Neuronal overexpression of hTDP-43 in Caenorhabditis elegans mimics the cellular pathology commonly observed in TDP-43 proteinopathies
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In Vivo Quantification of Protein Turnover in Aging C. Elegans using Photoconvertible Dendra2
Published on: June 13, 2020
Mandy Koopman1, Lale Güngördü1, Renée I Seinstra1
1European Research Institute for the Biology of Ageing, University of Groningen, University Medical Centre Groningen, The Netherlands.
Abstract:
Inclusions consisting of transactive response DNA-binding protein 43 (TDP-43) are a characteristic feature of amyotrophic lateral sclerosis (ALS). Caenorhabditis elegans has been instrumental in studying the underlying mechanisms of TDP-43 pathology. Here, we extend the possibilities of previous studies by examining a C. elegans model expressing human wild-type TDP-43 ( hTDP-43 ) pan-neuronally. We show that disease-related (hyper)phosphorylation and cytosolic localisation of hTDP-43 are present in hTDP-43 worms and that these features can be enhanced by adjusting the environmental temperature.

