Cognitive Neuroscience | Neurobiology of Disease & Regeneration | Neuronal Signaling Mechanisms | Control of Gene Expression | Cytoskeleton | Alzheimer's, Dementia & Cognitive Neurology | Movement Disorders
The frontotemporal dementia mutation R406W blocks tau’s interaction with the membrane cortex and affects tau distribution in an annexin A2-dependent manner
Anne Gauthier-Kemper, Carina Weissmann, Nataliya Golovyashkina, Zsofia Seboe-Lemke, Gerard Drewes, Volker Gerke, Jürgen J Heinisch, Roland Brandt*
*Corresponding author: Roland Brandt
Department of Neurobiology, University of Osnabrück, Osnabrück, Germany
F1000Posters 2011, 2: 1 (poster) [ENGLISH]
Poster [9.62 MB]
American Society for Cell Biology Annual Meeting 2010 , 11 - 15 Dec 2010, 131
Changes in the distribution and function of the microtubule-associated protein tau comprise histopathological hallmarks of tauopathies such as Alzheimer’s disease (AD), Frontotemporal dementia (FTD) and Parkinsonism linked to chromosome 17 (FTDP-17). In AD, increased phosphorylation contributes to tau pathology, whereas the functional consequence of FTDP-17 tau mutations is not known.
To scrutinize the effect of the frontotemporal dementia R406W mutation, which causes a tauopathy closely reflecting AD, we expressed human wild type and R406W-mutated tau in neuronally differentiated PC12 cells and analyzed their distribution and interaction by subcellular fractionation and live cell imaging using fluorescence photoactivation.
The data indicates that tau´s association with the membrane cortex contributes to its subcellular distribution and the enrichment of tau in the distal axon. They suggest that the pathological effect of the R406W mutation is caused by impaired membrane interaction, which involves annexin A2 as a membrane-cytoskeleton linker.
No relevant conflicts of interest declared.
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