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.

Although many animal species sense gravity for spatial orientation, the molecular bases remain uncertain. Therefore, we studied Drosophila melanogaster, which possess an inherent upward movement against gravity-negative geotaxis. Negative geotaxis requires Johnston's organ, a mechanosensory structure located in the antenna that also detects near-field sound. Because channels of the transient receptor potential (TRP) superfamily can contribute to mechanosensory signaling, we asked whether they are important for negative geotaxis. We identified distinct expression patterns for 5 TRP genes; the TRPV genes nanchung and inactive were present in most Johnston's organ neurons, the TRPN gene nompC and the TRPA gene painless were localized to 2 subpopulations of neurons, and the TRPA gene pyrexia was expressed in cap cells that may interact with the neurons. Likewise, mutating specific TRP genes produced distinct phenotypes, disrupting negative geotaxis (painless and pyrexia), hearing (nompC), or both (nanchung and inactive). Our genetic, physiological and behavioral data indicate that the sensory component of negative geotaxis involves multiple TRP genes. The results also distinguish between different mechanosensory modalities and set the stage for understanding how TRP channels contribute to mechanosensation. Drosophila ͉ transient receptor potential ͉ geotaxis T he primary mechanosensory organ that detects gravity in Drosophila appears to be Johnston's organ (1). This organ is located in the second antennal segment. It consists of over 200 scolopidia arrayed in a bowl shape (2), with each scolopidium containing mechanosensory chordotonal neurons and their support cells (3-5) (Fig. 1A). Johnston's organ is well known as a detector of near-field sound (3-6). Air particle displacement vibrates the third antennal segment, deforming the cuticle at the joint between segments 2 and 3 where the sensory units of Johnston's organ attach. It was proposed that the third segment may also be deflected by gravity (7), and the geometry of Johnston's organ suggests it could respond to gravity irrespective of head orientation (2). Indeed, recent work indicates that Johnston's organ can also respond to gravity, as well as to wind (1,8). Thus, Johnston's organ may detect multiple different mechanosensory stimuli, and investigations of specific molecular mechanisms underlying these sensory functions may benefit our understanding of other polymodal sensory structures such as the inner ear and dorsal root ganglion in mammals.Almost 50 years ago, Hirsch and colleagues demonstrated that negative geotaxis is genetically encoded in Drosophila (9, 10). Since then, several genes influencing this behavior have been identified (11-13). However, those genes are expressed in both central and peripheral nervous systems, and the nature of their role in the sensory organ that detects gravity remains unknown. The goal of this work was to identify genes involved in sensory aspects of negative geotaxis and in so doing to obtain genetic data to discriminate...

KAP plays an essential role in Kinesin II function, which is required for the axoneme growth and maintenance of the cilia in Drosophila type I sensory neurons. However, the flagellar assembly in Drosophila spermatids does not require Kinesin II and is independent of IFT.

Rhythmic movements, such as peristaltic contraction, are initiated by output from central pattern generator (CPG) networks in the CNS. These oscillatory networks elicit locomotion in the absence of external sensory or descending inputs, but CPG circuits produce more directed and behaviorally relevant movement via peripheral nervous system (PNS) input. Drosophila melanogaster larval locomotion results from patterned muscle contractions moving stereotypically along the body segments, but without PNS feedback, contraction of body segments is uncoordinated. We have dissected the role of a subset of mechanosensory neurons in the larval PNS, the chordotonal organs (chos), in providing sensory feedback to the locomotor CPG circuit with DIAS (Dynamic Image Analysis System) software. We analyzed mutants carrying cho mutations including atonal, a cho proneural gene, beethoven, a cho cilia class mutant, smetana and touch-insensitive larva B, two axonemal mutants, and 5D10, a weak cho mutant. All cho mutants have defects in gross path morphology compared to controls. These mutants exhibit increased frequency and duration of turning (decision-making) and reduced duration of linear locomotion. Furthermore, cho mutants affect locomotor parameters, including reduced average speed, direction change, and persistence. DIAS analysis of peristaltic waves indicates that mutants exhibit reduced average speed, positive flow and negative flow, and increased stride period. Thus, cho sensilla are major proprioceptive components that underlie touch sensitivity, locomotion, and peristaltic contraction by providing sensory feedback to the locomotor CPG circuit in larvae.R hythmic movements, such as peristaltic contraction, are initiated by output from central pattern generators (CPGs) in the CNS. These oscillatory networks elicit locomotion in the absence of external sensory or descending inputs, but without feedback from the peripheral nervous system (PNS), contraction of body segments is uncoordinated (1-5). The Drosophila peristaltic CPGs form and become active during late embryogenesis and persist throughout larval stages (5-9). Coordinated peristalsis in Drosophila embryos, therefore, relies on output from the preformed CPG circuits as well as sensory feedback from the PNS. Here, we use DIAS (Dynamic Image Analysis System) software (10, 11) to demonstrate that chordotonal organs (chos), type I sense organs of the larval PNS (12, 13), constitute a major feedback mechanism that provides peripheral input to the CPG for normal locomotion.Suster and Bate (5) demonstrated that blocking neurotransmitter release in the entire embryonic PNS with tetanus toxin (TeTx) prevented normal peristalsis during late embryogenesis (14, 15). Interestingly, the peristaltic defects seen in TeTx embryos phenocopied those exhibited in senseless (sens) null mutants (5, 16). DIAS motility software was used to dissect the dysfunctional locomotor parameters of first-instar TeTx and sens larvae and the role of sensory input from the PNS in driving CPGs (5). Wang et ...