Kittelmann, Maike

[["dc.bibliographiccitation.firstpage","234"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","ABI Technik"],["dc.bibliographiccitation.lastpage","244"],["dc.bibliographiccitation.volume","38"],["dc.contributor.author","Glaab-Kühn, Friederike"],["dc.contributor.author","Kittelmann, Maike"],["dc.date.accessioned","2018-10-25T08:23:32Z"],["dc.date.available","2018-10-25T08:23:32Z"],["dc.date.issued","2018"],["dc.description.abstract","Mit der wachsenden Zahl an zugänglichen FID-Lizenzen wurde es immer wichtiger, die FID-Lizenzen zentral nachzuweisen. Zu diesem Zweck hat das Kompetenzzentrum für Lizenzierung elektronischer Ressourcen im DFG-geförderten System der „Fachinformationsdienste für die Wissenschaft“ einen Zentralen Nachweis mit Informationen zu allen verfügbaren FID-Lizenzen aufgebaut. Der Artikel präsentiert die damit verbundenen konzeptionellen Überlegungen sowie die Festlegungen zur Umsetzung. Anhand von Workflows, Dokumentation und Qualitätsmanagement wird veranschaulicht, wie das Datenmanagement für den Zentralen Nachweis umgesetzt wurde."],["dc.description.abstract","The increasing number of resources licensed under the new FID-license scheme resulted in a growing demand for a central catalogue. In response, the “Kompetenzzentrum für Lizenzierung” (KfL) created a catalogue that records all FID-licenses in one place. The project was funded by the DFG within the frame of “Specialist Information Services for Academic Purposes”. This article outlines the conceptual design and implementation of this catalogue. Using selected examples, it takes a closer look at the catalogue’s data management, its workflows, documentation, and quality management."],["dc.identifier.doi","10.1515/abitech-2018-3004"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/15382"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/16098"],["dc.language.iso","de"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.relation","Kompetenzzentrum für Lizenzierung (KfL)"],["dc.relation.orgunit","Niedersächsische Staats- und Universitätsbibliothek Göttingen"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","FID-Lizenzen sichtbar und suchbar machen: Der Zentrale Nachweis für FID-Lizenzen – Konzept, Umsetzung und Datenmanagement"],["dc.title.alternative","Making FID-licenses visible and searchable. The catalogue for FID-licenses – concept, implementation and data management"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["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","745"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Genetics"],["dc.bibliographiccitation.lastpage","+"],["dc.bibliographiccitation.volume","196"],["dc.contributor.author","Hoover, Christopher M."],["dc.contributor.author","Edwards, Stacey L."],["dc.contributor.author","Yu, Szi-chieh"],["dc.contributor.author","Kittelmann, Maike"],["dc.contributor.author","Richmond, Janet E."],["dc.contributor.author","Eimer, Stefan"],["dc.contributor.author","Yorks, Rosalina M."],["dc.contributor.author","Miller, Kenneth G."],["dc.date.accessioned","2018-11-07T09:42:52Z"],["dc.date.available","2018-11-07T09:42:52Z"],["dc.date.issued","2014"],["dc.description.abstract","Neurons release neuropeptides via the regulated exocytosis of dense core vesicles (DCVs) to evoke or modulate behaviors. We found that Caenorhabditis elegans motor neurons send most of their DCVs to axons, leaving very few in the cell somas. How neurons maintain this skewed distribution and the extent to which it can be altered to control DCV numbers in axons or to drive release from somas for different behavioral impacts is unknown. Using a forward genetic screen, we identified loss-of-function mutations in UNC-43 (CaM kinase II) that reduce axonal DCV levels by approximate to 90% and cell soma/dendrite DCV levels by approximate to 80%, leaving small synaptic vesicles largely unaffected. Blocking regulated secretion in unc-43 mutants restored near wild-type axonal levels of DCVs. Time-lapse video microscopy showed no role for CaM kinase II in the transport of DCVs from cell somas to axons. In vivo secretion assays revealed that much of the missing neuropeptide in unc-43 mutants is secreted via a regulated secretory pathway requiring UNC-31 (CAPS) and UNC-18 (nSec1). DCV cargo levels in unc-43 mutants are similarly low in cell somas and the axon initial segment, indicating that the secretion occurs prior to axonal transport. Genetic pathway analysis suggests that abnormal neuropeptide function contributes to the sluggish basal locomotion rate of unc-43 mutants. These results reveal a novel pathway controlling the location of DCV exocytosis and describe a major new function for CaM kinase II."],["dc.identifier.doi","10.1534/genetics.113.158568"],["dc.identifier.isi","000333905500014"],["dc.identifier.pmid","24653209"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/34061"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Genetics Soc Am"],["dc.relation.issn","1943-2631"],["dc.title","A Novel CaM Kinase II Pathway Controls the Location of Neuropeptide Release from Caenorhabditis elegans Motor Neurons"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","5862"],["dc.bibliographiccitation.issue","15"],["dc.bibliographiccitation.journal","Proceedings of the National Academy of Sciences of the United States of America"],["dc.bibliographiccitation.lastpage","5867"],["dc.bibliographiccitation.volume","109"],["dc.contributor.author","Chua, John Jia En"],["dc.contributor.author","Butkevich, Eugenia"],["dc.contributor.author","Worseck, Josephine M."],["dc.contributor.author","Kittelmann, Maike"],["dc.contributor.author","Gronborg, Mads"],["dc.contributor.author","Behrmann, Elmar"],["dc.contributor.author","Stelzl, Ulrich"],["dc.contributor.author","Pavlos, Nathan J."],["dc.contributor.author","Lalowski, Maciej M."],["dc.contributor.author","Eimer, Stefan"],["dc.contributor.author","Wanker, Erich E."],["dc.contributor.author","Klopfenstein, Dieter Robert"],["dc.contributor.author","Jahn, Reinhard"],["dc.date.accessioned","2018-11-07T09:11:12Z"],["dc.date.available","2018-11-07T09:11:12Z"],["dc.date.issued","2012"],["dc.description.abstract","Presynaptic nerve terminals are formed from preassembled vesicles that are delivered to the prospective synapse by kinesin-mediated axonal transport. However, precisely how the various cargoes are linked to the motor proteins remains unclear. Here, we report a transport complex linking syntaxin 1a (Stx) and Munc18, two proteins functioning in synaptic vesicle exocytosis at the presynaptic plasma membrane, to the motor protein Kinesin-1 via the kinesin adaptor FEZ1. Mutation of the FEZ1 ortholog UNC-76 in Caenorhabditis elegans causes defects in the axonal transport of Stx. We also show that binding of FEZ1 to Kinesin-1 and Munc18 is regulated by phosphorylation, with a conserved site (serine 58) being essential for binding. When expressed in C. elegans, wild-type but not phosphorylation-deficient FEZ1 (S58A) restored axonal transport of Stx. We conclude that FEZ1 operates as a kinesin adaptor for the transport of Stx, with cargo loading and unloading being regulated by protein kinases."],["dc.identifier.doi","10.1073/pnas.1113819109"],["dc.identifier.isi","000302533500062"],["dc.identifier.pmid","22451907"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/26667"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Natl Acad Sciences"],["dc.relation.issn","0027-8424"],["dc.title","Phosphorylation-regulated axonal dependent transport of syntaxin 1 is mediated by a Kinesin-1 adapter"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","399"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","Development Genes and Evolution"],["dc.bibliographiccitation.lastpage","407"],["dc.bibliographiccitation.volume","219"],["dc.contributor.author","Kittelmann, Maike"],["dc.contributor.author","Schinko, Johannes B."],["dc.contributor.author","Winkler, Marco"],["dc.contributor.author","Bucher, Gregor"],["dc.contributor.author","Wimmer, Ernst A."],["dc.contributor.author","Prpic, Nikola-Michael"],["dc.date.accessioned","2018-11-07T11:25:55Z"],["dc.date.available","2018-11-07T11:25:55Z"],["dc.date.issued","2009"],["dc.description.abstract","The genetic control of leg development is well characterized in the fly Drosophila melanogaster. These control mechanisms, however, must differ to some degree between different insect species to account for the morphological diversity of thoracic legs in the insects. The legs of the flour beetle Tribolium castaneum differ from the Drosophila legs in their developmental mode as well as in their specific morphology especially at the larval stage. In order to identify genes involved in the morphogenesis of the Tribolium larval legs, we have analyzed EGFP enhancer trap lines of Tribolium. We have identified the zfh2 gene as a novel factor required for normal leg development in Tribolium. RNA interference with zfh2 function leads to two alternative classes of leg phenotype. The loss of a leg segment boundary and the generation of ectopic outgrowths in one class of phenotype suggest a role in leg segmentation and segment growth. The malformation of the pretarsal claw in the second class of phenotype suggests a role in distal development and the morphogenesis of the claw-shaped morphology of the pretarsus. This suggests that zfh2 is involved in the regulation of an unidentified target gene in a concentration-dependent manner. Our results demonstrate that enhancer trap screens in T. castaneum have the potential to identify novel gene functions regulating specific developmental processes."],["dc.identifier.doi","10.1007/s00427-009-0303-y"],["dc.identifier.isi","000271397600002"],["dc.identifier.pmid","19760181"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?goescholar/3758"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/56738"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","0949-944X"],["dc.rights.access","openAccess"],["dc.subject.ddc","570"],["dc.title","Insertional mutagenesis screening identifies the zinc finger homeodomain 2 (zfh2) gene as a novel factor required for embryonic leg development in Tribolium castaneum"],["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","264"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Neuroforum"],["dc.bibliographiccitation.lastpage","270"],["dc.bibliographiccitation.volume","20"],["dc.contributor.author","Kittelmann, Maike"],["dc.contributor.author","Göpfert, Martin C."],["dc.date.accessioned","2018-11-07T09:35:29Z"],["dc.date.available","2018-11-07T09:35:29Z"],["dc.date.issued","2014"],["dc.description.abstract","The fruit fly Drosophila melanogaster communicates acoustically and hears with its antennae. Fundamental aspects of hearing can be studied in these antenna! ears. Their auditory sensory cells are evolutionarily related with vertebrate hair cells and are developmentally specified by homologous transcription factors. Like vertebrate hair cells, Drosophila auditory sensory cells are also motile and actively amplify the mechanical vibrations that they transduce. This transduction and amplification rely on the interplay between mechanically activated ion channels and motor proteins, whose movement impacts on the macroscopic performance of the ear. First molecular transducer components have been identified and various auditory relevant proteins have been described. Several of these proteins are conserved components of cilia, putting forward the fly's ear as a model for human ciliopathies. Also the evolution of sensory signalling cascades can be studied using the fly's ear as the fly employs key Chemo- and Photoreceptor proteins to hear. Evidence is also accumulating that the fly's ear is a multifunctional sensory organ that, in addition to mediating hearing, serves the detection of wind and gravity and, presumably, temperature."],["dc.identifier.isi","000350178500005"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/32395"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Spektrum Akademischer Verlag-springer-verlag Gmbh"],["dc.relation.issn","0947-0875"],["dc.title","Drosophila hearing: mechanisms and genes"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1391"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Cell"],["dc.bibliographiccitation.lastpage","1403"],["dc.bibliographiccitation.volume","162"],["dc.contributor.author","Zhang, W."],["dc.contributor.author","Cheng, Li E."],["dc.contributor.author","Kittelmann, Maike"],["dc.contributor.author","Li, Jiefu"],["dc.contributor.author","Petkovic, Maja"],["dc.contributor.author","Cheng, Tong"],["dc.contributor.author","Jin, Peng"],["dc.contributor.author","Guo, Zhenhao"],["dc.contributor.author","Göpfert, Martin C."],["dc.contributor.author","Jan, Lily Yeh"],["dc.contributor.author","Jan, Yuh Nung"],["dc.date.accessioned","2018-11-07T09:51:42Z"],["dc.date.available","2018-11-07T09:51:42Z"],["dc.date.issued","2015"],["dc.description.abstract","Howmetazoanmechanotransduction channels sense mechanical stimuli is not well understood. The NOMPC channel in the transient receptor potential (TRP) family, a mechanotransduction channel for Drosophila touch sensation and hearing, contains 29 Ankyrin repeats (ARs) that associate with microtubules. These ARs have been postulated to act as a tether that conveys force to the channel. Here, we report that these N-terminal ARs form a cytoplasmicdomain essential forNOMPC mechanogating in vitro, mechanosensitivity of touch receptor neurons in vivo, and touch-induced behaviors of Drosophila larvae. Duplicating the ARs elongates the filaments that tether NOMPC to microtubules in mechanosensory neurons. Moreover, microtubule association is required for NOMPC mechanogating. Importantly, transferring the NOMPC ARs to mechanoinsensitive voltage-gated potassium channels confers mechanosensitivity to the chimeric channels. These experiments strongly support a tethermechanismofmechanogating for the NOMPC channel, providing insights into the basis ofmechanosensitivity ofmechanotransduction channels."],["dc.identifier.doi","10.1016/j.cell.2015.08.024"],["dc.identifier.isi","000361247900026"],["dc.identifier.pmid","26359990"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/35969"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Cell Press"],["dc.relation.issn","1097-4172"],["dc.relation.issn","0092-8674"],["dc.title","Ankyrin Repeats Convey Force to Gate the NOMPC Mechanotransduction Channel"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","E3007"],["dc.bibliographiccitation.issue","32"],["dc.bibliographiccitation.journal","PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA"],["dc.bibliographiccitation.lastpage","E3016"],["dc.bibliographiccitation.volume","110"],["dc.contributor.author","Kittelmann, Maike"],["dc.contributor.author","Liewald, Jana F."],["dc.contributor.author","Hegermann, Jan"],["dc.contributor.author","Schultheis, Christian"],["dc.contributor.author","Brauner, Martin"],["dc.contributor.author","Costa, Wagner Steuer"],["dc.contributor.author","Wabnig, Sebastian"],["dc.contributor.author","Eimer, Stefan"],["dc.contributor.author","Gottschalk, Alexander"],["dc.date.accessioned","2018-11-07T09:21:23Z"],["dc.date.available","2018-11-07T09:21:23Z"],["dc.date.issued","2013"],["dc.description.abstract","Local recycling of synaptic vesicles (SVs) allows neurons to sustain transmitter release. Extreme activity (e.g., during seizure) may exhaust synaptic transmission and, in vitro, induces bulk endocytosis to recover SV membrane and proteins; how this occurs in animals is unknown. Following optogenetic hyperstimulation of Caenorhabditis elegans motoneurons, we analyzed synaptic recovery by time-resolved behavioral, electrophysiological, and ultrastructural assays. Recovery of docked SVs and of evoked-release amplitudes (indicating readily-releasable pool refilling) occurred within similar to 8-20 s (tau = 9.2 s and tau = 11.9 s), whereas locomotion recovered only after similar to 60 s (tau = 20 s). During similar to 11-s stimulation, 50- to 200-nm noncoated vesicles (\"100nm vesicles\") formed, which disappeared similar to 8 s poststimulation, likely representing endocytic intermediates from which SVs may regenerate. In endophilin, synaptojanin, and dynamin mutants, affecting endocytosis and vesicle scission, resolving 100nm vesicles was delayed (>20 s). In dynamin mutants, 100nm vesicles were abundant and persistent, sometimes continuous with the plasma membrane; incomplete budding of smaller vesicles from 100nm vesicles further implicates dynamin in regenerating SVs from bulk-endocytosed vesicles. Synaptic recovery after exhaustive activity is slow, and different time scales of recovery at ultrastructural, physiological, and behavioral levels indicate multiple contributing processes. Similar processes may jointly account for slow recovery from acute seizures also in higher animals."],["dc.identifier.doi","10.1073/pnas.1305679110"],["dc.identifier.isi","000322771100013"],["dc.identifier.pmid","23878262"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/29092"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Natl Acad Sciences"],["dc.relation.issn","0027-8424"],["dc.title","In vivo synaptic recovery following optogenetic hyperstimulation"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]