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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.

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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.

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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.