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The Journal of Neuroscience, August 15, 2000, 20(16):5981-5988
Genetically Similar Transduction Mechanisms for Touch and Hearing in Drosophila
Daniel F. Eberl1, Robert W. Hardy2, and Maurice J. Kernan1 1 Department of Neurobiology and Behavior, The State University of New York at Stony Brook, Stony Brook, New York 11794-5230, and 2 Howard Hughes Medical Institute, University of California San Diego, La Jolla, California 92093-0649
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.
Key words: Drosophila; mutant; hearing; touch; mechanoreceptor; mechanotransduction; chordotonal organ; cilium; axoneme
Copyright © 2000 Society for Neuroscience 0270-6474/00/20165981-08$05.00/0
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