Marquardt, Till

[["dc.bibliographiccitation.firstpage","974"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Current opinion in neurobiology"],["dc.bibliographiccitation.lastpage","982"],["dc.bibliographiccitation.volume","23"],["dc.contributor.author","Wang, Liang"],["dc.contributor.author","Marquardt, Till"],["dc.date.accessioned","2019-07-09T11:40:47Z"],["dc.date.available","2019-07-09T11:40:47Z"],["dc.date.issued","2013-12-01"],["dc.description.abstract","A remarkable feature of nervous system development is the ability of axons emerging from newly formed neurons to traverse, by cellular scale, colossal distances to appropriate targets. The earliest axons achieve this in an essentially axon-free environment, but the vast majority of axons eventually grow along a scaffold of nerve tracts created by earlier extending axons. Signal exchange between sequentially or simultaneously extending axons may well represent the predominant mode of axonal navigation, but proportionally few efforts have so far been directed at deciphering the underlying mechanisms. This review intends to provide a conceptual update on the cellular and molecular principles driving axon-axon interactions, with emphasis on those contributing to the fidelity of axonal navigation, sorting and connectivity during nerve and circuit assembly."],["dc.identifier.doi","10.1016/j.conb.2013.08.004"],["dc.identifier.pmid","23973157"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/11325"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/58250"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","1873-6882"],["dc.rights","CC BY 3.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/3.0"],["dc.subject.mesh","Animals"],["dc.subject.mesh","Axons"],["dc.subject.mesh","Cell Communication"],["dc.subject.mesh","Humans"],["dc.subject.mesh","Neurogenesis"],["dc.subject.mesh","Signal Transduction"],["dc.title","What axons tell each other: axon-axon signaling in nerve and circuit assembly."],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e12247"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","PloS one"],["dc.bibliographiccitation.volume","5"],["dc.contributor.author","Voigt, Aaron"],["dc.contributor.author","Herholz, David"],["dc.contributor.author","Fiesel, Fabienne C."],["dc.contributor.author","Kaur, Kavita"],["dc.contributor.author","Müller, Daniel"],["dc.contributor.author","Karsten, Peter"],["dc.contributor.author","Weber, Stephanie S."],["dc.contributor.author","Kahle, Philipp J."],["dc.contributor.author","Marquardt, Till"],["dc.contributor.author","Schulz, Jörg"],["dc.date.accessioned","2019-07-09T11:53:07Z"],["dc.date.available","2019-07-09T11:53:07Z"],["dc.date.issued","2010"],["dc.description.abstract","Alteration and/or mutations of the ribonucleoprotein TDP-43 have been firmly linked to human neurodegenerative diseases, including amyotrophic lateral sclerosis (ALS) and frontotemporal lobar degeneration (FTLD). The relative impacts of TDP-43 alteration, mutation, or inherent protein function on neural integrity, however, remain less clear--a situation confounded by conflicting reports based on transient and/or random-insertion transgenic expression. We therefore performed a stringent comparative investigation of impacts of these TDP-43 modifications on neural integrity in vivo. To achieve this, we systematically screened ALS/FTLD-associated and synthetic TDP-43 isoforms via same-site gene insertion and neural expression in Drosophila; followed by transposon-based motor neuron-specific transgenesis in a chick vertebrate system. Using this bi-systemic approach we uncovered a requirement of inherent TDP-43 RNA-binding function--but not ALS/FTLD-linked mutation, mislocalization, or truncation--for TDP-43-mediated neurotoxicity in vivo."],["dc.identifier.doi","10.1371/journal.pone.0012247"],["dc.identifier.fs","573853"],["dc.identifier.pmid","20806063"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/6913"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/60347"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","1932-6203"],["dc.rights","CC BY 2.5"],["dc.rights.uri","https://creativecommons.org/licenses/by/2.5"],["dc.subject.ddc","610"],["dc.subject.mesh","Amyotrophic Lateral Sclerosis"],["dc.subject.mesh","Animals"],["dc.subject.mesh","Cell Line"],["dc.subject.mesh","Chickens"],["dc.subject.mesh","DNA-Binding Proteins"],["dc.subject.mesh","Drosophila melanogaster"],["dc.subject.mesh","Frontotemporal Lobar Degeneration"],["dc.subject.mesh","Gene Expression Regulation"],["dc.subject.mesh","Humans"],["dc.subject.mesh","Intracellular Space"],["dc.subject.mesh","Locomotion"],["dc.subject.mesh","Longevity"],["dc.subject.mesh","Male"],["dc.subject.mesh","Motor Neurons"],["dc.subject.mesh","Mutation"],["dc.subject.mesh","Neurons"],["dc.subject.mesh","Organ Specificity"],["dc.subject.mesh","Protein Binding"],["dc.subject.mesh","Protein Transport"],["dc.subject.mesh","RNA"],["dc.title","TDP-43-mediated neuron loss in vivo requires RNA-binding activity."],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["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"]]

[["dc.bibliographiccitation.firstpage","4037"],["dc.bibliographiccitation.issue","24"],["dc.bibliographiccitation.journal","Development"],["dc.bibliographiccitation.lastpage","4047"],["dc.bibliographiccitation.volume","135"],["dc.contributor.author","Oron-Karni, Varda"],["dc.contributor.author","Farhy, Chen"],["dc.contributor.author","Elgart, Michael"],["dc.contributor.author","Marquardt, Till"],["dc.contributor.author","Remizova, Lena"],["dc.contributor.author","Yaron, Orly"],["dc.contributor.author","Xie, Qing"],["dc.contributor.author","Cvekl, Ales"],["dc.contributor.author","Ashery-Padan, Ruth"],["dc.date.accessioned","2018-11-07T11:07:56Z"],["dc.date.available","2018-11-07T11:07:56Z"],["dc.date.issued","2008"],["dc.description.abstract","Throughout the developing central nervous system, pre-patterning of the ventricular zone into discrete neural progenitor domains is one of the predominant strategies used to produce neuronal diversity in a spatially coordinated manner. In the retina, neurogenesis proceeds in an intricate chronological and spatial sequence, yet it remains unclear whether retinal progenitor cells (RPCs) display intrinsic heterogeneity at any given time point. Here, we performed a detailed study of RPC fate upon temporally and spatially confined inactivation of Pax6. Timed genetic removal of Pax6 appeared to unmask a cryptic divergence of RPCs into qualitatively divergent progenitor pools. In the more peripheral RPCs under normal circumstances, Pax6 seemed to prevent premature activation of a photoreceptor-differentiation pathway by suppressing expression of the transcription factor Crx. More centrally, Pax6 contributed to the execution of the comprehensive potential of RPCs: Pax6 ablation resulted in the exclusive generation of amacrine interneurons. Together, these data suggest an intricate dual role for Pax6 in retinal neurogenesis, while pointing to the cryptic divergence of RPCs into distinct progenitor pools."],["dc.identifier.doi","10.1242/dev.028308"],["dc.identifier.isi","000261151000007"],["dc.identifier.pmid","19004853"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/52685"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Company Of Biologists Ltd"],["dc.relation.issn","0950-1991"],["dc.title","Dual requirement for Pax6 in retinal progenitor cells"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2008"],["dc.bibliographiccitation.issue","18"],["dc.bibliographiccitation.journal","The EMBO Journal"],["dc.bibliographiccitation.lastpage","2025"],["dc.bibliographiccitation.volume","35"],["dc.contributor.author","Vingill, Siv"],["dc.contributor.author","Brockelt, David"],["dc.contributor.author","Lancelin, Camille"],["dc.contributor.author","Tatenhorst, Lars"],["dc.contributor.author","Dontcheva, Guergana"],["dc.contributor.author","Preisinger, Christian"],["dc.contributor.author","Schwedhelm-Domeyer, Nicola"],["dc.contributor.author","Joseph, Sabitha"],["dc.contributor.author","Mitkovski, Miso"],["dc.contributor.author","Goebbels, Sandra"],["dc.contributor.author","Nave, Klaus-Armin"],["dc.contributor.author","Schulz, Joerg B."],["dc.contributor.author","Marquardt, Till"],["dc.contributor.author","Lingor, Paul"],["dc.contributor.author","Stegmueller, Judith"],["dc.date.accessioned","2018-11-07T10:08:31Z"],["dc.date.available","2018-11-07T10:08:31Z"],["dc.date.issued","2016"],["dc.description.abstract","Mutations in the FBXO7 (PARK15) gene have been implicated in a juvenile form of parkinsonism termed parkinsonian pyramidal syndrome (PPS), characterized by Parkinsonian symptoms and pyramidal tract signs. FBXO7 (F-box protein only 7) is a subunit of the SCF (SKP1/cullin-1/F-box protein) E3 ubiquitin ligase complex, but its relevance and function in neurons remain to be elucidated. Here, we report that the E3 ligase FBXO7-SCF binds to and ubiquitinates the proteasomal subunit PSMA2. In addition, we show that FBXO7 is a proteasome-associated protein involved in proteasome assembly. In FBXO7 knockout mice, we find reduced proteasome activity and early-onset motor deficits together with premature death. In addition, we demonstrate that NEX (neuronal helix-loop-helix protein-1)-Cre-induced deletion of the FBXO7 gene in forebrain neurons or the loss of FBXO7 in tyrosine hydroxylase (TH)-positive neurons results in motor defects, reminiscent of the phenotype in PARK15 patients. Taken together, our study establishes a vital role for FBXO7 in neurons, which is required for proper motor control and accentuates the importance of FBXO7 in proteasome function."],["dc.identifier.doi","10.15252/embj.201593585"],["dc.identifier.isi","000384084900006"],["dc.identifier.pmid","27497298"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/39477"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","1460-2075"],["dc.relation.issn","0261-4189"],["dc.title","Loss of FBXO7 (PARK15) results in reduced proteasome activity and models a parkinsonism-like phenotype in mice"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","514"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Translational Psychiatry"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Goldberg, Maria"],["dc.contributor.author","Islam, Md Rezaul"],["dc.contributor.author","Kerimoglu, Cemil"],["dc.contributor.author","Lancelin, Camille"],["dc.contributor.author","Gisa, Verena"],["dc.contributor.author","Burkhardt, Susanne"],["dc.contributor.author","Krüger, Dennis M."],["dc.contributor.author","Marquardt, Till"],["dc.contributor.author","Malchow, Berend"],["dc.contributor.author","Schmitt, Andrea"],["dc.contributor.author","Fischer, André"],["dc.date.accessioned","2021-12-01T09:23:16Z"],["dc.date.available","2021-12-01T09:23:16Z"],["dc.date.issued","2021"],["dc.description.abstract","Abstract MicroRNAs have been linked to synaptic plasticity and memory function and are emerging as potential biomarkers and therapeutic targets for cognitive diseases. Most of these data stem from the analysis of model systems or postmortem tissue from patients which mainly represents an advanced stage of pathology. Due to the in-accessibility of human brain tissue upon experimental manipulation, it is still challenging to identify microRNAs relevant to human cognition, which is however a key step for future translational studies. Here, we employ exercise as an experimental model for memory enhancement in healthy humans with the aim to identify microRNAs linked to memory function. By analyzing the circulating smallRNAome we find a cluster of 18 microRNAs that are highly correlated to cognition. MicroRNA-409-5p and microRNA-501-3p were the most significantly regulated candidates. Functional analysis revealed that the two microRNAs are important for neuronal integrity, synaptic plasticity, and morphology. In conclusion, we provide a novel approach to identify microRNAs linked to human memory function."],["dc.identifier.doi","10.1038/s41398-021-01627-w"],["dc.identifier.pii","1627"],["dc.identifier.pmid","34625536"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/94605"],["dc.identifier.url","https://mbexc.uni-goettingen.de/literature/publications/350"],["dc.identifier.url","https://sfb1286.uni-goettingen.de/literature/publications/137"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-478"],["dc.relation","EXC 2067: Multiscale Bioimaging"],["dc.relation","SFB 1286: Quantitative Synaptologie"],["dc.relation","SFB 1286 | B06: Die Rolle von RNA in Synapsenphysiologie und Neurodegeneration"],["dc.relation.eissn","2158-3188"],["dc.relation.workinggroup","RG A. Fischer (Epigenetics and Systems Medicine in Neurodegenerative Diseases)"],["dc.rights","CC BY 4.0"],["dc.title","Exercise as a model to identify microRNAs linked to human cognition: a role for microRNA-409 and microRNA-501"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]