Nap ts, a Mutation affecting sodium channel activity in Drosophila, Is an allele of mle a regulator of X chromosome transcription

Abstract

nap ts 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 nap ts 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 nap ts activities are encoded by the same open reading frame and suggest that nap ts is due to a single amino acid substitution. Although nap ts 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.