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The Journal of Neuroscience, August 1, 1999, 19(15):6446-6456

Bcl-2 Overexpression Does Not Protect Neurons from Mutant Neurofilament-Mediated Motor Neuron Degeneration

Megan K. Houseweart^{1, 2} and Don W. Cleveland^{1, 2, 3, 4}

¹ Ludwig Institute for Cancer Research, ² Program in Biomedical Sciences, ³ Division of Cellular and Molecular Medicine, and ⁴ Department of Neuroscience, University of California at San Diego, La Jolla, California 92093

Transgenic mice with a point mutation in the light neurofilament gene develop amyotrophic lateral sclerosis-like motor neuron disease characterized by selective spinal motor neuron loss, neurofilamentous accumulations, and severe muscle atrophy. To test whether the large motor neurons at risk in this disease could be protected from mutant neurofilament-mediated killing, these mice were bred to mice overexpressing the human Bcl-2 proto-oncogene. Elevated levels of Bcl-2 increased the numbers of motor and sensory axons surviving after the developmental period of naturally occurring cell death but did not greatly reduce the number of degenerating axons or protect the large motor neurons from mutant neurofilament-mediated death.

Key words: Bcl-2; amyotrophic lateral sclerosis; transgenic mice; motor neuron; cell death; neurofilament

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Copyright © 1999 Society for Neuroscience  0270-6474/99/19156446-11$05.00/0

This article has been cited by other articles:

				J.-M. Beaulieu, H. Jacomy, and J.-P. Julien Formation of Intermediate Filament Protein Aggregates with Disparate Effects in Two Transgenic Mouse Models Lacking the Neurofilament Light Subunit J. Neurosci., July 15, 2000; 20(14): 5321 - 5328. [Abstract] [Full Text] [PDF]

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