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  ATM phosphorylation of the actin-binding protein drebrin controls oxidation stress-resistance in mammalian neurons and C. elegans

Kreis, P., Gallrein, C., Rojas-Puente, E., Mack, T. G. A., Kroon, C., Dinkel, V., et al. (2019). ATM phosphorylation of the actin-binding protein drebrin controls oxidation stress-resistance in mammalian neurons and C. elegans. Nat Commun, 10(1), 486. doi:10.1038/s41467-019-08420-w.

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Datensatz-Permalink: https://hdl.handle.net/21.11116/0000-0007-EEF7-7 Versions-Permalink: https://hdl.handle.net/21.11116/0000-0007-EEF8-6
Genre: Zeitschriftenartikel

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https://www.ncbi.nlm.nih.gov/pubmed/30700723 (beliebiger Volltext)
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 Urheber:
Kreis, P., Autor
Gallrein, C., Autor
Rojas-Puente, E., Autor
Mack, T. G. A., Autor
Kroon, C., Autor
Dinkel, V., Autor
Willmes, C., Autor
Murk, K., Autor
Tom-Dieck, S., Autor
Schuman, Erin M.1, Autor           
Kirstein, J., Autor
Eickholt, B. J., Autor
Affiliations:
1Synaptic Plasticity Department, Max Planck Institute for Brain Research, Max Planck Society, ou_2461710              

Inhalt

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Schlagwörter: Actins/genetics/*metabolism Alzheimer Disease/genetics/metabolism Amino Acid Motifs Animals Ataxia Telangiectasia Mutated Proteins/genetics/metabolism Caenorhabditis elegans Cells, Cultured Dendritic Spines/genetics/metabolism Female Humans Male Mice Mice, Inbred C57BL Mice, Knockout Neurons/*metabolism Neuropeptides/genetics/*metabolism *Oxidative Stress Phosphorylation Rats Rats, Wistar Reactive Oxygen Species/metabolism
 Zusammenfassung: Drebrin (DBN) regulates cytoskeletal functions during neuronal development, and is thought to contribute to structural and functional synaptic changes associated with aging and Alzheimer's disease. Here we show that DBN coordinates stress signalling with cytoskeletal dynamics, via a mechanism involving kinase ataxia-telangiectasia mutated (ATM). An excess of reactive oxygen species (ROS) stimulates ATM-dependent phosphorylation of DBN at serine-647, which enhances protein stability and accounts for improved stress resilience in dendritic spines. We generated a humanized DBN Caenorhabditis elegans model and show that a phospho-DBN mutant disrupts the protective ATM effect on lifespan under sustained oxidative stress. Our data indicate a master regulatory function of ATM-DBN in integrating cytosolic stress-induced signalling with the dynamics of actin remodelling to provide protection from synapse dysfunction and ROS-triggered reduced lifespan. They further suggest that DBN protein abundance governs actin filament stability to contribute to the consequences of oxidative stress in physiological and pathological conditions.

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 Datum: 2019-02-01
 Publikationsstatus: Erschienen
 Seiten: -
 Ort, Verlag, Ausgabe: -
 Inhaltsverzeichnis: -
 Art der Begutachtung: -
 Identifikatoren: Anderer: 30700723
DOI: 10.1038/s41467-019-08420-w
ISSN: 2041-1723 (Electronic)2041-1723 (Linking)
 Art des Abschluß: -

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Titel: Nat Commun
Genre der Quelle: Zeitschrift
 Urheber:
Affiliations:
Ort, Verlag, Ausgabe: -
Seiten: - Band / Heft: 10 (1) Artikelnummer: - Start- / Endseite: 486 Identifikator: -