napts, a mutation affecting sodium channel activity in Drosophila, is an allele of mle, a regulator of X chromosome transcription

Cell. 1991 Sep 6;66(5):949-59. doi: 10.1016/0092-8674(91)90440-a.


napts is a recessive mutation that affects the level of sodium channel activity and, at high temperature, causes paralysis associated with a loss of action potentials. We show, by genetic complementation tests, germline transformation, and analysis of mutations, that napts is a gain-of-function mutation of mle, a gene required for X chromosome dosage compensation and male viability. Molecular analyses of nap and mle mutations indicate that mle+, nap+, and napts activities are encoded by the same open reading frame and suggest that napts is due to a single amino acid substitution. Although napts is known to act via para+, an X-linked sodium channel structural gene, its effect is not due to a simple defect in para+ dosage compensation.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Action Potentials
  • Alleles
  • Animals
  • Dosage Compensation, Genetic
  • Drosophila melanogaster / genetics*
  • Gene Expression Regulation
  • Genes, Regulator*
  • Genetic Complementation Test
  • Mutation
  • Paralysis / genetics
  • Sodium Channels / metabolism*
  • Temperature
  • Transcription, Genetic
  • Transformation, Genetic
  • X Chromosome


  • Sodium Channels