scholarly journals Myosin IIB assembly state determines its mechanosensitive dynamics

2019 ◽  
Vol 218 (3) ◽  
pp. 895-908 ◽  
Author(s):  
Eric S. Schiffhauer ◽  
Yixin Ren ◽  
Vicente A. Iglesias ◽  
Priyanka Kothari ◽  
Pablo A. Iglesias ◽  
...  
Keyword(s):  
Mathematical Modeling ◽  
Cell Shape ◽  
Cellular Response ◽  
Myosin Ii ◽  
3T3 Cells ◽  
Dictyostelium Myosin ◽  
Highly Sensitive ◽  
Key Players ◽  
Nih 3T3 ◽  
Shape Changes

Dynamical cell shape changes require a highly sensitive cellular system that can respond to chemical and mechanical inputs. Myosin IIs are key players in the cell’s ability to react to mechanical inputs, demonstrating an ability to accumulate in response to applied stress. Here, we show that inputs that influence the ability of myosin II to assemble into filaments impact the ability of myosin to respond to stress in a predictable manner. Using mathematical modeling for Dictyostelium myosin II, we predict that myosin II mechanoresponsiveness will be biphasic with an optimum established by the percentage of myosin II assembled into bipolar filaments. In HeLa and NIH 3T3 cells, heavy chain phosphorylation of NMIIB by PKCζ, as well as expression of NMIIA, can control the ability of NMIIB to mechanorespond by influencing its assembly state. These data demonstrate that multiple inputs to the myosin II assembly state integrate at the level of myosin II to govern the cellular response to mechanical inputs.

scholarly journals Myosin-dependent remodeling of adherens junctions protects junctions from Snail-dependent disassembly

2016 ◽  
Vol 212 (2) ◽  
pp. 219-229 ◽  
Author(s):  
Mo Weng ◽  
Eric Wieschaus
Keyword(s):  
Cell Shape ◽  
Adherens Junctions ◽  
Myosin Ii ◽  
Cell Junctions ◽  
Snail Expression ◽  
Quantitative Image ◽  
Early Expression ◽  
Temporally Correlated ◽  
Shape Changes

Although Snail is essential for disassembly of adherens junctions during epithelial–mesenchymal transitions (EMTs), loss of adherens junctions in Drosophila melanogaster gastrula is delayed until mesoderm is internalized, despite the early expression of Snail in that primordium. By combining live imaging and quantitative image analysis, we track the behavior of E-cadherin–rich junction clusters, demonstrating that in the early stages of gastrulation most subapical clusters in mesoderm not only persist, but move apically and enhance in density and total intensity. All three phenomena depend on myosin II and are temporally correlated with the pulses of actomyosin accumulation that drive initial cell shape changes during gastrulation. When contractile myosin is absent, the normal Snail expression in mesoderm, or ectopic Snail expression in ectoderm, is sufficient to drive early disassembly of junctions. In both cases, junctional disassembly can be blocked by simultaneous induction of myosin contractility. Our findings provide in vivo evidence for mechanosensitivity of cell–cell junctions and imply that myosin-mediated tension can prevent Snail-driven EMT.

Second-Site Noncomplementation Identifies Genomic Regions Required for Drosophila Nonmuscle Myosin Function During Morphogenesis

Genetics ◽  
1998 ◽  
Vol 148 (4) ◽  
pp. 1845-1863
Author(s):  
Susan R Halsell ◽  
Daniel P Kiehart
Keyword(s):  
Cell Shape ◽  
Myosin Ii ◽  
Nonmuscle Myosin ◽  
Genetic Screens ◽  
Nonmuscle Myosin Ii ◽  
Cell Shape Changes ◽  
Genomic Regions ◽  
Shape Changes ◽  
Strong Interactors

Abstract Drosophila is an ideal metazoan model system for analyzing the role of nonmuscle myosin-II (henceforth, myosin) during development. In Drosophila, myosin function is required for cytokinesis and morphogenesis driven by cell migration and/or cell shape changes during oogenesis, embryogenesis, larval development and pupal metamorphosis. The mechanisms that regulate myosin function and the supramolecular structures into which myosin incorporates have not been systematically characterized. The genetic screens described here identify genomic regions that uncover loci that facilitate myosin function. The nonmuscle myosin heavy chain is encoded by a single locus, zipper. Contiguous chromosomal deficiencies that represent approximately 70% of the euchromatic genome were screened for genetic interactions with two recessive lethal alleles of zipper in a second-site noncomplementation assay for the malformed phenotype. Malformation in the adult leg reflects aberrations in cell shape changes driven by myosin-based contraction during leg morphogenesis. Of the 158 deficiencies tested, 47 behaved as second-site noncomplementors of zipper. Two of the deficiencies are strong interactors, 17 are intermediate and 28 are weak. Finer genetic mapping reveals that mutations in cytoplasmic tropomyosin and viking (collagen IV) behave as second-site noncomplementors of zipper during leg morphogenesis and that zipper function requires a previously uncharacterized locus, E3.10/J3.8, for leg morphogenesis and viability.

scholarly journals Downregulation of basal myosin‐ II is required for cell shape changes and tissue invagination

2018 ◽  
Vol 37 (23) ◽  
Author(s):  
Daniel Krueger ◽  
Pietro Tardivo ◽  
Congtin Nguyen ◽  
Stefano De Renzis
Keyword(s):  
Cell Shape ◽  
Myosin Ii ◽  
Cell Shape Changes ◽  
Shape Changes

scholarly journals Myosin-II-mediated cell shape changes and cell intercalation contribute to primitive streak formation

2015 ◽  
Vol 17 (4) ◽  
pp. 397-408 ◽  
Author(s):  
Emil Rozbicki ◽  
Manli Chuai ◽  
Antti I. Karjalainen ◽  
Feifei Song ◽  
Helen M. Sang ◽  
...  
Keyword(s):  
Cell Shape ◽  
Myosin Ii ◽  
Primitive Streak ◽  
Cell Shape Changes ◽  
Cell Intercalation ◽  
Shape Changes

scholarly journals Viscoelastic dissipation stabilizes cell shape changes during tissue morphogenesis

2017 ◽  
Author(s):  
R Clément ◽  
C. Collinet ◽  
B. Dehapiot ◽  
T. Lecuit ◽  
P.-F. Lenne
Keyword(s):  
Optical Tweezers ◽  
Cell Shape ◽  
Myosin Ii ◽  
Force Generation ◽  
Tissue Morphogenesis ◽  
Cell Shape Changes ◽  
Cellular Forces ◽  
Transient Forces ◽  
Shape Changes

Tissue morphogenesis relies on the production of active cellular forces. Understanding how such forces are mechanically converted into cell shape changes is essential to our understanding of morphogenesis. Here we use Myosin II pulsatile activity during Drosophila embryogenesis to study how transient forces generate irreversible cell shape changes. Analyzing the dynamics of junction shortening and elongation resulting from Myosin II pulses, we find that long pulses yield less reversible deformations, typically a signature of dissipative mechanics. This is consistent with a simple viscoelastic description, which we use to model individual shortening and elongation events. The model predicts that dissipation typically occurs on the minute timescale, a timescale commensurate with that of force generation by Myosin II pulses. We test this estimate by applying time-controlled forces on junctions with optical tweezers. Our results argue that active junctional deformation is stabilized by dissipation. Hence, tissue morphogenesis requires coordination between force generation and dissipation.

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