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Tyrosine hydroxylase expression and Cdk5 kinase activity in ataxic cerebellum

K-John J Cheung1, Jesusa L Rosales, Byung-Chul Lee

  • 1Department of Cell Biology and Anatomy, Southern Alberta Cancer Research Institute and Hotchkiss Brain Institute, The University of Calgary, Heritage Medical Research Building, Calgary, AB, Canada, T2N4N1.

Molecular and Cellular Biochemistry
|July 12, 2008
PubMed

Insights

Abnormal cerebellar tyrosine hydroxylase (TH) expression in ataxic mice may not be regulated by Cyclin-dependent kinase 5 (Cdk5) activity, suggesting alternative regulatory mechanisms are involved.

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Genetics

Background:

  • Ataxia is linked to neuronal differentiation and migration issues, processes regulated by Cyclin-dependent kinase 5 (Cdk5).
  • Cerebellar abnormalities in Cdk5-deficient mice resemble those in ataxic mouse models.
  • Aberrant cerebellar tyrosine hydroxylase (TH) expression is observed in ataxic mice, including the pogo/pogo model.

Purpose of the Study:

  • To investigate the relationship between Cdk5 activity and TH expression in the cerebellum of ataxic mice.
  • To determine if reduced Cdk5 activity in p35-/- and p39-/- mice affects TH expression.

Main Methods:

  • Assessed Cdk5 activity in the cerebellum of pogo/pogo mice with abnormal TH expression.
  • Examined TH expression in the cerebellum of p35-/- and p39-/- mice with reduced Cdk5 activity.

Main Results:

  • Increased TH expression in pogo cerebellum correlated with decreased Cdk5 activity.
  • Reduced Cdk5 activity in p35-/- and p39-/- mice did not result in altered TH expression.

Conclusions:

  • Cdk5 activity may not be the primary regulator of abnormal TH expression in the cerebellum.
  • Other mechanisms likely control TH expression in ataxic cerebellar pathology.

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