Search

The full complement of ion channels which influence insect auditory mechanotransduction and the mechanisms by which their influence is exerted remain unclear. Shal (K v 4), a Shaker family member encoding voltage-gated potassium channels in Drosophila melanogaster , has been shown to localize to dendrites in some neuron types, suggesting the potential role of Shal in Drosophila hearing, including mechanotransduction. A GFP trap was used to visualize the localization of the Shal channel in Johnston's organ neurons responsible for hearing in the antenna. Shal protein was localized strongly to the cell body and inner dendritic segment of sensory neurons. It was also detectable in the sensory cilium, suggesting its involvement not only in general auditory function but specifically in mechanotransduction. Electrophysiological recordings to assess neural responses to auditory stimuli in mutant Shal flies revealed significant decreases in auditory responses. Laser Doppler vibrometer recordings indicated abnormal antennal free fluctuation frequencies in mutant lines, indicating an effect on active antennal tuning, and thus active transduction mechanisms. This suggests that Shal participates in coordinating energy-dependent antennal movements in Drosophila that are essential for tuning the antenna to courtship song frequencies., Competing Interests: The authors declare no competing financial interests., (Copyright © 2025 Gregory et al.)

The fruit fly Drosophila melanogaster has provided important insights into how sensory information is transduced by transient receptor potential (TRP) channels in the peripheral nervous system (PNS). However, TRP channels alone have not been able to completely model mechanosensitive transduction in mechanoreceptive chordotonal neurons (CNs). Here, we show that, in addition to TRP channels, the sole voltage-gated sodium channel (Na V ) in Drosophila , Para, is localized to the dendrites of CNs. Para is localized to the distal tip of the dendrites in all CNs, from embryos to adults, and is colocalized with the mechanosensitive TRP channels No mechanoreceptor potential C (NompC) and Inactive/Nanchung (Iav/Nan). Para localization also demarcates spike initiation zones (SIZs) in axons and the dendritic localization of Para is indicative of a likely dendritic SIZ in fly CNs. Para is not present in the dendrites of other peripheral sensory neurons. In both multipolar and bipolar neurons in the PNS, Para is present in a proximal region of the axon, comparable to the axonal initial segment (AIS) in vertebrates, 40-60 μm from the soma in multipolar neurons and 20-40 μm in bipolar neurons. Whole-cell reduction of para expression using RNAi in CNs of the adult Johnston's organ (JO) severely affects sound-evoked potentials (SEPs). However, the duality of Para localization in the CN dendrites and axons identifies a need to develop resources to study compartment-specific roles of proteins that will enable us to better understand Para's role in mechanosensitive transduction., Competing Interests: The authors declare no competing financial interests., (Copyright © 2023 Ravenscroft et al.)

To test the effects of mechanosensory mutations on hearing in Drosophila, we have recorded sound-evoked potentials originating from ciliated sensory neurons in Johnston's organ, the chordotonal organ that is the sensory element of the fly's antennal ear. Electrodes inserted close to the antennal nerve were used to record extracellular compound potentials evoked by near-field sound stimuli. Sound-evoked potentials are absent in atonal mutant flies, which lack Johnston's organ. Mutations in many genes involved in mechanotransduction by tactile bristles also eliminate or reduce the Johnston's organ response, indicating that related transduction mechanisms operate in each type of mechanosensory organ. In addition, the sound-evoked response is affected by two mutations that do not affect bristle mechanotransduction, beethoven (btv) and touch-insensitive-larvaB (tilB). btv shows defects in the ciliary dilation, an elaboration of the axoneme that is characteristic of chordotonal cilia. tilB, which also causes male sterility, shows structural defects in sperm flagellar axonemes. This suggests that in addition to the shared transduction mechanism, axonemal integrity and possibly ciliary motility are required for signal amplification or transduction by chordotonal sensory neurons.

The Dmca1D gene encodes a Drosophila calcium channel alpha1 subunit. We describe the first functional characterization of a mutation in this gene. This alpha1 subunit mediates the dihydropyridine-sensitive calcium channel current in larval muscle but does not contribute to the amiloride-sensitive current in that tissue. A mutation, which changes a highly conserved Cys to Tyr in transmembrane domain IS1, identifies a residue important for channel function not only in Drosophila muscle but also in mammalian cardiac channels. In both cases, mutations in this Cys residue slow channel activation and reduce expressed currents. Amino acid substitutions at this Cys position in the cardiac alpha1 subunit show that the size of the side chain, rather than its ability to form disulfide bonds, affects channel activation.