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Updated: Jul 16, 2026
Ex vivo Culturing of Whole, Developing Drosophila Brains
Published on: July 27, 2012
Drosophila lacking the Cdk5 activator, p35, display defective axon guidance, age-dependent behavioral deficits and
Lisa Connell-Crowley1, Duc Vo, Lori Luke
1Basic Neuroscience Program, National Institute of Neurological Disorders and Stroke (NINDS), National Human Genome Research Institute (NHGRI), National Institutes of Health Bldg 37, Rm 1016, 37 Convent Drive, Bethesda, MD 20892, USA.
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.
