Extracellular Matrix Geometry and Initial Adhesive Position Determine Stress Fiber Network Organization during Cell Spreading

Kassianidou, Elena; Probst, Dimitri; Jäger, Julia; Lee, Stacey; Roguet, Anne-Lou; Schwarz, Ulrich S.; Kumar, Sanjay

doi:10.1016/j.celrep.2019.04.035

Cited by 38 publications

(31 citation statements)

References 69 publications

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“…Previous work has suggested that discrete connections of a peripheral stress fiber to other internal fibers can affect its relaxation pattern after severing (Kassianidou et al, 2017(Kassianidou et al, , 2019. However, the incomplete relaxation pattern of the severed peripheral stress fibers we observed here was not systematically associated with interconnections with internal fibers, as illustrated by the absence of visible fibers connected to the peripheral stress fibers in Figure 2a.…”

Section: Stress Fibers Are Still Under Tension Following Laser Photoacontrasting

confidence: 56%

Stress fibers are embedded in a contractile cortical network

Vignaud

Copos

Leterrier

et al. 2020

Preprint

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Contractile actomyosin networks generate intracellular forces essential for the regulation of cell shape, migration, and cell-fate decisions, ultimately leading to the remodeling and patterning of tissues. Although actin filaments aligned in bundles represent the main source of traction-force production in adherent cells, there is increasing evidence that these bundles form interconnected and interconvertible structures with the rest of the intracellular actin network. In this study, we explored how these bundles are connected to the surrounding cortical network and the mechanical impact of these interconnected structures on the production and distribution of traction forces on the extracellular matrix and throughout the cell. By using a combination of hydrogel micropatterning, traction-force microscopy and laser photoablation, we measured the relaxation of the cellular traction field in response to local photoablations at various positions within the cell. Our experimental results and modeling of the mechanical response of the network revealed that bundles were fully embedded along their entire length in a continuous and contractile network of cortical filaments. Moreover, the propagation of the contraction of these bundles throughout the entire cell was dependent on this embedding. In addition, these bundles appeared to originate from the alignment and coalescence of thin and unattached cortical actin filaments from the surrounding mesh.

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Section: Stress Fibers Are Still Under Tension Following Laser Photoacontrasting

confidence: 56%

Stress fibers are embedded in a contractile cortical network

Vignaud

Copos

Leterrier

et al. 2020

Preprint

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“…We produced cross-shaped FN-micropatterns via microcontact printing, which restrict FA formation to the pattern but still provide a sufficient adhesive area for the spreading of U2OS cells (see methods section for details). U2OS WT and all KO cell lines adapted their shape to the pattern and gained a striking phenotype with concave, inward bent actin arcs that line the cell contour as previously described for various cell types (Figure 2) (Bischofs et al, 2008;Brand et al, 2017;Kassianidou et al, 2019;Labouesse et al, 2015;Tabdanov et al, 2018;Thery et al, 2006). These arcs bridge passivated substrate areas and have a circular shape.…”

Section: Micropatterned Substrates Reveal Distinct Functions Of Nm IImentioning

confidence: 57%

Distinct roles of nonmuscle myosin II isoforms for establishing tension and elasticity during cell morphodynamics

Weißenbruch

Grewe

Hippler

et al. 2020

Preprint

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Nonmuscle myosin II (NM II) is an integral part of essential cellular processes, including adhesion and migration. Mammalian cells express up to three isoforms termed NM IIA, B, and C. We used U2OS cells to create CRISPR/Cas9-based knockouts of all three isoforms and analyzed the phenotypes on homogeneous and micropatterned substrates. We find that NM IIA is essential to build up cellular tension during initial stages of force generation, while NM IIB is necessary to elastically stabilize NM IIA-generated tension. The knockout of NM IIC has no detectable effects. A scale-bridging mathematical model explains our observations by relating actin fiber stability to the molecular rates of the myosin crossbridge cycle. We also find that NM IIA initiates and guides co-assembly of NM IIB into heterotypic minifilaments. We finally use mathematical modeling to explain the different exchange dynamics of NM IIA and B in minifilaments, as measured in FRAP experiments.

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“…Cell attachment is dependent on ECM components such as fibronectin, collagen, or laminin, which allow, for instance, integrin signaling pathways activation [47]. To better understand how the spatial organization of these ECM components influences cell adhesion and spreading, several groups have relied on photolithography microfabrication [48], a high spatial resolution photoprinting process [49,50], which allows the transfer of ECM features of controlled shapes and sizes to a surface or even the creation of nano- and micro-structured patterns (Figure 2A).…”

Section: Use Of Microfabrication and Microfluidic Systems To Enginmentioning

confidence: 99%

Coupling Microfluidic Platforms, Microfabrication, and Tissue Engineered Scaffolds to Investigate Tumor Cells Mechanobiology

et al. 2019

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The tumor microenvironment (TME) is composed of dynamic and complex networks composed of matrix substrates, extracellular matrix (ECM), non-malignant cells, and tumor cells. The TME is in constant evolution during the disease progression, most notably through gradual stiffening of the stroma. Within the tumor, increased ECM stiffness drives tumor growth and metastatic events. However, classic in vitro strategies to study the TME in cancer lack the complexity to fully replicate the TME. The quest to understand how the mechanical, geometrical, and biochemical environment of cells impacts their behavior and fate has been a major force driving the recent development of new technologies in cell biology research. Despite rapid advances in this field, many challenges remain in order to bridge the gap between the classical culture dish and the biological reality of actual tissue. Microfabrication coupled with microfluidic approaches aim to engineer the actual complexity of the TME. Moreover, TME bioengineering allows artificial modulations with single or multiple cues to study different phenomena occurring in vivo. Some innovative cutting-edge tools and new microfluidic approaches could have an important impact on the fields of biology and medicine by bringing deeper understanding of the TME, cell behavior, and drug effects.

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Extracellular Matrix Geometry and Initial Adhesive Position Determine Stress Fiber Network Organization during Cell Spreading

Cited by 38 publications

References 69 publications

Stress fibers are embedded in a contractile cortical network

Stress fibers are embedded in a contractile cortical network

Distinct roles of nonmuscle myosin II isoforms for establishing tension and elasticity during cell morphodynamics

Coupling Microfluidic Platforms, Microfabrication, and Tissue Engineered Scaffolds to Investigate Tumor Cells Mechanobiology

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