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Genetic alteration of nerve membrane excitability in temperature-sensitive paralytic mutants of Drosophila melanogaster

Nature volume 286, pages 814816 (21 August 1980) | Download Citation

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Abstract

Single mutations that disrupt basic physiological processes such as axonal conduction and synaptic transmission provide one means to study the membrane components and mechanisms that underlie these processes1,8. Temperature-sensitive paralytic mutants of Drosophila melanogaster which behave normally at a permissive temperature (23–25 °C) but become paralysed at a restrictive temperature (usually 29–37 °C) have been utilized in such studies. An example is napts (no action potential, temperature-sensitive), a recessive second-chromosome mutation that causes paralysis of larvae and adults at 37 °C. Electrophysiological recordings have demonstrated that napts specifically affects a component of axonal membranes5. Here we show that axonal conduction in napts larvae is abnormally sensitive to tetrodotoxin (TTX), a specific blocker of voltage-sensitive sodium channels9, and that the refractory period of action potentials differs from wild type, consistent with the idea that napts alters the function of sodium channels. It is further shown that parats (paralysed, temperature-sensitive), a recessive X-linked mutation1, also specifically disrupts axonal conduction and that the two mutations affect functionally related membrane components. Identification of other mutants defective in associated components of nerve membranes is made feasible by using techniques described here.

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Affiliations

  1. Division of Biology, California Institute of Technology, Pasadena, California 91125

    • Chun-Fang Wu
    •  & Barry Ganetzky
  2. Department of Zoology, University of Iowa, Iowa City, Iowa 52242

    • Chun-Fang Wu
  3. Laboratory of Genetics, University of Wisconsin, Madison, Wisconsin 53706

    • Barry Ganetzky

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https://doi.org/10.1038/286814a0

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