Marquardt, Till

[["dc.bibliographiccitation.firstpage","1264"],["dc.bibliographiccitation.issue","6176"],["dc.bibliographiccitation.journal","Science"],["dc.bibliographiccitation.lastpage","1266"],["dc.bibliographiccitation.volume","343"],["dc.contributor.author","Mueller, Daniel"],["dc.contributor.author","Cherukuri, Pitchaiah"],["dc.contributor.author","Henningfeld, Kristine A."],["dc.contributor.author","Poh, Chor Hoon"],["dc.contributor.author","Wittler, Lars"],["dc.contributor.author","Grote, Phillip"],["dc.contributor.author","Schlüter, Oliver M."],["dc.contributor.author","Schmidt, Jennifer"],["dc.contributor.author","Laborda, Jorge"],["dc.contributor.author","Bauer, Steven R."],["dc.contributor.author","Brownstone, Robert M."],["dc.contributor.author","Marquardt, Till"],["dc.date.accessioned","2018-11-07T09:42:34Z"],["dc.date.available","2018-11-07T09:42:34Z"],["dc.date.issued","2014"],["dc.description.abstract","Motor neurons, which relay neural commands to drive skeletal muscle movements, encompass types ranging from \"slow\" to \"fast,\" whose biophysical properties govern the timing, gradation, and amplitude of muscle force. Here we identify the noncanonical Notch ligand Delta-like homolog 1 (Dlk1) as a determinant of motor neuron functional diversification. Dlk1, expressed by similar to 30% of motor neurons, is necessary and sufficient to promote a fast biophysical signature in the mouse and chick. Dlk1 suppresses Notch signaling and activates expression of the K+ channel subunit Kcng4 to modulate delayed-rectifier currents. Dlk1 inactivation comprehensively shifts motor neurons toward slow biophysical and transcriptome signatures, while abolishing peak force outputs. Our findings provide insights into the development of motor neuron functional diversity and its contribution to the execution of movements."],["dc.identifier.doi","10.1126/science.1246448"],["dc.identifier.isi","000332728500040"],["dc.identifier.pmid","24626931"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/12046"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/33989"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Assoc Advancement Science"],["dc.relation.issn","1095-9203"],["dc.relation.issn","0036-8075"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Dlk1 Promotes a Fast Motor Neuron Biophysical Signature Required for Peak Force Execution"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","submitted_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","233"],["dc.bibliographiccitation.issue","5873"],["dc.bibliographiccitation.journal","Science"],["dc.bibliographiccitation.lastpage","236"],["dc.bibliographiccitation.volume","320"],["dc.contributor.author","Gallarda, Benjamin W."],["dc.contributor.author","Bonanomi, Dario"],["dc.contributor.author","Mueller, Daniel"],["dc.contributor.author","Brown, Arthur"],["dc.contributor.author","Alaynick, William A."],["dc.contributor.author","Andrews, Shane E."],["dc.contributor.author","Lemke, Greg"],["dc.contributor.author","Pfaff, Samuel L."],["dc.contributor.author","Marquardt, Till"],["dc.date.accessioned","2018-11-07T11:16:07Z"],["dc.date.available","2018-11-07T11:16:07Z"],["dc.date.issued","2008"],["dc.description.abstract","Execution of motor behaviors relies on circuitries effectively integrating immediate sensory feedback to efferent pathways controlling muscle activity. It remains unclear how, during neuromuscular circuit assembly, sensory and motor projections become incorporated into tightly coordinated, yet functionally separate pathways. We report that, within axial nerves, establishment of discrete afferent and efferent pathways depends on coordinate signaling between coextending sensory and motor projections. These heterotypic axon-axon interactions require motor axonal EphA3/EphA4 receptor tyrosine kinases activated by cognate sensory axonal ephrin-A ligands. Genetic elimination of trans-axonal ephrin-A -> EphA signaling in mice triggers drastic motor-sensory miswiring, culminating in functional efferents within proximal afferent pathways. Effective assembly of a key circuit underlying motor behaviors thus critically depends on trans-axonal signaling interactions resolving motor and sensory projections into discrete pathways."],["dc.identifier.doi","10.1126/science.1153758"],["dc.identifier.isi","000254836700044"],["dc.identifier.pmid","18403711"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/54519"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Assoc Advancement Science"],["dc.relation.issn","0036-8075"],["dc.title","Segregation of axial motor and sensory pathways via heterotypic trans-axonal signaling"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]