Llorens-Martín, M;
López-Doménech, G;
Soriano, E;
Avila, J;
(2011)
GSK3β is involved in the relief of mitochondria pausing in a Tau-dependent manner.
PLoS One
, 6
(11)
, Article e27686. 10.1371/journal.pone.0027686.
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Abstract
Mitochondrial trafficking deficits have been implicated in the pathogenesis of several neurological diseases, including Alzheimer's disease (AD). The Ser/Thre kinase GSK3β is believed to play a fundamental role in AD pathogenesis. Given that GSK3β substrates include Tau protein, here we studied the impact of GSK3β on mitochondrial trafficking and its dependence on Tau protein. Overexpression of GSK3β in neurons resulted in an increase in motile mitochondria, whereas a decrease in the activity of this kinase produced an increase in mitochondria pausing. These effects were dependent on Tau proteins, as Tau (-/-) neurons did not respond to distinct GSK3β levels. Furthermore, differences in GSK3β expression did not affect other parameters like mitochondria velocity or mitochondria run length. We conclude that GSK3B activity regulates mitochondrial axonal trafficking largely in a Tau-dependent manner.
| Type: | Article |
|---|---|
| Title: | GSK3β is involved in the relief of mitochondria pausing in a Tau-dependent manner. |
| Location: | United States |
| Open access status: | An open access version is available from UCL Discovery |
| DOI: | 10.1371/journal.pone.0027686 |
| Publisher version: | http://dx.doi.org/10.1371/journal.pone.0027686 |
| Language: | English |
| Additional information: | © 2011 Llorens-Martin et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. This study was funded by grants from the Spanish Ministry of Health (SAF 2006-02424, BFU-2008-03980), the Comunidad de Madrid (SAL/0202/2006), the Fundación M. Botín, the Fundación Caixa Catalunya Obra Social, and an institutional grant from the Fundación R. Areces. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. |
| Keywords: | Animals, Axons, Biological Transport, Cell Survival, Glycogen Synthase Kinase 3, Mice, Mitochondria, Molecular Imaging, tau Proteins |
| UCL classification: | UCL UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Life Sciences UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Life Sciences > Div of Biosciences UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Life Sciences > Div of Biosciences > Neuro, Physiology and Pharmacology |
| URI: | https://discovery.ucl.ac.uk/id/eprint/1332666 |
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