Phenotypes associated with this allele
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| Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ank2tm1Bnt mutation
(1 available);
any
Ank2 mutation
(184 available)
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behavior/neurological
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• slight in the acquisition phase of a Morris water maze
• however, performance in the reversal phase is normal
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• males make small or no territory markings in response to female urine
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• fewer ultrasonic vocalization
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| Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ank2tm1Bnt mutation
(1 available);
any
Ank2 mutation
(184 available)
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nervous system
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• axon initial segments are normal
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| Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ank2tm1Bnt mutation
(1 available);
any
Ank2 mutation
(184 available)
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Small body size in Ank2tm1Bnt/Ank2tm1Bnt mouse compared to wild type
mortality/aging
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• over half of homozygotes are moribund (and therefore killed) at P1
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• 95% of remaining homozygotes die by P8; only a few (4 out of 8) survive to P20
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behavior/neurological
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• homozygotes that survive to 2 weeks of age exhibit impaired balance
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• homozygotes that survive to 2 weeks of age exhibit abnormal locomotor activity
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growth/size/body
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• homozygotes that survive to 2 weeks of age exhibit a 75% reduction in body weight relative to wild-type littermates
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vision/eye
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• at P9, many mutant optic nerve axons become dilated with diameters up to 8-fold greater than normal, and contain multivescicular bodies
• axon fasciculation is also impaired with frequent loss of direct axon-axon contacts
• a nearly complete degeneration of the optic nerve is noted by P21
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• disruption of secondary lens fiber organization at anterior pole
(J:52124)
• organization of secondary lens fibers at the anterior pole was severely disturbed at postnatal day 1
(J:70385)
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nervous system
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• at P1, homozygotes show a 7-fold enlargement of the lateral ventricles
• enlargement of lateral ventricles is not associated with occlusion of the cerebral aqueduct
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• at P1-P5, ~61.5% homozygotes display a size reduction or absence of the corpus callosum; a nearly complete absence of the anterior portion is observed
• the corpus callosum cannot be visualized in parasagittal sections and appears greatly reduced in coronal sections of mutant brain
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• at P1, homozygotes exhibit a size reduction or absence of the internal capsule
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• at P1, homozygotes exhibit hypoplasia or absence of the pyramidal tracts
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• at P1, homozygotes exhibit hypoplasia or absence of the pyramidal tracts
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• homozygotes display decreased L1 staining in premyelinated axons of long fiber tracts, including the corpus callosum, fimbria, and internal capsule in the brain, and pyramidal tracts and lateral columns of the spinal cord
• L1 staining is unreduced in the mutant optic nerve at P1-P3 but disappears by P7, although the optic nerve itself is still present
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• at P9, many mutant optic nerve axons become dilated with diameters up to 8-fold greater than normal, and contain multivescicular bodies
• axon fasciculation is also impaired with frequent loss of direct axon-axon contacts
• a nearly complete degeneration of the optic nerve is noted by P21
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Allelic
Composition |
Ank2tm1Bnt/Ank2+
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Genetic
Background |
involves: 129 |
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| Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ank2tm1Bnt mutation
(1 available);
any
Ank2 mutation
(184 available)
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cardiovascular system
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• in isoproterenol-treated mice
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• isoproterenol-treated mice exhibit disorganized shifts of the leading pacemaker and competing multiple pacemakers compared with similarly treated wild-type mice
• acetylcholine-treated mice exhibit reduced sensitivity of pacemaker function compared with similarly treated wild-type mice
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homeostasis/metabolism
adipose tissue
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• mouse embryonic fibroblasts exhibit increased adipogenesis with both increased in adipocyte numbers and enlarged lipid droplets compared with wild-type cells.
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• decreased basal adipocyte glucose uptake
• however, insulin-stimulated uptake is normal
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cellular
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• mouse embryonic fibroblasts exhibit increased adipogenesis with both increased in adipocyte numbers and enlarged lipid droplets compared with wild-type cells.
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• decreased basal adipocyte glucose uptake
• however, insulin-stimulated uptake is normal
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Analysis Tools