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Direct gating and mechanical integrity of Drosophila auditory transducers require TRPN1

A Corrigendum to this article was published on 21 November 2014

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Abstract

The elusive transduction channels for hearing are directly gated mechanically by the pull of gating springs. We found that the transient receptor potential (TRP) channel TRPN1 (NOMPC) is essential for this direct gating of Drosophila auditory transduction channels and that the channel-spring complex was disrupted if TRPN1 was lost. Our results identify TRPN1 as a mechanical constituent of the fly's auditory transduction complex that may act as the channel and/or gating spring.

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Figure 1: Correlates of transducer gating depend on TRPN1.
Figure 2: TRPN1 is required for auditory transducer gating and integrity.

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  • 13 May 2013

    In the version of this article initially published, grant acknowledgments for the Human Frontier Science Program (J.T.A.) and the Bernstein Centre Göttingen (M.C.G.) were missing. The error has been corrected in the HTML and PDF versions of the article.

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Acknowledgements

We thank R. Walker, L. Cheng, Y.-N. Jan, the Bloomington Stock Center, the Exelixis Collection at Harvard Medical School and the Nippon Consortium for fly strains. This work was supported by the Volkswagen Foundation (B.N.), the German National Academic Foundation (D.P.), Biotechnology and Biological Sciences Research Council (BB/G004455/1) and the Human Frontier Science Program (J.T.A.), and the Bernstein Centre Göttingen and German Science Foundation (DFG, SFB889-A1, M.C.G.).

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T.E. performed the experiments with the help of D.P. B.N. devised models and T.E. analyzed the data. J.T.A. devised methods and performed pilot studies. M.C.G. supervised the project and wrote the manuscript with T.E., B.N., D.P. and J.T.A.

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Correspondence to Jörg T Albert or Martin C Göpfert.

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The authors declare no competing financial interests.

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Effertz, T., Nadrowski, B., Piepenbrock, D. et al. Direct gating and mechanical integrity of Drosophila auditory transducers require TRPN1. Nat Neurosci 15, 1198–1200 (2012). https://doi.org/10.1038/nn.3175

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