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Callosal axon guidance defects in p35(-/-) mice
Y T Kwon1, L H Tsai, J E Crandall
1Howard Hughes Medical Institute, Department of Pathology, Harvard Medical School, Boston, Massachusetts 02115, USA.
The Journal of Comparative Neurology
|November 2, 1999
Summary
Mice lacking p35, a key brain protein, show severe defects in how nerve fibers connect in the brain. This study reveals p35 is crucial for guiding axons during development.
Area of Science:
- Neuroscience
- Developmental Biology
- Molecular Biology
Background:
- p35 is an activator of cyclin-dependent kinase 5 (cdk5) in the central nervous system (CNS).
- Mice lacking p35 display disrupted neocortical lamination and altered axonal tracts.
Purpose of the Study:
- To investigate the role of p35 in axonal guidance and fasciculation during CNS development.
- To determine if defects in cortical lamination directly cause axonal guidance issues.
Main Methods:
- Analysis of p35 mutant mice exhibiting CNS structural defects.
- Tracer injection experiments in adult p35 mutant mice to track cortical axon projection.
- Examination of embryonic callosal axon tracts and thalamocortical afferents.
Main Results:
- p35 mutant mice show impaired assimilation of cortical axons into the corpus callosum.
- Cortical axons in p35 mutants defasciculate prematurely and take oblique paths.
- Defective fasciculation is observed in embryonic callosal tracts and thalamocortical afferents.
- The callosal phenotype in p35 mutants differs from reeler mice, suggesting it's not solely due to cortical lamination defects.
Conclusions:
- Loss of p35 leads to primary defects in axonal fasciculation and guidance.
- The p35/cdk5 kinase pathway is essential for proper guidance of specific axons during embryonic development.