title: GSK3β 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 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.
authors: Departmento de Neurobiología Molecular, Centro de Biología Molecular Severo Ochoa, Madrid, Spain.
authors: María
authors: M
authors: Llorens-Martín
authors: Guillermo
authors: G
authors: López-Doménech
authors: Eduardo
authors: E
authors: Soriano
authors: Jesús
authors: J
authors: Avila
mesh_terms: D000818:Animals; D001369:Axons / Q000378:metabolism; D001692:Biological Transport; D002470:Cell Survival; D038362:Glycogen Synthase Kinase 3 / Q000235:genetics / Q000378:metabolism*; D000071679:Glycogen Synthase Kinase 3 beta; D051379:Mice; D008928:Mitochondria / Q000378:metabolism*; D057054:Molecular Imaging; D016875:tau Proteins / Q000378:metabolism*
chemical_list: D016875:tau Proteins; D000071679:Glycogen Synthase Kinase 3 beta; C000605507:Gsk3b protein, mouse; D038362:Glycogen Synthase Kinase 3