Drosophila lacking the Cdk5 activator, p35, display defective axon guidance, age-dependent behavioral deficits and reduced lifespan

Mech Dev. 2007 May;124(5):341-9. doi: 10.1016/j.mod.2007.02.002. Epub 2007 Feb 15.

Abstract

The cyclin-dependent kinase Cdk5 has attracted a great deal of attention both because of its roles in cell migration and axon patterning, and the extensive data implicating it in adult-onset neurodegeneration in mammals. Both the kinase activity and the biological effects of Cdk5 are absolutely dependent on association with an activating subunit, called p35. We show here that Drosophila lacking the Cdk5 activator, D-p35, display a wide range of defects in embryonic axon patterning. We further show that, while viable and fertile, p35 mutant adults display progressive, age-dependent loss of motor function and have a significantly shortened lifespan.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, N.I.H., Intramural

MeSH terms

  • Age Factors
  • Alleles
  • Animals
  • Animals, Genetically Modified
  • Axons / ultrastructure
  • Behavior, Animal
  • Cyclin-Dependent Kinase 5 / genetics
  • Cyclin-Dependent Kinase 5 / metabolism*
  • Drosophila Proteins / genetics
  • Drosophila Proteins / metabolism*
  • Drosophila melanogaster / genetics
  • Drosophila melanogaster / growth & development
  • Drosophila melanogaster / metabolism*
  • Drosophila melanogaster / physiology
  • Female
  • Genes, Insect
  • Longevity
  • Male
  • Motor Neurons / physiology
  • Mutation
  • Nerve Tissue Proteins / genetics
  • Nerve Tissue Proteins / metabolism*

Substances

  • Drosophila Proteins
  • Nerve Tissue Proteins
  • neuronal Cdk5 activator (p25-p35)
  • Cyclin-Dependent Kinase 5
  • Cdk5 protein, Drosophila