Phenotypes associated with this allele

• Allele Symbol: Bicd2^tm1Hgrd
• Allele Name: targeted mutation 1, Casper Hoogenraad
• Allele ID: MGI:5618153
• Summary: 4 genotypes

Jump to	Allelic Composition	Genetic Background	Genotype ID
cn1	Bicd2^tm1Hgrd/Bicd2^tm1Hgrd Emx1^tm1(cre)Krj/Emx1^+	involves: C57BL/6	MGI:5810138
cn2	Bicd2^tm1Hgrd/Bicd2^tm1Hgrd Tg(Nes-cre)1Atp/0	involves: C57BL/6 * FVB/N	MGI:5810135
cn3	Bicd2^tm1Hgrd/Bicd2^tm1Hgrd Tg(GFAP-cre)25Mes/0	involves: C57BL/6 * FVB/N	MGI:5810136
cn4	Bicd2^tm1Hgrd/Bicd2^tm1Hgrd Tg(Atoh1-cre/Esr1*)14Fsh/0	involves: C57BL/6 * FVB/N	MGI:5810139

Genotype
MGI:5810138

cn1

• Allelic Composition: Bicd2^tm1Hgrd/Bicd2^tm1Hgrd; Emx1^tm1(cre)Krj/Emx1⁺
• Genetic Background: involves: C57BL/6

• ♀: 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 Bicd2^tm1Hgrd/Bicd2^tm1HgrdEmx1^tm1(cre)Krj/Emx1⁺ mice

nervous system

nervous system phenotype ( J:210236 )

N • mice survive to >8 weeks (when they are sacrificed) and do not develop hydrocephalus

abnormal neuronal migration ( J:210236 )

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

abnormal hippocampus layer morphology ( J:210236 )

• mice exhibit disrupted laminar organization in the hippocampus

abnormal stratification in cerebral cortex ( J:210236 )

• mice exhibit disrupted laminar organization in the cerebral cortex

cellular

abnormal neuronal migration ( J:210236 )

• 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: Bicd2^tm1Hgrd/Bicd2^tm1Hgrd; Tg(Nes-cre)1Atp/0
• Genetic Background: involves: C57BL/6 * FVB/N

mortality/aging

premature death ( J:210236 )

• mice die by 3-4 weeks of age

nervous system

hydrocephaly ( J:210236 )

• mice develop severe progressive hydrocephalus

abnormal hippocampus layer morphology ( J:210236 )

• mice exhibit disrupted laminar organization in the hippocampus

abnormal stratification in cerebral cortex ( J:210236 )

• mice exhibit disrupted laminar organization in the cortex

abnormal cerebellar layer morphology ( J:210236 )

• mice exhibit disrupted laminar organization in the cerebellar cortex

Genotype
MGI:5810136

cn3

• Allelic Composition: Bicd2^tm1Hgrd/Bicd2^tm1Hgrd; Tg(GFAP-cre)25Mes/0
• Genetic Background: involves: C57BL/6 * FVB/N

Disrupted laminar organization of the cortex in Bicd2^tm1Hgrd/Bicd2^tm1Hgrd Tg(GFAP-cre)25Mes/0 mice

mortality/aging

premature death ( J:210236 )

• mice with hydrocephalus die by 3-4 weeks of age

• mice without hydrocephalus survive to >8 weeks

nervous system

abnormal neuronal migration ( J:210236 )

• 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

abnormal cerebellar granule cell migration ( J:210236 )

• mice exhibit the same cerebellar granule cell migration defects observed in Bicd2^tm1.1Hgrd homozygotes

hydrocephaly ( J:210236 )

• some mice develop less severe hydrocephalus than that observed in Bicd2^tm1.1Hgrd mice

• others do not develop hydrocephalus

decreased corpus callosum size ( J:210236 )

• mice exhibit a thin corpus callosum

decreased brain external capsule size ( J:210236 )

• mice exhibit a thin capsula externa

abnormal hippocampus layer morphology ( J:210236 )

• mice without hydrocephalus exhibit disrupted laminar organization in the hippocampus

abnormal hippocampus pyramidal cell layer ( J:210236 )

• at P20, the hippocampus pyramidal cell layer appears disorganized in the CA1 region

abnormal stratification in cerebral cortex ( J:210236 )

• 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

abnormal cerebellar layer morphology ( J:210236 )

• mice without hydrocephalus exhibit disrupted laminar organization in the cerebellar cortex

absent cerebellar granule layer ( J:210236 )

• mice do not develop an internal granule cell layer

cellular

abnormal neuronal migration ( J:210236 )

• 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

abnormal cerebellar granule cell migration ( J:210236 )

• mice exhibit the same cerebellar granule cell migration defects observed in Bicd2^tm1.1Hgrd homozygotes

Genotype
MGI:5810139

cn4

• Allelic Composition: Bicd2^tm1Hgrd/Bicd2^tm1Hgrd; Tg(Atoh1-cre/Esr1*)14Fsh/0
• Genetic Background: involves: C57BL/6 * FVB/N

normal phenotype

no abnormal phenotype detected ( J:210236 )

• 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