scholarly journals Dynamic myosin phosphorylation regulates contractile pulses and tissue integrity during epithelial morphogenesis

2014 ◽  
Vol 206 (3) ◽  
pp. 435-450 ◽  
Author(s):  
Claudia G. Vasquez ◽  
Mike Tworoger ◽  
Adam C. Martin
Keyword(s):  
Cell Shape ◽  
Shape Change ◽  
Epithelial Morphogenesis ◽  
Nonmuscle Myosin ◽  
Apical Constriction ◽  
Tissue Integrity ◽  
Cell Shape Change ◽  
Nonmuscle Myosin Ii ◽  
A Cell ◽  
Coupling Dynamic

Apical constriction is a cell shape change that promotes epithelial bending. Activation of nonmuscle myosin II (Myo-II) by kinases such as Rho-associated kinase (Rok) is important to generate contractile force during apical constriction. Cycles of Myo-II assembly and disassembly, or pulses, are associated with apical constriction during Drosophila melanogaster gastrulation. It is not understood whether Myo-II phosphoregulation organizes contractile pulses or whether pulses are important for tissue morphogenesis. Here, we show that Myo-II pulses are associated with pulses of apical Rok. Mutants that mimic Myo-II light chain phosphorylation or depletion of myosin phosphatase inhibit Myo-II contractile pulses, disrupting both actomyosin coalescence into apical foci and cycles of Myo-II assembly/disassembly. Thus, coupling dynamic Myo-II phosphorylation to upstream signals organizes contractile Myo-II pulses in both space and time. Mutants that mimic Myo-II phosphorylation undergo continuous, rather than incremental, apical constriction. These mutants fail to maintain intercellular actomyosin network connections during tissue invagination, suggesting that Myo-II pulses are required for tissue integrity during morphogenesis.

scholarly journals Apical constriction: A cell shape change that can drive morphogenesis

2010 ◽  
Vol 341 (1) ◽  
pp. 5-19 ◽  
Author(s):  
Jacob M. Sawyer ◽  
Jessica R. Harrell ◽  
Gidi Shemer ◽  
Jessica Sullivan-Brown ◽  
Minna Roh-Johnson ◽  
...  
Keyword(s):  
Cell Shape ◽  
Shape Change ◽  
Apical Constriction ◽  
Cell Shape Change ◽  
A Cell

scholarly journals Triggering a Cell Shape Change by Exploiting Preexisting Actomyosin Contractions

Science ◽  
2012 ◽  
Vol 335 (6073) ◽  
pp. 1232-1235 ◽  
Author(s):  
Minna Roh-Johnson ◽  
Gidi Shemer ◽  
Christopher D. Higgins ◽  
Joseph H. McClellan ◽  
Adam D. Werts ◽  
...  
Keyword(s):  
Cell Shape ◽  
Shape Change ◽  
Cell Shape Change ◽  
A Cell

scholarly journals The Drosophila afadin homologue Canoe regulates linkage of the actin cytoskeleton to adherens junctions during apical constriction

2009 ◽  
Vol 186 (1) ◽  
pp. 57-73 ◽  
Author(s):  
Jessica K. Sawyer ◽  
Nathan J. Harris ◽  
Kevin C. Slep ◽  
Ulrike Gaul ◽  
Mark Peifer
Keyword(s):  
Actin Cytoskeleton ◽  
Cell Shape ◽  
Shape Change ◽  
Adherens Junctions ◽  
Apical Constriction ◽  
Cell Shape Change ◽  
Mediate Cell Adhesion ◽  
Mediate Cell ◽  
Actomyosin Cytoskeleton ◽  
Core Part

Cadherin-based adherens junctions (AJs) mediate cell adhesion and regulate cell shape change. The nectin–afadin complex also localizes to AJs and links to the cytoskeleton. Mammalian afadin has been suggested to be essential for adhesion and polarity establishment, but its mechanism of action is unclear. In contrast, Drosophila melanogaster’s afadin homologue Canoe (Cno) has suggested roles in signal transduction during morphogenesis. We completely removed Cno from embryos, testing these hypotheses. Surprisingly, Cno is not essential for AJ assembly or for AJ maintenance in many tissues. However, morphogenesis is impaired from the start. Apical constriction of mesodermal cells initiates but is not completed. The actomyosin cytoskeleton disconnects from AJs, uncoupling actomyosin constriction and cell shape change. Cno has multiple direct interactions with AJ proteins, but is not a core part of the cadherin–catenin complex. Instead, Cno localizes to AJs by a Rap1- and actin-dependent mechanism. These data suggest that Cno regulates linkage between AJs and the actin cytoskeleton during morphogenesis.

scholarly journals RhoA GTPase inhibition organizes contraction during epithelial morphogenesis

2016 ◽  
Vol 214 (5) ◽  
pp. 603-617 ◽  
Author(s):  
Frank M. Mason ◽  
Shicong Xie ◽  
Claudia G. Vasquez ◽  
Michael Tworoger ◽  
Adam C. Martin
Keyword(s):  
Cell Shape ◽  
Shape Change ◽  
Critical Role ◽  
Central Position ◽  
Nucleotide Exchange ◽  
Apical Constriction ◽  
Cell Contractility ◽  
Rhoa Activity ◽  
Cell Shape Change ◽  
Rhoa Gtpase

During morphogenesis, contraction of the actomyosin cytoskeleton within individual cells drives cell shape changes that fold tissues. Coordination of cytoskeletal contractility is mediated by regulating RhoA GTPase activity. Guanine nucleotide exchange factors (GEFs) activate and GTPase-activating proteins (GAPs) inhibit RhoA activity. Most studies of tissue folding, including apical constriction, have focused on how RhoA is activated by GEFs to promote cell contractility, with little investigation as to how GAPs may be important. Here, we identify a critical role for a RhoA GAP, Cumberland GAP (C-GAP), which coordinates with a RhoA GEF, RhoGEF2, to organize spatiotemporal contractility during Drosophila melanogaster apical constriction. C-GAP spatially restricts RhoA pathway activity to a central position in the apical cortex. RhoGEF2 pulses precede myosin, and C-GAP is required for pulsation, suggesting that contractile pulses result from RhoA activity cycling. Finally, C-GAP expression level influences the transition from reversible to irreversible cell shape change, which defines the onset of tissue shape change. Our data demonstrate that RhoA activity cycling and modulating the ratio of RhoGEF2 to C-GAP are required for tissue folding.

scholarly journals Charting the unknown currents of cellular flows and forces

Development ◽  
2020 ◽  
Vol 147 (24) ◽  
pp. dev186403 ◽  
Author(s):  
Christian Dahmann ◽  
Anne-Kathrin Classen
Keyword(s):  
Cell Shape ◽  
Shape Change ◽  
Tissue Level ◽  
Tissue Mechanics ◽  
Epithelial Morphogenesis ◽  
Mechanical Forces ◽  
Cell Behaviors ◽  
Cell Shape Change ◽  
Active Generation ◽  
Correct Size

ABSTRACTOne of the central questions in developmental biology concerns how cells become organized into tissues of the correct size, shape and polarity. This organization depends on the implementation of a cell's genetic information to give rise to specific and coordinated cell behaviors, including cell division and cell shape change. The execution of these cell behaviors requires the active generation of mechanical forces. However, understanding how force generation is controlled and, importantly, coordinated among many cells in a tissue was little explored until the early 2000s. Suzanne Eaton was one of the pioneers in this emerging field of developmental tissue mechanics. As we briefly review here, she connected the quantitative analysis of cell behaviors with genetic assays, and integrated physical modeling with measurements of mechanical forces to reveal fundamental insights into epithelial morphogenesis at cell- and tissue-level scales.

scholarly journals In vivo embryonic expression of laminin and its involvement in cell shape change in the sea urchin Sphaerechinus granularis

Development ◽  
1987 ◽  
Vol 101 (4) ◽  
pp. 659-671 ◽  
Author(s):  
R.A. McCarthy ◽  
M.M. Burger
Keyword(s):  
Monoclonal Antibody ◽  
Sea Urchin ◽  
Basal Lamina ◽  
Cell Shape ◽  
Shape Change ◽  
Cell Shape Change ◽  
A Cell ◽  
Mesenchyme Cells ◽  
Embryonic Epithelium

Laminin, a component of the embryonic sea urchin basal lamina, is recognized by monoclonal antibody BL1 (Mab BL1). Our results demonstrate that laminin is secreted into the blastcoel at the early blastula stage at a time when the blastomeres undergo a cell shape change and are organized into an epithelium. Laminin is present on the basal surfaces of ectodermal cells and is absent or reduced on migrating primary mesenchyme cells. Microinjection of a monoclonal antibody directed against laminin induces a morphological change in cell shape and a deformation of the embryonic epithelium. Investigation of selected stages of live embryos suggests that the distribution of laminin may be heterogeneous within the basal lamina during early development. The results implicate laminin as a mediator of cell shape change during early morphogenesis.

Sign in / Sign up

Export Citation Format

Share Document