Sigrist, Stephan J.

[["dc.bibliographiccitation.firstpage","1318"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Nature Communications"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Bhukel, Anuradha"],["dc.contributor.author","Beuschel, Christine Brigitte"],["dc.contributor.author","Maglione, Marta"],["dc.contributor.author","Lehmann, Martin"],["dc.contributor.author","Juhász, Gabor"],["dc.contributor.author","Madeo, Frank"],["dc.contributor.author","Sigrist, Stephan J."],["dc.date.accessioned","2022-08-19T09:57:31Z"],["dc.date.available","2022-08-19T09:57:31Z"],["dc.date.issued","2019"],["dc.description.abstract","Macroautophagy is an evolutionarily conserved cellular maintenance program, meant to protect the brain from premature aging and neurodegeneration. How neuronal autophagy, usually loosing efficacy with age, intersects with neuronal processes mediating brain maintenance remains to be explored. Here, we show that impairing autophagy in the Drosophila learning center (mushroom body, MB) but not in other brain regions triggered changes normally restricted to aged brains: impaired associative olfactory memory as well as a brain-wide ultrastructural increase of presynaptic active zones (metaplasticity), a state non-compatible with memory formation. Mechanistically, decreasing autophagy within the MBs reduced expression of an NPY-family neuropeptide, and interfering with autocrine NPY signaling of the MBs provoked similar brain-wide metaplastic changes. Our results in an exemplary fashion show that autophagy-regulated signaling emanating from a higher brain integration center can execute high-level control over other brain regions to steer life-strategy decisions such as whether or not to form memories."],["dc.identifier.doi","10.1038/s41467-019-09262-2"],["dc.identifier.pmid","30899013"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/113039"],["dc.identifier.url","https://for2705.de/literature/publications/4"],["dc.language.iso","en"],["dc.relation","FOR 2705: Dissection of a Brain Circuit: Structure, Plasticity and Behavioral Function of the Drosophila Mushroom Body"],["dc.relation.issn","2041-1723"],["dc.relation.workinggroup","RG Sigrist (Genetics)"],["dc.rights","CC BY 4.0"],["dc.title","Autophagy within the mushroom body protects from synapse aging in a non-cell autonomous manner"],["dc.type","journal_article"],["dc.type.internalPublication","no"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","108941"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Cell Reports"],["dc.bibliographiccitation.volume","35"],["dc.contributor.author","Liang, YongTian"],["dc.contributor.author","Piao, Chengji"],["dc.contributor.author","Beuschel, Christine B."],["dc.contributor.author","Toppe, David"],["dc.contributor.author","Kollipara, Laxmikanth"],["dc.contributor.author","Bogdanow, Boris"],["dc.contributor.author","Maglione, Marta"],["dc.contributor.author","Lützkendorf, Janine"],["dc.contributor.author","See, Jason Chun Kit"],["dc.contributor.author","Huang, Sheng"],["dc.contributor.author","Conrad, Tim O. F."],["dc.contributor.author","Kintscher, Ulrich"],["dc.contributor.author","Madeo, Frank"],["dc.contributor.author","Liu, Fan"],["dc.contributor.author","Sickmann, Albert"],["dc.contributor.author","Sigrist, Stephan J."],["dc.date.accessioned","2022-08-19T11:57:50Z"],["dc.date.available","2022-08-19T11:57:50Z"],["dc.date.issued","2021"],["dc.description.abstract","Mitochondrial function declines during brain aging and is suspected to play a key role in age-induced cognitive decline and neurodegeneration. Supplementing levels of spermidine, a body-endogenous metabolite, has been shown to promote mitochondrial respiration and delay aspects of brain aging. Spermidine serves as the amino-butyl group donor for the synthesis of hypusine (Nε-[4-amino-2-hydroxybutyl]-lysine) at a specific lysine residue of the eukaryotic translation initiation factor 5A (eIF5A). Here, we show that in the Drosophila brain, hypusinated eIF5A levels decline with age but can be boosted by dietary spermidine. Several genetic regimes of attenuating eIF5A hypusination all similarly affect brain mitochondrial respiration resembling age-typical mitochondrial decay and also provoke a premature aging of locomotion and memory formation in adult Drosophilae. eIF5A hypusination, conserved through all eukaryotes as an obviously critical effector of spermidine, might thus be an important diagnostic and therapeutic avenue in aspects of brain aging provoked by mitochondrial decline."],["dc.identifier.doi","10.1016/j.celrep.2021.108941"],["dc.identifier.pmid","33852845"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/113058"],["dc.identifier.url","https://for2705.de/literature/publications/36"],["dc.language.iso","en"],["dc.relation","FOR 2705: Dissection of a Brain Circuit: Structure, Plasticity and Behavioral Function of the Drosophila Mushroom Body"],["dc.relation","FOR 2705 | TP 5: Postsynaptic receptor plasticity and transsynaptic communication in storage of memory components in the mushroom bodies"],["dc.relation.eissn","2211-1247"],["dc.relation.workinggroup","RG Sigrist (Genetics)"],["dc.rights","CC BY-NC-ND 4.0"],["dc.title","eIF5A hypusination, boosted by dietary spermidine, protects from premature brain aging and mitochondrial dysfunction"],["dc.type","journal_article"],["dc.type.internalPublication","no"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]