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Prestin is an anion transporter dispensable for mechanical feedback amplification in Drosophila hearing

In mammals, the membrane-based protein Prestin confers unique electromotile properties to cochlear outer hair cells, which contribute to the cochlear amplifier. Like mammals, the ears of insects, such as those of Drosophila melanogaster, mechanically amplify sound stimuli and have also been reported...

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Autores principales: Kavlie, Ryan G., Fritz, Janice L., Nies, Florian, Göpfert, Martin C., Oliver, Dominik, Albert, Joerg T., Eberl, Daniel F.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Springer Berlin Heidelberg 2014
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4282873/
https://www.ncbi.nlm.nih.gov/pubmed/25412730
http://dx.doi.org/10.1007/s00359-014-0960-9
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author Kavlie, Ryan G.
Fritz, Janice L.
Nies, Florian
Göpfert, Martin C.
Oliver, Dominik
Albert, Joerg T.
Eberl, Daniel F.
author_facet Kavlie, Ryan G.
Fritz, Janice L.
Nies, Florian
Göpfert, Martin C.
Oliver, Dominik
Albert, Joerg T.
Eberl, Daniel F.
author_sort Kavlie, Ryan G.
collection PubMed
description In mammals, the membrane-based protein Prestin confers unique electromotile properties to cochlear outer hair cells, which contribute to the cochlear amplifier. Like mammals, the ears of insects, such as those of Drosophila melanogaster, mechanically amplify sound stimuli and have also been reported to express Prestin homologs. To determine whether the D. melanogaster Prestin homolog (dpres) is required for auditory amplification, we generated and analyzed dpres mutant flies. We found that dpres is robustly expressed in the fly’s antennal ear. However, dpres mutant flies show normal auditory nerve responses, and intact non-linear amplification. Thus we conclude that, in D. melanogaster, auditory amplification is independent of Prestin. This finding resonates with prior phylogenetic analyses, which suggest that the derived motor function of mammalian Prestin replaced, or amended, an ancestral transport function. Indeed, we show that dpres encodes a functional anion transporter. Interestingly, the acquired new motor function in the phylogenetic lineage leading to birds and mammals coincides with loss of the mechanotransducer channel NompC (=TRPN1), which has been shown to be required for auditory amplification in flies. The advent of Prestin (or loss of NompC, respectively) may thus mark an evolutionary transition from a transducer-based to a Prestin-based mechanism of auditory amplification. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1007/s00359-014-0960-9) contains supplementary material, which is available to authorized users.
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spelling pubmed-42828732015-01-08 Prestin is an anion transporter dispensable for mechanical feedback amplification in Drosophila hearing Kavlie, Ryan G. Fritz, Janice L. Nies, Florian Göpfert, Martin C. Oliver, Dominik Albert, Joerg T. Eberl, Daniel F. J Comp Physiol A Neuroethol Sens Neural Behav Physiol Original Paper In mammals, the membrane-based protein Prestin confers unique electromotile properties to cochlear outer hair cells, which contribute to the cochlear amplifier. Like mammals, the ears of insects, such as those of Drosophila melanogaster, mechanically amplify sound stimuli and have also been reported to express Prestin homologs. To determine whether the D. melanogaster Prestin homolog (dpres) is required for auditory amplification, we generated and analyzed dpres mutant flies. We found that dpres is robustly expressed in the fly’s antennal ear. However, dpres mutant flies show normal auditory nerve responses, and intact non-linear amplification. Thus we conclude that, in D. melanogaster, auditory amplification is independent of Prestin. This finding resonates with prior phylogenetic analyses, which suggest that the derived motor function of mammalian Prestin replaced, or amended, an ancestral transport function. Indeed, we show that dpres encodes a functional anion transporter. Interestingly, the acquired new motor function in the phylogenetic lineage leading to birds and mammals coincides with loss of the mechanotransducer channel NompC (=TRPN1), which has been shown to be required for auditory amplification in flies. The advent of Prestin (or loss of NompC, respectively) may thus mark an evolutionary transition from a transducer-based to a Prestin-based mechanism of auditory amplification. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1007/s00359-014-0960-9) contains supplementary material, which is available to authorized users. Springer Berlin Heidelberg 2014-11-21 2015 /pmc/articles/PMC4282873/ /pubmed/25412730 http://dx.doi.org/10.1007/s00359-014-0960-9 Text en © The Author(s) 2014 https://creativecommons.org/licenses/by/4.0/ Open AccessThis article is distributed under the terms of the Creative Commons Attribution License which permits any use, distribution, and reproduction in any medium, provided the original author(s) and the source are credited.
spellingShingle Original Paper
Kavlie, Ryan G.
Fritz, Janice L.
Nies, Florian
Göpfert, Martin C.
Oliver, Dominik
Albert, Joerg T.
Eberl, Daniel F.
Prestin is an anion transporter dispensable for mechanical feedback amplification in Drosophila hearing
title Prestin is an anion transporter dispensable for mechanical feedback amplification in Drosophila hearing
title_full Prestin is an anion transporter dispensable for mechanical feedback amplification in Drosophila hearing
title_fullStr Prestin is an anion transporter dispensable for mechanical feedback amplification in Drosophila hearing
title_full_unstemmed Prestin is an anion transporter dispensable for mechanical feedback amplification in Drosophila hearing
title_short Prestin is an anion transporter dispensable for mechanical feedback amplification in Drosophila hearing
title_sort prestin is an anion transporter dispensable for mechanical feedback amplification in drosophila hearing
topic Original Paper
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4282873/
https://www.ncbi.nlm.nih.gov/pubmed/25412730
http://dx.doi.org/10.1007/s00359-014-0960-9
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