Phenotypes associated with this allele
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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)
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Abnormally oriented axonal bundles coursing from the superficial lamina towards the capsula interna in neocortex of Bicd2tm1Hgrd/Bicd2tm1HgrdEmx1tm1(cre)Krj/Emx1+ mice
nervous system
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• mice survive to >8 weeks (when they are sacrificed) and do not develop hydrocephalus
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• immunofluorescence of neurofilament-M revealed abnormally oriented axonal bundles coursing from the superficial lamina towards the capsula interna in the neocortex
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• mice exhibit disrupted laminar organization in the hippocampus
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• mice exhibit disrupted laminar organization in the cerebral cortex
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cellular
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• immunofluorescence of neurofilament-M revealed abnormally oriented axonal bundles coursing from the superficial lamina towards the capsula interna in the neocortex
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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)
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mortality/aging
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• mice die by 3-4 weeks of age
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nervous system
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• mice develop severe progressive hydrocephalus
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• mice exhibit disrupted laminar organization in the hippocampus
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• mice exhibit disrupted laminar organization in the cortex
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• mice exhibit disrupted laminar organization in the cerebellar cortex
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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)
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Disrupted laminar organization of the cortex in Bicd2tm1Hgrd/Bicd2tm1Hgrd Tg(GFAP-cre)25Mes/0 mice
mortality/aging
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• mice with hydrocephalus die by 3-4 weeks of age
• mice without hydrocephalus survive to >8 weeks
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nervous system
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• 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
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• mice exhibit the same cerebellar granule cell migration defects observed in Bicd2tm1.1Hgrd homozygotes
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• some mice develop less severe hydrocephalus than that observed in Bicd2tm1.1Hgrd mice
• others do not develop hydrocephalus
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• mice exhibit a thin corpus callosum
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• mice exhibit a thin capsula externa
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• mice without hydrocephalus exhibit disrupted laminar organization in the hippocampus
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• at P20, the hippocampus pyramidal cell layer appears disorganized in the CA1 region
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• 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
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• mice without hydrocephalus exhibit disrupted laminar organization in the cerebellar cortex
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• mice do not develop an internal granule cell layer
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cellular
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• 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
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• mice exhibit the same cerebellar granule cell migration defects observed in Bicd2tm1.1Hgrd homozygotes
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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)
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normal phenotype
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• 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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