Abstract
Mutations in the mitochondrial fusion protein Mitofusin 2 (MFN2) are the most common identified cause of dominantly inherited axonal sensory-motor neuropathies (CMT2). The mechanisms by which mutations in MFN2, a ubiquitously expressed mitochondrial fusion protein, lead to peripheral neuropathy have not been elucidated. To determine how MFN2 mutations lead to degeneration of peripheral axons, we used recombinant lentiviruses to express disease-mutated forms of MFN2 in mouse dorsal root ganglion neurons in vitro.
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