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Effects of kinesin mutations on neuronal functions.

Authors
  • M, Gho
  • K, Mcdonald
  • B, Ganetzky
  • Wm, Saxton
Type
Published Article
Journal
Science
Publisher
American Association for the Advancement of Science (AAAS)
Volume
258
Issue
5080
Pages
313–316
Source
UCSC Neuro biomedical-ucsc
License
Unknown

Abstract

Kinesin is believed to generate force for the movement of organelles in anterograde axonal transport. The identification of genes that encode kinesin-like proteins suggests that other motors may provide anterograde force instead of or in addition to kinesin. To gain insight into the specific functions of kinesin, the effects of mutations in the kinesin heavy chain gene (khc) on the physiology and ultrastructure of Drosophila larval neurons were studied. Mutations in khc impair both action potential propagation in axons and neurotransmitter release at nerve terminals but have no apparent effect on the concentration of synaptic vesicles in nerve terminal cytoplasm. Thus kinesin is required in vivo for normal neuronal function and may be active in the transport of ion channels and components of the synaptic release machinery to their appropriate cellular locations. Kinesin appears not to be required for the anterograde transport of synaptic vesicles or their components.

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