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First published online 8 April 2008
doi: 10.1242/jcs.017665

Journal of Cell Science 121, 1415-1425 (2008)
Published by The Company of Biologists 2008
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Research Article

Dynamics of an F-actin aggresome generated by the actin-stabilizing toxin jasplakinolide

Francisco Lázaro-Diéguez1,2,3, Carmen Aguado4, Eugenia Mato1,2, Yován Sánchez-Ruíz1, Inmaculada Esteban4, Jordi Alberch1,2, Erwin Knecht4 and Gustavo Egea1,2,3,*

1 Departament de Biologia Cel·lular i Anatomia Patològica, Facultat de Medicina, Universitat de Barcelona, E-08036 Barcelona, Spain
2 Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Universitat de Barcelona, E-08036 Barcelona, Spain
3 Institut de Nanociència i Nanotecnologia (IN2UB), Universitat de Barcelona, E-08036 Barcelona, Spain
4 Laboratorio de Biología Celular, Centro de Investigación Príncipe Felipe and CIBERER, E-46013 Valencia, Spain

* Author for correspondence (e-mail: gegea{at}ub.edu)

Accepted 31 January 2008

In this study, we report the formation of several cytoplasmic inclusion bodies composed of filamentous actin (F-actin) and generated by experimental treatments using depolymerizing or stabilizing actin toxins in neuronal and non-neuronal mammalian cell lines. The actin-stabilizing toxin jasplakinolide (Jpk) induced, in a microtubule-dependent manner, a single, large F-actin aggregate, which contained β- and {gamma}-actin, ADF/cofilin, cortactin, and the actin nucleator Arp2/3. This aggregate was tightly associated with the Golgi complex and mitochondria, and was surrounded by vimentin intermediate filaments, microtubules and MAP4. Therefore, the Jpk-induced single, large F-actin aggregate fits the established criteria for being considered an aggresome. Lysosomes and/or autophagic vacuoles, proteasomes and microtubules were found to directly participate in the dissolution of this F-actin aggresome. Finally, the model reported here is simple, highly reproducible and reversible, and it provides an opportunity to test pharmacological agents that interfere with the formation, maintenance and/or disappearance of F-actin-enriched pathological inclusion bodies.

Key words: Actin, Aggresome, Autophagy, Inclusion bodies, Cytoskeleton, Huntingtin, Jasplakinolide, Microtubules, Proteasome






© The Company of Biologists Ltd 2008