TY - JOUR
AU - Riemenschneider, Henrick
AU - Guo, Qiang
AU - Bader, Jakob
AU - Frottin, Frédéric
AU - Farny, Daniel
AU - Kleinberger, Gernot
AU - Haass, Christian
AU - Mann, Matthias
AU - Hartl, F Ulrich
AU - Baumeister, Wolfgang
AU - Hipp, Mark S
AU - Meissner, Felix
AU - Fernández-Busnadiego, Rubén
AU - Edbauer, Dieter
TI - Gel-like inclusions of C-terminal fragments of TDP-43 sequester stalled proteasomes in neurons.
JO - EMBO reports
VL - 23
IS - 6
SN - 1469-221X
CY - Hoboken, NJ [u.a.]
PB - Wiley
M1 - DZNE-2022-00611
SP - e53890
PY - 2022
N1 - (CC BY)
AB - Aggregation of the multifunctional RNA-binding protein TDP-43 defines large subgroups of amyotrophic lateral sclerosis and frontotemporal dementia and correlates with neurodegeneration in both diseases. In disease, characteristic C-terminal fragments of 25 kDa ('TDP-25') accumulate in cytoplasmic inclusions. Here, we analyze gain-of-function mechanisms of TDP-25 combining cryo-electron tomography, proteomics, and functional assays. In neurons, cytoplasmic TDP-25 inclusions are amorphous, and photobleaching experiments reveal gel-like biophysical properties that are less dynamic than nuclear TDP-43. Compared with full-length TDP-43, the TDP-25 interactome is depleted of low-complexity domain proteins. TDP-25 inclusions are enriched in 26S proteasomes adopting exclusively substrate-processing conformations, suggesting that inclusions sequester proteasomes, which are largely stalled and no longer undergo the cyclic conformational changes required for proteolytic activity. Reporter assays confirm that TDP-25 impairs proteostasis, and this inhibitory function is enhanced by ALS-causing TDP-43 mutations. These findings support a patho-physiological relevance of proteasome dysfunction in ALS/FTD.
KW - Amyotrophic Lateral Sclerosis: genetics
KW - Amyotrophic Lateral Sclerosis: metabolism
KW - DNA-Binding Proteins: genetics
KW - DNA-Binding Proteins: metabolism
KW - Frontotemporal Dementia: genetics
KW - Frontotemporal Dementia: metabolism
KW - Humans
KW - Inclusion Bodies: metabolism
KW - Neurons: metabolism
KW - Peptide Fragments: genetics
KW - Peptide Fragments: metabolism
KW - Proteasome Endopeptidase Complex: metabolism
KW - ALS (Other)
KW - TDP-43 (Other)
KW - neurodegeneration (Other)
KW - phase separation (Other)
KW - proteasome (Other)
LB - PUB:(DE-HGF)16
C2 - pmc:PMC9171420
C6 - pmid:35438230
DO - DOI:10.15252/embr.202153890
UR - https://pub.dzne.de/record/163937
ER -