle ear is absent (J:105980)
• at E15.5-E17.5, middle ear ossicles do not start the condensation process and thus fail to develop (J:109536)

cardiovascular system
• all null mutants have aortic arch defects
• mutants have retroesophageal right subclavian artery
• at E10.5 all conditional mutants display hypoplasia of the outflow tract
• all conditional null mutants have a single outflow tract
• in mutants the left ventricle communicates with the right through a large VSD

endocrine/exocrine glands
• thyroid glands are smaller than wild-type and ectopically placed in conditional null embryos while conditional heterozygous embryos have ectopically placed thyroid glands

immune system

muscle
• in conditional mutants, the masseter muscle is absent
• in conditional mutants, pterygoid muscles are absent

hematopoietic system

digestive/alimentary system
• observed at E17.5 (J:105980)
• at E17.5, mutants exhibit cleft palate (J:109536)

nervous system
• at E10.5, the otic vesicle is surrounded by an expanded cochleovestibular ganglion rudiment
• at E11.5, the cochleovestibular ganglion is duplicated around the otic vesicle anterior-posterior midline

embryo
• at E10.5, the first pharyngeal pouch fails to outgrow, preventing middle ear bone condensations

integument
• at E17.5, mutants appear edematous

growth/size/body
• observed at E17.5 (J:105980)
• at E17.5, mutants exhibit cleft palate (J:109536)
• at E15.5-E17.5, the pinnae do not start the condensation process and thus fail to develop (J:109536)

Mouse Models of Human Disease
OMIM ID Ref(s)
DiGeorge Syndrome; DGS 188400 J:105980 , J:109536




Genotype
MGI:3624332
cn49
Allelic
Composition
Jag1tm1Jlew/Jag1tm1Jlew
Foxg1tm1(cre)Skm/Foxg1+
Genetic
Background
involves: C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Foxg1tm1(cre)Skm mutation (2 available); any Foxg1 mutation (12 available)
Jag1tm1Jlew mutation (0 available); any Jag1 mutation (35 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
hearing/vestibular/ear
• at E17.5, the middle part of the cochlea has two disorganized rows of hair cells instead of the normal stereotyped pattern of 3 rows of outer hair cells and 1 row of inner hair cells: towards base of the cochlea, the number of hair cells is severely reduced and instead of a continuous band of two rows, the rows are broken up and irregular islands of hair cells are present
• in mutants, the number of hair cells per 100 microns of cochlea length is reduced to 25.8 as compared to 63.5 in wild-type controls
• in conditional Jag1 knockouts, outer hair cells are missing completely
• number of inner hair cells is almost doubled from 15.3 per 100 microns cochlea length to 25.8
• epithelium where the horizontal crista and utricular macula would be lacks hair cells
• in Jag1 mutants, all three semicircular canals are truncated
• epithelium where the utricular macula would be is thickened

nervous system
• at E17.5, the middle part of the cochlea has two disorganized rows of hair cells instead of the normal stereotyped pattern of 3 rows of outer hair cells and 1 row of inner hair cells: towards base of the cochlea, the number of hair cells is severely reduced and instead of a continuous band of two rows, the rows are broken up and irregular islands of hair cells are present
• in mutants, the number of hair cells per 100 microns of cochlea length is reduced to 25.8 as compared to 63.5 in wild-type controls
• in conditional Jag1 knockouts, outer hair cells are missing completely
• number of inner hair cells is almost doubled from 15.3 per 100 microns cochlea length to 25.8
• epithelium where the horizontal crista and utricular macula would be lacks hair cells




Genotype
MGI:5427352
cx50
Allelic
Composition
Smarca1tm1.1Pick/Y
Foxg1tm1(cre)Skm/Foxg1+
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * CD-1
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Foxg1tm1(cre)Skm mutation (2 available); any Foxg1 mutation (12 available)
Smarca1tm1.1Pick mutation (0 available); any Smarca1 mutation (7 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
N
• no increase in the proportion of mitotic cells or fraction of intermediate/basal progenitor cells is detected at E15.5 unlike in mutant mice wild-type for Foxg1





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last database update
11/29/2016
MGI 6.06
The Jackson Laboratory