Jahn, Olaf

[["dc.bibliographiccitation.artnumber","2530.e5"],["dc.bibliographiccitation.firstpage","2521"],["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","Cell Reports"],["dc.bibliographiccitation.volume","26"],["dc.contributor.author","López-Murcia, Francisco José"],["dc.contributor.author","Reim, Kerstin"],["dc.contributor.author","Jahn, Olaf"],["dc.contributor.author","Taschenberger, Holger"],["dc.contributor.author","Brose, Nils"],["dc.date.accessioned","2019-07-09T11:50:32Z"],["dc.date.available","2019-07-09T11:50:32Z"],["dc.date.issued","2019"],["dc.description.abstract","SNARE-mediated synaptic vesicle (SV) fusion is controlled by multiple regulatory proteins that determine neurotransmitter release efficiency. Complexins are essential SNARE regulators whose mode of action is unclear, as available evidence indicates positive SV fusion facilitation and negative \"fusion clamp\"-like activities, with the latter occurring only in certain contexts. Because these contradictory findings likely originate in part from different experimental perturbation strategies, we attempted to resolve them by examining a conditional complexin-knockout mouse line as the most stringent genetic perturbation model available. We found that acute complexin loss after synaptogenesis in autaptic and mass-cultured hippocampal neurons reduces SV fusion probability and thus abates the rates of spontaneous, synchronous, asynchronous, and delayed transmitter release but does not affect SV priming or cause \"unclamping\" of spontaneous SV fusion. Thus, complexins act as facilitators of SV fusion but are dispensable for \"fusion clamping\" in mammalian forebrain neurons."],["dc.identifier.doi","10.1016/j.celrep.2019.02.030"],["dc.identifier.pmid","30840877"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/15955"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59788"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation","info:eu-repo/grantAgreement/EC/H2020/670283/EU//SYNPRIME"],["dc.relation.issn","2211-1247"],["dc.rights","CC BY-NC-ND 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc-nd/4.0"],["dc.subject.ddc","573"],["dc.subject.ddc","612"],["dc.title","Acute Complexin Knockout Abates Spontaneous and Evoked Transmitter Release"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Frontiers in Molecular Neuroscience"],["dc.bibliographiccitation.volume","12"],["dc.contributor.author","Akula, Asha Kiran"],["dc.contributor.author","Zhang, Xin"],["dc.contributor.author","Viotti, Julio S."],["dc.contributor.author","Nestvogel, Dennis"],["dc.contributor.author","Rhee, Jeong-Seop"],["dc.contributor.author","Ebrecht, Rene"],["dc.contributor.author","Reim, Kerstin"],["dc.contributor.author","Wouters, Fred"],["dc.contributor.author","Liepold, Thomas"],["dc.contributor.author","Jahn, Olaf"],["dc.contributor.author","Bogeski, Ivan"],["dc.contributor.author","Dresbach, Thomas"],["dc.date.accessioned","2020-12-10T18:44:35Z"],["dc.date.available","2020-12-10T18:44:35Z"],["dc.date.issued","2019"],["dc.description.abstract","Neurotransmitter release is mediated by an evolutionarily conserved machinery. The synaptic vesicle (SV) associated protein Mover/TPRGL/SVAP30 does not occur in all species and all synapses. Little is known about its molecular properties and how it may interact with the conserved components of the presynaptic machinery. Here, we show by deletion analysis that regions required for homomeric interaction of Mover are distributed across the entire molecule, including N-terminal, central and C-terminal regions. The same regions are also required for the accumulation of Mover in presynaptic terminals of cultured neurons. Mutating two phosphorylation sites in N-terminal regions did not affect these properties. In contrast, a point mutation in the predicted Calmodulin (CaM) binding sequence of Mover abolished both homomeric interaction and presynaptic targeting. We show that this sequence indeed binds Calmodulin, and that recombinant Mover increases Calmodulin signaling upon heterologous expression. Our data suggest that presynaptic accumulation of Mover requires homomeric interaction mediated by regions distributed across large areas of the protein, and corroborate the hypothesis that Mover functionally interacts with Calmodulin signaling."],["dc.identifier.doi","10.3389/fnmol.2019.00249"],["dc.identifier.eissn","1662-5099"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16645"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/78512"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.notes.intern","Merged from goescholar"],["dc.publisher","Frontiers Media S.A."],["dc.relation.eissn","1662-5099"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","The Calmodulin Binding Region of the Synaptic Vesicle Protein Mover Is Required for Homomeric Interaction and Presynaptic Targeting"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1011"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","The Journal of Cell Biology"],["dc.bibliographiccitation.lastpage","1026"],["dc.bibliographiccitation.volume","218"],["dc.contributor.author","Scholz, Nicole"],["dc.contributor.author","Ehmann, Nadine"],["dc.contributor.author","Sachidanandan, Divya"],["dc.contributor.author","Imig, Cordelia"],["dc.contributor.author","Cooper, Benjamin H."],["dc.contributor.author","Jahn, Olaf"],["dc.contributor.author","Reim, Kerstin"],["dc.contributor.author","Brose, Nils"],["dc.contributor.author","Meyer, Jutta"],["dc.contributor.author","Lamberty, Marius"],["dc.contributor.author","Altrichter, Steffen"],["dc.contributor.author","Bormann, Anne"],["dc.contributor.author","Hallermann, Stefan"],["dc.contributor.author","Pauli, Martin"],["dc.contributor.author","Heckmann, Manfred"],["dc.contributor.author","Stigloher, Christian"],["dc.contributor.author","Langenhan, Tobias"],["dc.contributor.author","Kittel, Robert J."],["dc.date.accessioned","2020-12-10T18:15:36Z"],["dc.date.available","2020-12-10T18:15:36Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.1083/jcb.201806155"],["dc.identifier.eissn","1540-8140"],["dc.identifier.issn","0021-9525"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/74898"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Complexin cooperates with Bruchpilot to tether synaptic vesicles to the active zone cytomatrix"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]