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@ARTICLE{Kirchenbchler:10586,
author = {Kirchenbüchler, D. and Born, S. and Kirchgeßner, N. and
Houben, S. and Hoffmann, B. and Merkel, R.},
title = {{S}ubstrate, focal adhesion and actin filaments: {A}
mechanical unit with a weak spot for mechanosensitive
proteins},
journal = {Journal of physics / Condensed matter},
volume = {22},
issn = {0953-8984},
address = {Bristol},
publisher = {IOP Publ.},
reportid = {PreJuSER-10586},
pages = {194109},
year = {2010},
note = {Record converted from VDB: 12.11.2012},
abstract = {Mechanosensing is a vital prerequisite for dynamic
remodeling of focal adhesions and cytoskeletal structures
upon substrate deformation. For example, tissue formation,
directed cell orientation or cell differentiation are
regulated by such mechanosensing processes. Focal adhesions
and the actin cytoskeleton are believed to be involved in
these processes, but where mechanosensing molecules are
located and how elastic substrate, focal adhesions and the
cytoskeleton couple with each other upon substrate
deformation still remains obscure. To approach these
questions we have developed a sensitive method to apply
defined spatially decaying deformation fields to cells
cultivated on ultrasoft elastic substrates and to accurately
quantify the resulting displacements of the actin
cytoskeleton, focal adhesions, as well as the substrate.
Displacement fields were recorded in live cell microscopy by
tracking either signals from fluorescent proteins or marker
particles in the substrate. As model cell type we used
myofibroblasts. These cells are characterized by highly
stable adhesion and force generating structures but are
still able to detect mechanical signals with high
sensitivity. We found a rigid connection between substrate
and focal adhesions. Furthermore, stress fibers were found
to be barely extendable almost over their whole lengths.
Plastic deformation took place only at the very ends of
actin filaments close to focal adhesions. As a result, this
area became elongated without extension of existing actin
filaments by polymerization. Both ends of the stress fibers
were mechanically coupled with detectable plastic
deformations on either site. Interestingly, traction force
dependent substrate deformation fields remained mostly
unaffected even when stress fiber elongations were released.
These data argue for a location of mechanosensing proteins
at the ends of actin stress fibers and describe, except for
these domains, the whole system to be relatively rigid for
tensile strain with a mechanical coupling between the front
and rear end of a cell.},
keywords = {Actin Cytoskeleton: physiology / Animals / Cell Adhesion:
physiology / Cells, Cultured / Fibroblasts: physiology /
Intracellular Signaling Peptides and Proteins: physiology /
Mechanotransduction, Cellular: physiology / Rats / Rats,
Wistar / Intracellular Signaling Peptides and Proteins (NLM
Chemicals) / J (WoSType)},
cin = {IBN-4},
ddc = {530},
cid = {I:(DE-Juel1)VDB802},
pnm = {BioSoft: Makromolekulare Systeme und biologische
Informationsverarbeitung},
pid = {G:(DE-Juel1)FUEK505},
shelfmark = {Physics, Condensed Matter},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:21386436},
UT = {WOS:000277033100012},
doi = {10.1088/0953-8984/22/19/194109},
url = {https://juser.fz-juelich.de/record/10586},
}