Differential Contributions of Nonmuscle Myosin II Isoforms and Functional Domains to Stress Fiber Mechanics

Chang, Ching-Wei; Kumar, Sanjay

doi:10.1038/srep13736

Cited by 25 publications

(34 citation statements)

References 54 publications

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“…, 2006; Beach et al. , 2011, 2014; Chang and Kumar, 2015), making it unable to rapidly supply subunits to distal assembling pulses. In addition, different kinases mediating NM2 RLC phosphorylation are spatially segregated in cells (Liang et al.…”

Section: Resultsmentioning

confidence: 99%

Local pulsatile contractions are an intrinsic property of the myosin 2A motor in the cortical cytoskeleton of adherent cells

Baird

Billington

Wang

et al. 2017

MBoC

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Section: Resultsmentioning

confidence: 99%

Local pulsatile contractions are an intrinsic property of the myosin 2A motor in the cortical cytoskeleton of adherent cells

Baird

Billington

Wang

et al. 2017

MBoC

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“…FRAP (Fluorescence Recovery After Photobleaching) analysis of Actin dynamics in stress fibers indicated a faster recovery in CAPZ KO cells (Fig. 1D), and thus a faster actin turnover previously associated to higher levels of Myosin-II activity [43,44]. Analysis of Vinculin dynamics in focal adhesions (FAs) indicated a slower recovery in CAPZ KO cells (Fig.…”

Section: Capzb Limits Actomyosin Contractility In Response To Ecm Mecmentioning

confidence: 88%

F-actin dynamics regulates mammalian organ growth and cell fate maintenance

Pocaterra

Santinon

Romani

et al. 2019

Journal of Hepatology

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Background & Aims In vitro, several data indicate that cell function can be regulated by the mechanical properties of cells and of the microenvironment. Cells measure these features by developing forces via their actomyosin cytoskeleton, and respond accordingly by transducing forces into biochemical signals that instruct cell behavior. Among these, the transcriptional coactivators YAP/TAZ recently emerged as key factors mediating multiple responses to actomyosin contractility. However, whether mechanical cues regulate adult liver tissue homeostasis, and whether this occurs through YAP/TAZ, remains largely unaddressed. Methods & Results Here we show that the F-actin capping protein CAPZ is a critical negative regulator of actomyosin contractility and mechanotransduction. Capzb inactivation alters stress fiber and focal adhesion dynamics leading to enhanced myosin activity, increased cellular traction forces, and increased liver stiffness. In vitro, this rescues YAP from inhibition by a small geometry; in vivo, inactivation of Capzb in the adult mouse liver induces YAP activation in parallel to the Hippo pathway, causing extensive hepatocyte proliferation and leading to striking organ overgrowth. Moreover, Capzb is required for the maintenance of the differentiated hepatocyte state, for metabolic zonation, and for gluconeogenesis. In keeping with changes in tissue mechanics, inhibition of the contractility regulator ROCK, or deletion of the Yap1 mechanotransducer, reverse the phenotypes emerging in Capzb-null livers. Conclusions These results indicate a previously unrecognized role for CAPZ in tuning the mechanical properties of cells and tissues, which is required in hepatocytes for the maintenance of the differentiated hepatocyte state and to regulate organ size. More in general, it indicates for the first time a physiological role of mechanotransduction in maintaining organ homeostasis in mammals.

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“…Despite structural similarities, NMIIA and NMIIB isoforms have been assigned both redundant and specific functions depending on cell types and processes 36 . NMIIA and NMIIB exhibit different ATPase activities and actin-binding properties 37–40 , in addition to their specific C-terminal tails that confer them unique functions 41–43 . These two isoforms can exist as activated monomers in cells, but they can also co-assemble as homotypic and heterotypic filaments 44,45 .…”

Section: Introductionmentioning

confidence: 99%

Myosin II isoforms play distinct roles in adherens junction biogenesis

Heuzé

Sankara

Dang

et al. 2019

Preprint

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29Adherens junction (AJ) assembly under force is essential for many biological processes like 30 epithelial monolayer bending, collective cell migration, cell extrusion and wound healing. The 31 acto-myosin cytoskeleton acts as a major force-generator during the de novo formation and 32 remodelling of AJ. Here, we investigated the role of myosinII isoforms in epithelial junction 33 assembly. Myosin IIA (NMIIA) and Myosin IIB (NMIIB) differentially regulate biogenesis of 34 adherens junction through association with distinct actin networks. Analysis of junction 35 dynamics, actin organization, and mechanical forces of control and knockdown cells for 36 myosins revealed that NMIIA provides the mechanical tugging force necessary for cell-cell 37 junction reinforcement and maintenance. NMIIB is involved in E-cadherin clustering, 38 maintenance of a branched actin layer connecting E-cadherin complexes and perijunctional 39 actin fibres leading to the building-up of anisotropic stress. These data reveal unanticipated 40 complementary functions of NMIIA and NMIIB in the biogenesis and integrity of AJ. 41 42 Introduction 43 Tissue integrity and plasticity rely on cell-cell adhesion and cell contractility. The formation, 44 remodelling and disassembly of cell-cell adhesions are fundamental events accompanying all 45 stages of morphogenesis, tissue homeostasis and healing. Adherens junctions (AJ) mediated 46 by E-cadherin/catenin complexes are key elements of epithelial cell-cell adhesions and the 47 first ones to assemble upon contact initiation 1-3 . They provide strong mechanical coupling 48 between neighbouring cells through association with the acto-myosin cytoskeleton 4 . 49The assembly of de novo AJ is crucial for cell-cell rearrangement 5,6 , tissue closure 7 and the 50 maintenance of epithelial cell integrity during wound healing or cell extrusion 8-10 . During de 51 novo cell-cell contacts formation, initial contacts between facing lamellipodia induce immediate 52 clustering of cadherin molecules by trans-and cis-oligomerization [11][12][13][14] . Subsequent signalling 53 events involving RhoGTPases trigger local remodelling of the actin cytoskeleton through 54 Arp2/3-or formin-mediated actin polarization in the vicinity of AJs 15-17 . These cytoskeletal 55 rearrangements drive the expansion of cell-cell contacts and inter-cellular adhesion 56 strengthening 2,18,19 . 57Non-muscle Myosin II (NMII) has emerged as a fundamental player in force-generation and 58 force-transmission at AJ both in vitro and in vivo [20][21][22] . NMII is essential for epithelial tissue 59 architecture 23 , epithelial tissue morphogenesis 24 , tissue repair 25,26 and cell extrusion 27 . NMII 60 protects junctions from disassembly during development 28 and provides the mechanical 61 tugging force necessary for AJ reinforcement 29 . In endothelial cells, NMII is recruited early in 62 filopodia-mediated bridge bundles and its activity is required for accumulation of VE-cadherin 63 in nascent AJs 30 . In epithelial cells, NMII favours local...

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Differential Contributions of Nonmuscle Myosin II Isoforms and Functional Domains to Stress Fiber Mechanics

Cited by 25 publications

References 54 publications

Local pulsatile contractions are an intrinsic property of the myosin 2A motor in the cortical cytoskeleton of adherent cells

Local pulsatile contractions are an intrinsic property of the myosin 2A motor in the cortical cytoskeleton of adherent cells

F-actin dynamics regulates mammalian organ growth and cell fate maintenance

Myosin II isoforms play distinct roles in adherens junction biogenesis

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