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Published version

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2011-11-14

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cc-by (c) Llorens Martín et al., 2011
Please use this identifier to cite or link to this item: https://hdl.handle.net/2445/43195

GSK3 is involved in the relief of mitochondria pausing in a tau-dependent manner.

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http://dx.doi.org/10.1371/journal.pone.0027686

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.

Subject

Glicogen, Malaltia de Parkinson, Malalties del sistema nerviós

Subject (English)

Glycogen, Parkinson's disease, Nervous system Diseases

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Articles publicats en revistes (Biologia Cel·lular, Fisiologia i Immunologia)

Citation

LLORENS MARTÍN, M., et al. GSK3 is involved in the relief of mitochondria pausing in a tau-dependent manner. PLoS One. 2011. Vol. 6, num. 11, pags. e27686. ISSN 1932-6203. [consulted: 14 of August of 2026]. Available at: https://hdl.handle.net/2445/43195

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