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


ABSTRACT: Mitochondrial trafficking deficits have been implicated in the pathogenesis of several neurological diseases, including Alzheimer's disease (AD). The Ser/Thre kinase GSK3? is believed to play a fundamental role in AD pathogenesis. Given that GSK3? substrates include Tau protein, here we studied the impact of GSK3? on mitochondrial trafficking and its dependence on Tau protein. Overexpression of GSK3? 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 GSK3? levels. Furthermore, differences in GSK3? 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.

SUBMITTER: Llorens-Martin M 

PROVIDER: S-EPMC3215736 | biostudies-literature | 2011

REPOSITORIES: biostudies-literature

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GSK3β is involved in the relief of mitochondria pausing in a Tau-dependent manner.

Llorens-Martín María M   López-Doménech Guillermo G   Soriano Eduardo E   Avila Jesús J  

PloS one 20111114 11


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  ...[more]

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