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Titolo:
In vivo detection of cytokeratin filament network breakdown in cells treated with the phosphatase inhibitor okadaic acid
Autore:
Strnad, P; Windoffer, R; Leube, RE;
Indirizzi:
Univ Mainz, Dept Anat, D-55128 Mainz, Germany Univ Mainz Mainz Germany D-55128 ainz, Dept Anat, D-55128 Mainz, Germany
Titolo Testata:
CELL AND TISSUE RESEARCH
fascicolo: 2, volume: 306, anno: 2001,
pagine: 277 - 293
SICI:
0302-766X(200111)306:2<277:IVDOCF>2.0.ZU;2-Y
Fonte:
ISI
Lingua:
ENG
Soggetto:
KERATIN INTERMEDIATE FILAMENTS; BRAIN TUMOR-CELLS; GLUCOSE-REGULATED PROTEIN; EPITHELIAL-CELLS; IN-VIVO; EPIDERMAL KERATINS; MOUSE HEPATOCYTES; SIZED FILAMENTS; RAT HEPATOCYTES; MALLORY BODIES;
Keywords:
cytoskeleton; intermediate filament; phosphorylation; green fluorescent protein; time-lapse fluorescence microscopy; cell culture; human;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
88
Recensione:
Indirizzi per estratti:
Indirizzo: Leube, RE Univ Mainz, Dept Anat, Becherweg 13, D-55128 Mainz, Germany UnivMainz Becherweg 13 Mainz Germany D-55128 28 Mainz, Germany
Citazione:
P. Strnad et al., "In vivo detection of cytokeratin filament network breakdown in cells treated with the phosphatase inhibitor okadaic acid", CELL TIS RE, 306(2), 2001, pp. 277-293

Abstract

We have previously described vulva carcinoma-derived A-431 subclone AK13-1, which stably expresses fluorescently labeled cytokeratin filaments (CKFs). Time-lapse fluorescence microscopy of these cells permits the continuous monitoring of the dynamics of the CKF cyloskeleton in vivo. To study mechanisms and principles of CKF disassembly as it occurs, e.g., during mitosis and liver disease, we have treated cells with the phosphatase inhibitor okadaic acid (OA), which induces complete CKF network breakdown within 3-5 h without significantly affecting the organization of the actin- and tubulin-based cytofilaments. In time-lapse movies, we find that the network breakdownstarts at the cell periphery and proceeds toward the cell center, where residual filaments become compacted into a prominent perinuclear ring. The progressing disassembly is paralleled by an increase of diffuse fluorescence throughout the cytoplasm and the appearance of non-filamentous spheroidal aggregates. They are formed in the filament-free cell periphery from non-filamentous precursors and can sometimes be detected in the proximity of desmosomes. Other aggregates are either found in close apposition to CKFs or aregenerated directly from the compacted perinuclear material. Primary granules later fuse, thereby producing structures of considerable size. We show that CKF network breakdown and granule formation rely on metabolic energy and that the continued presence of OA is needed for its completion. We conclude that phosphorylation/dephosphorylation is an important mechanism regulating CKF network dynamics in vivo with far-reaching implications for the understanding of epithelial plasticity and pathology.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 23/09/20 alle ore 06:27:45