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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Bicd2tm1Hgrd
targeted mutation 1, Casper Hoogenraad
MGI:5618153
Summary 4 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
cn1
Bicd2tm1Hgrd/Bicd2tm1Hgrd
Emx1tm1(cre)Krj/Emx1+
involves: C57BL/6 MGI:5810138
cn2
Bicd2tm1Hgrd/Bicd2tm1Hgrd
Tg(Nes-cre)1Atp/0
involves: C57BL/6 * FVB/N MGI:5810135
cn3
Bicd2tm1Hgrd/Bicd2tm1Hgrd
Tg(GFAP-cre)25Mes/0
involves: C57BL/6 * FVB/N MGI:5810136
cn4
Bicd2tm1Hgrd/Bicd2tm1Hgrd
Tg(Atoh1-cre/Esr1*)14Fsh/0
involves: C57BL/6 * FVB/N MGI:5810139


Genotype
MGI:5810138
cn1
Allelic
Composition
Bicd2tm1Hgrd/Bicd2tm1Hgrd
Emx1tm1(cre)Krj/Emx1+
Genetic
Background
involves: C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Bicd2tm1Hgrd mutation (0 available); any Bicd2 mutation (31 available)
Emx1tm1(cre)Krj mutation (2 available); any Emx1 mutation (34 available)
phenotype observed in females
phenotype observed in males
N normal phenotype

Abnormally oriented axonal bundles coursing from the superficial lamina towards the capsula interna in neocortex of Bicd2tm1Hgrd/Bicd2tm1HgrdEmx1tm1(cre)Krj/Emx1+ mice

nervous system
N
• mice survive to >8 weeks (when they are sacrificed) and do not develop hydrocephalus
• immunofluorescence of neurofilament-M revealed abnormally oriented axonal bundles coursing from the superficial lamina towards the capsula interna in the neocortex
• mice exhibit disrupted laminar organization in the hippocampus
• mice exhibit disrupted laminar organization in the cerebral cortex

cellular
• immunofluorescence of neurofilament-M revealed abnormally oriented axonal bundles coursing from the superficial lamina towards the capsula interna in the neocortex




Genotype
MGI:5810135
cn2
Allelic
Composition
Bicd2tm1Hgrd/Bicd2tm1Hgrd
Tg(Nes-cre)1Atp/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 (31 available)
Tg(Nes-cre)1Atp mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mice die by 3-4 weeks of age

nervous system
• mice develop severe progressive hydrocephalus
• mice exhibit disrupted laminar organization in the hippocampus
• mice exhibit disrupted laminar organization in the cortex
• mice exhibit disrupted laminar organization in the cerebellar cortex




Genotype
MGI:5810136
cn3
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 (31 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:5810139
cn4
Allelic
Composition
Bicd2tm1Hgrd/Bicd2tm1Hgrd
Tg(Atoh1-cre/Esr1*)14Fsh/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 (31 available)
Tg(Atoh1-cre/Esr1*)14Fsh mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
normal phenotype
• tamoxifen-treated mice survive to >8 weeks (when they are sacrificed) and do not exhibit hydrocephalus or disrupted laminar organization in the cerebral cortex, cerebellum or hippocampus
• at P25, all post-migratory granule cells are found in the cerebellar internal granule cell layer, indicating that cerebellar granule cell migration is normal





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last database update
04/23/2024
MGI 6.23
The Jackson Laboratory