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Lis1 reduction causes tangential migratory errors in mouse spinal cord.

Katherine D Moore1, Renee Chen, Marianne Cilluffo

  • 1Department of Integrative Biology and Physiology, UCLA, Los Angeles, California 90095-7239, USA.

The Journal of Comparative Neurology
|September 22, 2011
PubMed
Summary
This summary is machine-generated.

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Lis1 gene mutations disrupt the migration of sympathetic and parasympathetic preganglionic neurons in mice. This gene is crucial for proper neuronal positioning in the developing spinal cord.

Area of Science:

  • Neuroscience
  • Developmental Biology
  • Genetics

Background:

  • Mutations in the LIS1 gene cause lissencephaly, a disorder characterized by abnormal neuronal migration.
  • LIS1 is highly expressed in embryonic neurons, suggesting a role in neuronal development.
  • Lis1 heterozygous mice exhibit defects in cerebral cortex and hippocampal formation lamination.

Purpose of the Study:

  • To investigate the role of Lis1 in the migration of sympathetic and parasympathetic preganglionic neurons (SPNs and PPNs).
  • To determine if Lis1 deficiency affects the tangential migration of these neurons in the developing spinal cord.

Main Methods:

  • Analysis of neuronal migration in Lis1 heterozygous (Lis1+/−) mice compared to wild-type (Lis1+/+) littermates.
  • Histological examination of spinal cord sections at various embryonic ages.

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  • Observation of the positioning and migratory trajectories of SPNs, PPNs, and somatic motor neurons.

    • Main Results:

    • While initial radial migration was unaffected, the subsequent dorsally directed tangential migration of SPNs and PPNs was aberrant in Lis1+/− mice.
    • The distribution of SPNs and PPNs was elongated dorsoventrally in Lis1+/− mice, with ectopic neurons found in the ventral spinal cord.
    • Mispositioned neurons persisted postnatally, indicating premature cessation of migration. A subset of somatic motor neurons also showed delayed migration.

    Conclusions:

    • Lis1 is essential for the correct dorsally directed tangential migration of many SPNs and PPNs.
    • Lis1 deficiency leads to premature migration arrest in a subset of these neurons.
    • The study highlights Lis1's critical role in spinal cord neuronal positioning during development.