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@ARTICLE{Moch:811941,
author = {Moch, Marcin and Windoffer, Reinhard and Schwarz, Nicole
and Pohl, Raphaela and Omenzetter, Andreas and Schnakenberg,
Uwe and Herb, Fabian and Chaisaowong, Kraisorn and Merhof,
Dorit and Ramms, Lena and Fabris, Gloria and Hoffmann, Bernd
and Merkel, Rudolf and Leube, Rudolf E.},
title = {{E}ffects of {P}lectin {D}epletion on {K}eratin {N}etwork
{D}ynamics and {O}rganization},
journal = {PLoS one},
volume = {11},
number = {3},
issn = {1932-6203},
address = {Lawrence, Kan.},
publisher = {PLoS},
reportid = {FZJ-2016-04251},
pages = {e0149106 -},
year = {2016},
abstract = {The keratin intermediate filament cytoskeleton protects
epithelial cells against various types of stress and is
involved in fundamental cellular processes such as
signaling, differentiation and organelle trafficking. These
functions rely on the cell type-specific arrangement and
plasticity of the keratin system. It has been suggested that
these properties are regulated by a complex cycle of
assembly and disassembly. The exact mechanisms responsible
for the underlying molecular processes, however, have not
been clarified. Accumulating evidence implicates the
cytolinker plectin in various aspects of the keratin cycle,
i.e., by acting as a stabilizing anchor at hemidesmosomal
adhesion sites and the nucleus, by affecting keratin
bundling and branching and by linkage of keratins to actin
filament and microtubule dynamics. In the present study we
tested these hypotheses. To this end, plectin was
downregulated by shRNA in vulvar carcinoma-derived A431
cells. As expected, integrin β4- and BPAG-1-positive
hemidesmosomal structures were strongly reduced and
cytosolic actin stress fibers were increased. In addition,
integrins α3 and β1 were reduced. The experiments
furthermore showed that loss of plectin led to a reduction
in keratin filament branch length but did not alter overall
mechanical properties as assessed by indentation analyses
using atomic force microscopy and by displacement analyses
of cytoplasmic superparamagnetic beads using magnetic
tweezers. An increase in keratin movement was observed in
plectin-depleted cells as was the case in control cells
lacking hemidesmosome-like structures. Yet, keratin turnover
was not significantly affected. We conclude that plectin
alone is not needed for keratin assembly and disassembly and
that other mechanisms exist to guarantee proper keratin
cycling under steady state conditions in cultured single
cells.},
cin = {ICS-7},
ddc = {500},
cid = {I:(DE-Juel1)ICS-7-20110106},
pnm = {552 - Engineering Cell Function (POF3-552)},
pid = {G:(DE-HGF)POF3-552},
typ = {PUB:(DE-HGF)16},
UT = {WOS:000372701200017},
doi = {10.1371/journal.pone.0149106},
url = {https://juser.fz-juelich.de/record/811941},
}