This title appears in the Scientific Report :
2022
Please use the identifier:
http://dx.doi.org/10.1101/2021.02.15.431234 in citations.
Please use the identifier: http://hdl.handle.net/2128/33587 in citations.
NECAB2 participates in an endosomal pathway of mitochondrial stress response at striatal synapses
NECAB2 participates in an endosomal pathway of mitochondrial stress response at striatal synapses
Synaptic signaling depends on ATP generated by mitochondria. Due to extensive connectivity, the striatum is especially vulnerable to mitochondrial dysfunction and thus requires efficient mitochondrial quality control and repair. We found that global knockout of the neuronal calcium-binding protein 2...
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Personal Name(s): | Bueno, Diones |
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Dey, Partha Narayan / Schacht, Teresa / Wolf, Christina / Wüllner, Verena / Morpurgo, Elena / Rojas-Charry, Liliana / Sessinghaus, Lena / Leukel, Petra / Sommer, Clemens / Radyushkin, Konstantin / Schäfer, Michael K. E. / Florin, Luise / Gomez-Zepeda, David / Tenzer, Stefan / Baumgart, Jan / Stamm, Paul / Daiber, Andreas / Horta, Guilherme / Nardi, Leonardo / Vasic, Verica / Schmeisser, Michael J. / Hellwig, Andrea / Oskamp, Angela / Bauer, Andreas / Anand, Ruchika / Reichert, Andreas / Ritz, Sandra / Peper, Jonas / Silies, Marion / Frauenknecht, Katrin B. M. / Methner, Axel | |
Contributing Institute: |
Molekulare Organisation des Gehirns; INM-2 |
Published in: | bioRxiv beta (2021) |
Imprint: |
Cold Spring Harbor
Cold Spring Harbor Laboratory, NY
2021
|
DOI: |
10.1101/2021.02.15.431234 |
Document Type: |
Preprint |
Research Program: |
Brain Dysfunction and Plasticity |
Link: |
OpenAccess |
Publikationsportal JuSER |
Please use the identifier: http://hdl.handle.net/2128/33587 in citations.
Synaptic signaling depends on ATP generated by mitochondria. Due to extensive connectivity, the striatum is especially vulnerable to mitochondrial dysfunction and thus requires efficient mitochondrial quality control and repair. We found that global knockout of the neuronal calcium-binding protein 2 (NECAB2) in the mouse causes loss of striatal synapses and behavioral phenotypes related to striatal dysfunction such as reduced motivation and altered sensory gating. Striatal mitochondria from Necab2 knockout mice are more abundant and smaller. They are characterized by increased respiration and superoxide production resulting in oxidative stress. This accumulation of dysfunctional mitochondria is caused by a defective assembly of mitochondria with early endosomes in a pathway that involves the small GTPase Rab5 and its guanine nucleotide exchange factor Alsin/ALS2. NECAB2 therefore participates in an endosomal pathway of mitochondrial stress response and repair important for striatal function. |