Göpfert, Martin C.

[["dc.bibliographiccitation.artnumber","17085"],["dc.bibliographiccitation.journal","Scientific Reports"],["dc.bibliographiccitation.volume","5"],["dc.contributor.author","Karak, Somdatta"],["dc.contributor.author","Jacobs, Julie S."],["dc.contributor.author","Kittelmann, Maike"],["dc.contributor.author","Spalthoff, Christian"],["dc.contributor.author","Katana, Radoslaw"],["dc.contributor.author","Sivan-Loukianova, Elena"],["dc.contributor.author","Schon, Michael A."],["dc.contributor.author","Kernan, Maurice J."],["dc.contributor.author","Eberl, Daniel F."],["dc.contributor.author","Göpfert, Martin C."],["dc.date.accessioned","2018-11-07T09:48:47Z"],["dc.date.available","2018-11-07T09:48:47Z"],["dc.date.issued","2015"],["dc.description.abstract","Much like vertebrate hair cells, the chordotonal sensory neurons that mediate hearing in Drosophila are motile and amplify the mechanical input of the ear. Because the neurons bear mechanosensory primary cilia whose microtubule axonemes display dynein arms, we hypothesized that their motility is powered by dyneins. Here, we describe two axonemal dynein proteins that are required for Drosophila auditory neuron function, localize to their primary cilia, and differently contribute to mechanical amplification in hearing. Promoter fusions revealed that the two axonemal dynein genes Dmdnah3 (=CG17150) and Dmdnai2 (=CG6053) are expressed in chordotonal neurons, including the auditory ones in the fly's ear. Null alleles of both dyneins equally abolished electrical auditory neuron responses, yet whereas mutations in Dmdnah3 facilitated mechanical amplification, amplification was abolished by mutations in Dmdnai2. Epistasis analysis revealed that Dmdnah3 acts downstream of Nan-Iav channels in controlling the amplificatory gain. Dmdnai2, in addition to being required for amplification, was essential for outer dynein arms in auditory neuron cilia. This establishes diverse roles of axonemal dyneins in Drosophila auditory neuron function and links auditory neuron motility to primary cilia and axonemal dyneins. Mutant defects in sperm competition suggest that both dyneins also function in sperm motility."],["dc.description.sponsorship","Open-Access Publikationsfonds 2015"],["dc.identifier.doi","10.1038/srep17085"],["dc.identifier.isi","000365389300001"],["dc.identifier.pmid","26608786"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/12601"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/35376"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Nature Publishing Group"],["dc.relation.issn","2045-2322"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Diverse Roles of Axonemal Dyneins in Drosophila Auditory Neuron Function and Mechanical Amplification in Hearing"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","7243"],["dc.bibliographiccitation.issue","26"],["dc.bibliographiccitation.journal","Proceedings of the National Academy of Sciences of the United States of America"],["dc.bibliographiccitation.lastpage","7248"],["dc.bibliographiccitation.volume","113"],["dc.contributor.author","Guo, Yanmeng"],["dc.contributor.author","Wang, Y."],["dc.contributor.author","Zhang, W."],["dc.contributor.author","Meltzer, Shan"],["dc.contributor.author","Zanini, Damiano"],["dc.contributor.author","Yu, Yue"],["dc.contributor.author","Li, Jiefu"],["dc.contributor.author","Cheng, Tong"],["dc.contributor.author","Guo, Zhenhao"],["dc.contributor.author","Wang, Qingxiu"],["dc.contributor.author","Jacobs, Julie S."],["dc.contributor.author","Sharma, Yashoda"],["dc.contributor.author","Eberl, Daniel F."],["dc.contributor.author","Göpfert, Martin C."],["dc.contributor.author","Jan, Lily Yeh"],["dc.contributor.author","Jan, Yuh Nung"],["dc.contributor.author","Wang, Z."],["dc.date.accessioned","2018-11-07T10:12:35Z"],["dc.date.available","2018-11-07T10:12:35Z"],["dc.date.issued","2016"],["dc.description.abstract","Drosophila larval locomotion, which entails rhythmic body contractions, is controlled by sensory feedback from proprioceptors. The molecular mechanisms mediating this feedback are little understood. By using genetic knock-in and immunostaining, we found that the Drosophila melanogaster transmembrane channel-like (tmc) gene is expressed in the larval class I and class II dendritic arborization (da) neurons and bipolar dendrite (bd) neurons, both of which are known to provide sensory feedback for larval locomotion. Larvae with knockdown or loss of tmc function displayed reduced crawling speeds, increased head cast frequencies, and enhanced backward locomotion. Expressing Drosophila TMC or mammalian TMC1 and/or TMC2 in the tmc-positive neurons rescued these mutant phenotypes. Bending of the larval body activated the tmc-positive neurons, and in tmc mutants this bending response was impaired. This implicates TMC's roles in Drosophila proprioception and the sensory control of larval locomotion. It also provides evidence for a functional conservation between Drosophila and mammalian TMCs."],["dc.identifier.doi","10.1073/pnas.1606537113"],["dc.identifier.isi","000379033400072"],["dc.identifier.pmid","27298354"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/40270"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Natl Acad Sciences"],["dc.relation.issn","0027-8424"],["dc.title","Transmembrane channel-like (tmc) gene regulates Drosophila larval locomotion"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","51"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Journal of Comparative Physiology. A, Neuroethology, Sensory, Neural, and Behavioral Physiology"],["dc.bibliographiccitation.lastpage","60"],["dc.bibliographiccitation.volume","201"],["dc.contributor.author","Kavlie, Ryan G."],["dc.contributor.author","Fritz, Janice L."],["dc.contributor.author","Nies, Florian"],["dc.contributor.author","Göpfert, Martin C."],["dc.contributor.author","Oliver, Dominik"],["dc.contributor.author","Albert, Joerg T."],["dc.contributor.author","Eberl, Daniel F."],["dc.date.accessioned","2018-11-07T10:04:00Z"],["dc.date.available","2018-11-07T10:04:00Z"],["dc.date.issued","2015"],["dc.description.abstract","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."],["dc.identifier.doi","10.1007/s00359-014-0960-9"],["dc.identifier.isi","000347289700005"],["dc.identifier.pmid","25412730"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/11154"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/38599"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","1432-1351"],["dc.relation.issn","0340-7594"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Prestin is an anion transporter dispensable for mechanical feedback amplification in Drosophila hearing"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]