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Full-length TDP-43 and its C-terminal domain form filaments <i>in vitro</i> having non-amyloid properties

Claudia Capitini, Giulia Fani, Mirella Vivoli, Amanda Penco, Claudio Canale, Lisa D. Cabrita, Martino Calamai, John Christodoulou, Annalisa Relini, Fabrizio Chiti

2020Amyloid17 citationsDOIOpen Access PDF

Abstract

Accumulation of ubiquitin-positive, tau- and α-synuclein-negative intracellular inclusions of TDP-43 in the central nervous system represents the major hallmark correlated to amyotrophic lateral sclerosis (ALS) and frontotemporal lobar degeneration with ubiquitin-positive inclusions (FTLD-U). Such inclusions have variably been described as amorphous aggregates or more structured deposits having amyloid properties. Here we have purified full-length TDP-43 (FL TDP-43) and its C-terminal domain (Ct TDP-43) to investigate the morphological, structural and tinctorial features of aggregates formed in vitro by them at pH 7.4 and 37 °C. AFM images indicate that both protein variants show a tendency to form filaments. Moreover, we show that both FL TDP-43 and Ct TDP-43 filaments possess a largely disordered secondary structure, as ascertained by far-UV circular dichroism and Fourier transform infra-red spectroscopy, do not bind Congo red and induce a very weak increase of thioflavin T fluorescence, indicating the absence of a clear amyloid-like signature.

Topics & Concepts

ThioflavinFrontotemporal lobar degenerationCongo redAmyloid (mycology)BiophysicsCircular dichroismUbiquitinIn vitroChemistryAmyotrophic lateral sclerosisCrystallographyC-terminusBiologyBiochemistryPathologyAlzheimer's diseaseFrontotemporal dementiaMedicineDementiaGeneAmino acidAdsorptionOrganic chemistryDiseaseInorganic chemistryAmyotrophic Lateral Sclerosis ResearchParkinson's Disease Mechanisms and TreatmentsAlzheimer's disease research and treatments
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