| Literature DB >> 15483124 |
Zhefeng Gong1, Wonseok Son, Yun Doo Chung, Janghwan Kim, Dong Wook Shin, Colleen A McClung, Yong Lee, Hye Won Lee, Deok-Jin Chang, Bong-Kiun Kaang, Hawon Cho, Uhtaek Oh, Jay Hirsh, Maurice J Kernan, Changsoo Kim.
Abstract
Hearing in Drosophila depends on the transduction of antennal vibration into receptor potentials by ciliated sensory neurons in Johnston's organ, the antennal chordotonal organ. We previously found that a Drosophila protein in the vanilloid receptor subfamily (TRPV) channel subunit, Nanchung (NAN), is localized to the chordotonal cilia and required to generate sound-evoked potentials (Kim et al., 2003). Here, we show that the only other Drosophila TRPV protein is mutated in the behavioral mutant inactive (iav). The IAV protein forms a hypotonically activated channel when expressed in cultured cells; in flies, it is specifically expressed in the chordotonal neurons, localized to their cilia and required for hearing. IAV and NAN are each undetectable in cilia of mutants lacking the other protein, indicating that they both contribute to a heteromultimeric transduction channel in vivo. A functional green fluorescence protein-IAV fusion protein shows that the channel is restricted to the proximal cilium, constraining models for channel activation.Entities:
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Year: 2004 PMID: 15483124 PMCID: PMC6730075 DOI: 10.1523/JNEUROSCI.1645-04.2004
Source DB: PubMed Journal: J Neurosci ISSN: 0270-6474 Impact factor: 6.167