napts, a mutation affecting sodium channel activity in Drosophila, is an allele of mle, a regulator of X chromosome transcription.
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.
Kernan
M J
MJ
Laboratory of Genetics, University of Wisconsin, Madison 53706.
Kuroda
M I
MI
Kreber
R
R
Baker
B S
BS
Ganetzky
B
B
D000200:Action Potentials; D000483:Alleles; D000818:Animals; D004303:Dosage Compensation, Genetic; D004331:Drosophila melanogaster / Q000235:genetics*; D005786:Gene Expression Regulation; D005809:Genes, Regulator; D005816:Genetic Complementation Test; D009154:Mutation; D010243:Paralysis / Q000235:genetics; D015222:Sodium Channels / Q000378:metabolism*; D013696:Temperature; D014158:Transcription, Genetic; D014170:Transformation, Genetic; D014960:X Chromosome
D015222:Sodium Channels