Reply to the ‘Comment on “Tensional homeostasis at different length scales” by J. Humphrey and C. Cyron, Soft Matter, 2022, 18, DOI: 10.1039/D1SM01151K’

Soft Matter ◽  
2022 ◽  
Author(s):  
Dimitrije Stamenović ◽  
Michael L. Smith
Keyword(s):  
Soft Matter ◽  
Focal Adhesions ◽  
Living Cells ◽  
Length Scales ◽  
Tensional Homeostasis

In this Reply to the Comment, we discuss data from the literature which show that the idea that tensional homeostasis in focal adhesions (FAs) of living cells exists over “a central range of FAs”, which is promulgated in the Comment, is not tenable.

Comment on “Tensional homeostasis at different length scales” by D. Stamenović and M. L. Smith, Soft Matter, 2021, 17, 10274–10285, DOI: 10.1039/D0SM01911A

Soft Matter ◽  
2022 ◽  
Author(s):  
Jay D. Humphrey ◽  
Christian J. Cyron
Keyword(s):  
Boundary Value Problems ◽  
Soft Matter ◽  
Boundary Value ◽  
Initial Boundary ◽  
Initial Boundary Value Problems ◽  
Length Scales ◽  
Mechanical Homeostasis ◽  
Tensional Homeostasis ◽  
Initial Boundary Value

Assessing potential mechanical homeostasis requires appropriate solutions to the initial-boundary value problems that define the biophysical situation of interest and appropriate definitions of what is meant by homeostasis, including its range.

Patterning of Soft Matter across Multiple Length Scales

2016 ◽  
Vol 26 (16) ◽  
pp. 2609-2616 ◽  
Author(s):  
Pim van der Asdonk ◽  
Hans C. Hendrikse ◽  
Marcos Fernandez-Castano Romera ◽  
Dion Voerman ◽  
Britta E. I. Ramakers ◽  
...  
Keyword(s):  
Soft Matter ◽  
Length Scales ◽  
Multiple Length Scales

scholarly journals Decipher the dynamic coordination between enzymatic activity and structural modulation at focal adhesions in living cells

2014 ◽  
Vol 4 (1) ◽  
Author(s):  
Shaoying Lu ◽  
Jihye Seong ◽  
Yi Wang ◽  
Shiou-chi Chang ◽  
John Paul Eichorst ◽  
...  
Keyword(s):  
Enzymatic Activity ◽  
Focal Adhesions ◽  
Living Cells ◽  
Dynamic Coordination ◽  
Structural Modulation

1. The science of softness

2020 ◽  
pp. 1-18
Author(s):  
Tom McLeish
Keyword(s):  
Scientific Community ◽  
Soft Matter ◽  
Soft Materials ◽  
Visionary Leadership ◽  
Slow Dynamics ◽  
Length Scales ◽  
New Science ◽  
Motion Structure

‘The science of softness’ provides a brief history and overview of soft matter science. The development of soft matter science was propelled by a combination of communication within the scientific community; intrinsic conceptual overlap and commonality; and visionary leadership from a small number of pioneering scientists. Chemistry proved as essential an ingredient to the new science of soft matter as ideas and techniques from physics. The characteristics of soft matter include motion; structure on intermediate length scales; slow dynamics; and universality. Microscopy is the most obvious and direct example of experimental tools applied across the gamut of soft materials.

Force-dependent vinculin binding to talin in live cells: a crucial step in anchoring the actin cytoskeleton to focal adhesions

2014 ◽  
Vol 306 (6) ◽  
pp. C607-C620 ◽  
Author(s):  
Hiroaki Hirata ◽  
Hitoshi Tatsumi ◽  
Chwee Teck Lim ◽  
Masahiro Sokabe
Keyword(s):  
Actin Cytoskeleton ◽  
Focal Adhesions ◽  
Living Cells ◽  
Live Cells ◽  
Mechanical Forces ◽  
Actin Network ◽  
Crucial Step

Mechanical forces play a pivotal role in the regulation of focal adhesions (FAs) where the actin cytoskeleton is anchored to the extracellular matrix through integrin and a variety of linker proteins including talin and vinculin. The localization of vinculin at FAs depends on mechanical forces. While in vitro studies have demonstrated the force-induced increase in vinculin binding to talin, it remains unclear whether such a mechanism exists at FAs in vivo. In this study, using fibroblasts cultured on elastic silicone substrata, we have examined the role of forces in modulating talin-vinculin binding at FAs. Stretching the substrata caused vinculin accumulation at talin-containing FAs, and this accumulation was abrogated by expressing the talin-binding domain of vinculin (domain D1, which inhibits endogenous vinculin from binding to talin). These results indicate that mechanical forces loaded to FAs facilitate vinculin binding to talin at FAs. In cell-protruding regions, the actin network moved backward over talin-containing FAs in domain D1-expressing cells while it was anchored to FAs in control cells, suggesting that the force-dependent vinculin binding to talin is crucial for anchoring the actin cytoskeleton to FAs in living cells.

A Theoretical Model of Stretch-Induced Stress Fiber Remodeling

2008 ◽  
Author(s):  
Roland Kaunas
Keyword(s):  
Focal Adhesion ◽  
Focal Adhesions ◽  
Dynamic Structure ◽  
Cytoskeletal Proteins ◽  
Stress Fibers ◽  
Cell Contractility ◽  
Maximum Stretch ◽  
Tensional Homeostasis ◽  
Tractional Forces ◽  
Actin Stress Fibers

Cyclic stretching of endothelial cells (ECs), such as occurs in arteries during the cardiac cycle, induces ECs and their actin stress fibers to orient perpendicular to the direction of maximum stretch. This perpendicular alignment response is strengthened by increasing the magnitudes of stretch and cell contractility (1). The actin cytoskeleton is a dynamic structure that regulates cell shape changes and mechanical properties. It has been shown that actin stress fibers are ‘prestretched’ under normal, non-perturbed, conditions (2), consistent with the ideas of ‘prestress’ that have motivated tensegrity cell models (3). It has also been shown that ‘tractional forces’ generated by cells at focal adhesions tend to increase proportionately with increasing focal adhesion area, thus suggesting that cells tend to maintain constant the stress borne by a focal adhesion (4). By implication, this suggests that cells try to maintain constant the stress in actin stress fibers. Thus, it seems that cells reorganize or turnover cytoskeletal proteins and adhesion complexes so as to maintain constant a preferred mechanical state. Mizutani et al. (5) referred to this as cellular tensional homeostasis, although they did not suggest a model or theory to account for this dynamic process.

scholarly journals Direct Observation of Catch-Bonds in Focal Adhesions of Living Cells

2012 ◽  
Vol 102 (3) ◽  
pp. 12a
Author(s):  
Navid Bonakdar ◽  
Achim Schilling ◽  
Claus Metzner ◽  
Ben Fabry
Keyword(s):  
Direct Observation ◽  
Focal Adhesions ◽  
Living Cells ◽  
Catch Bonds

Mechanical forces alter zyxin unbinding kinetics within focal adhesions of living cells

2006 ◽  
Vol 207 (1) ◽  
pp. 187-194 ◽  
Author(s):  
Tanmay P. Lele ◽  
Jay Pendse ◽  
Sanjay Kumar ◽  
Matthew Salanga ◽  
John Karavitis ◽  
...  
Keyword(s):  
Focal Adhesions ◽  
Living Cells ◽  
Mechanical Forces

scholarly journals Focal adhesions are hotspots for keratin filament precursor formation

2006 ◽  
Vol 173 (3) ◽  
pp. 341-348 ◽  
Author(s):  
Reinhard Windoffer ◽  
Anne Kölsch ◽  
Stefan Wöll ◽  
Rudolf E. Leube
Keyword(s):  
Focal Adhesions ◽  
Living Cells ◽  
Stress Fibers ◽  
Regulatory Function ◽  
Cell Cortex ◽  
Hairpin Rna ◽  
Actin Turnover ◽  
Keratin Filament ◽  
Short Hairpin ◽  
Multicolor Fluorescence

Recent studies showed that keratin filament (KF) formation originates primarily from sites close to the actin-rich cell cortex. To further characterize these sites, we performed multicolor fluorescence imaging of living cells and found drastically increased KF assembly in regions of elevated actin turnover, i.e., in lamellipodia. Abundant KF precursors (KFPs) appeared within these areas at the distal tips of actin stress fibers, moving alongside the stress fibers until their integration into the peripheral KF network. The earliest KFPs were detected next to actin-anchoring focal adhesions (FAs) and were only seen after the establishment of FAs in emerging lamellipodia. Tight spatiotemporal coupling of FAs and KFP formation were not restricted to epithelial cells, but also occurred in nonepithelial cells and cells producing mutant keratins. Finally, interference with FA formation by talin short hairpin RNA led to KFP depletion. Collectively, our results support a major regulatory function of FAs for KF assembly, thereby providing the basis for coordinated shaping of the entire cytoskeleton during cell relocation and rearrangement.

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