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PMID: 12651870 Published · ppublish English Journal Article Research Support, U.S. Gov't, P.H.S.

Aggresomes protect cells by enhancing the degradation of toxic polyglutamine-containing protein.

Human molecular genetics ·Vol. 12 ·No. 7 ·2003-04-01 ·Pages 749-57

Taylor JP, Tanaka F, Robitschek J, Sandoval CM, Taye A, Markovic-Plese S, Fischbeck KH

Abstract

Expression of misfolded protein in cultured cells frequently leads to the formation of juxtanuclear inclusions that have been termed 'aggresomes'. Aggresome formation is an active cellular response that involves trafficking of the offending protein along microtubules, reorganization of intermediate filaments and recruitment of components of the ubiquitin proteasome system. Whether aggresomes are benevolent or noxious is unknown, but they are of particular interest because of the appearance of similar inclusions in protein deposition diseases. Here we present evidence that aggresomes serve a cytoprotective function and are associated with accelerated turnover of mutant proteins. We show that mutant androgen receptor (AR), the protein responsible for X-linked spinobulbar muscular atrophy, forms insoluble aggregates and is toxic to cultured cells. Mutant AR was also found to form aggresomes in a process distinct from aggregation. Molecular and pharmacological interventions were used to disrupt aggresome formation, revealing their cytoprotective function. Aggresome-forming proteins were found to have an accelerated rate of turnover, and this turnover was slowed by inhibition of aggresome formation. Finally, we show that aggresome-forming proteins become membrane-bound and associate with lysosomal structures. Together, these findings suggest that aggresomes are cytoprotective, serving as cytoplasmic recruitment centers to facilitate degradation of toxic proteins.

MeSH Terms
Autophagy Blotting, Western Cell Line Cell Nucleus/metabolism Cysteine Endopeptidases/metabolism Humans Inclusion Bodies/metabolism Lysosomes/metabolism,ultrastructure Multienzyme Complexes/metabolism Mutation Peptides Proteasome Endopeptidase Complex Protein Folding Protein Transport Proteins/metabolism Receptors, Androgen/genetics Transfection
Chemicals
Multienzyme Complexes Peptides Proteins Receptors, Androgen polyglutamine Cysteine Endopeptidases Proteasome Endopeptidase Complex
Authors & Affiliations
7 authors, click to expand affiliations / ORCID
Taylor J Paul
Neurogenetics Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, 10 Center Drive, Building 10, Room 3B-14, Bethesda, MD 20892-1250, USA. [email protected]
Tanaka Fumiaki
Robitschek Jon
Sandoval C Miguel
Taye Addis
Markovic-Plese Silva
Fischbeck Kenneth H
Article Info
Journal
Human molecular genetics
Abbr.
Hum Mol Genet
ISSN
0964-6906
Published
2003-04-01
Pages
749-57
Language
English
Region
England
NLM ID
9208958
Subset
IM
Grants
NINDS NIH HHS · K22-NS44125-01 · United States
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