scholarly journals A contractile actomyosin network linked to adherens junctions by Canoe/afadin helps drive convergent extension

2011 ◽  
Vol 22 (14) ◽  
pp. 2491-2508 ◽  
Author(s):  
Jessica K. Sawyer ◽  
Wangsun Choi ◽  
Kuo-Chen Jung ◽  
Li He ◽  
Nathan J. Harris ◽  
...  
Keyword(s):  
Cell Shape ◽  
Shape Change ◽  
Adherens Junction ◽  
Tissue Level ◽  
The Body ◽  
Convergent Extension ◽  
Planar Polarity ◽  
Cell Shape Change ◽  
Apical Polarity ◽  
Polarity Proteins

Integrating individual cell movements to create tissue-level shape change is essential to building an animal. We explored mechanisms of adherens junction (AJ):cytoskeleton linkage and roles of the linkage regulator Canoe/afadin during Drosophila germband extension (GBE), a convergent-extension process elongating the body axis. We found surprising parallels between GBE and a quite different morphogenetic movement, mesoderm apical constriction. Germband cells have an apical actomyosin network undergoing cyclical contractions. These coincide with a novel cell shape change—cell extension along the anterior–posterior (AP) axis. In Canoe's absence, GBE is disrupted. The apical actomyosin network detaches from AJs at AP cell borders, reducing coordination of actomyosin contractility and cell shape change. Normal GBE requires planar polarization of AJs and the cytoskeleton. Canoe loss subtly enhances AJ planar polarity and dramatically increases planar polarity of the apical polarity proteins Bazooka/Par3 and atypical protein kinase C. Changes in Bazooka localization parallel retraction of the actomyosin network. Globally reducing AJ function does not mimic Canoe loss, but many effects are replicated by global actin disruption. Strong dose-sensitive genetic interactions between canoe and bazooka are consistent with them affecting a common process. We propose a model in which an actomyosin network linked at AP AJs by Canoe and coupled to apical polarity proteins regulates convergent extension.

scholarly journals A Putative Catenin–Cadherin System Mediates Morphogenesis of the Caenorhabditis elegans Embryo

1998 ◽  
Vol 141 (1) ◽  
pp. 297-308 ◽  
Author(s):  
Michael Costa ◽  
William Raich ◽  
Cristina Agbunag ◽  
Ben Leung ◽  
Jeff Hardin ◽  
...  
Keyword(s):  
Cell Adhesion ◽  
Caenorhabditis Elegans ◽  
Cell Shape ◽  
Shape Change ◽  
Adherens Junctions ◽  
The Body ◽  
C Elegans ◽  
Cell Shape Change ◽  
Filament Bundles ◽  
Cell Adhesion Proteins

During morphogenesis of the Caenorhabditis elegans embryo, hypodermal (or epidermal) cells migrate to enclose the embryo in an epithelium and, subsequently, change shape coordinately to elongate the body (Priess, J.R., and D.I. Hirsh. 1986. Dev. Biol. 117:156– 173; Williams-Masson, E.M., A.N. Malik, and J. Hardin. 1997. Development [Camb.]. 124:2889–2901). We have isolated mutants defective in morphogenesis that identify three genes required for both cell migration during body enclosure and cell shape change during body elongation. Analyses of hmp-1, hmp-2, and hmr-1 mutants suggest that products of these genes anchor contractile actin filament bundles at the adherens junctions between hypodermal cells and, thereby, transmit the force of bundle contraction into cell shape change. The protein products of all three genes localize to hypodermal adherens junctions in embryos. The sequences of the predicted HMP-1, HMP-2, and HMR-1 proteins are related to the cell adhesion proteins α-catenin, β-catenin/Armadillo, and classical cadherin, respectively. This putative catenin–cadherin system is not essential for general cell adhesion in the C. elegans embryo, but rather mediates specific aspects of morphogenetic cell shape change and cytoskeletal organization.

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 Uncoupling apical constriction from tissue invagination

eLife ◽  
2017 ◽  
Vol 6 ◽  
Author(s):  
SeYeon Chung ◽  
Sangjoon Kim ◽  
Deborah J Andrew
Keyword(s):  
Cell Shape ◽  
Shape Change ◽  
Rho Kinase ◽  
Tissue Level ◽  
Tube Formation ◽  
Intrinsic Properties ◽  
Apical Constriction ◽  
Cell Shape Change ◽  
Polarized Epithelia ◽  
Muscle Myosin

Apical constriction is a widely utilized cell shape change linked to folding, bending and invagination of polarized epithelia. It remains unclear how apical constriction is regulated spatiotemporally during tissue invagination and how this cellular process contributes to tube formation in different developmental contexts. Using Drosophila salivary gland (SG) invagination as a model, we show that regulation of folded gastrulation expression by the Fork head transcription factor is required for apicomedial accumulation of Rho kinase and non-muscle myosin II, which coordinate apical constriction. We demonstrate that neither loss of spatially coordinated apical constriction nor its complete blockage prevent internalization and tube formation, although such manipulations affect the geometry of invagination. When apical constriction is disrupted, compressing force generated by a tissue-level myosin cable contributes to SG invagination. We demonstrate that fully elongated polarized SGs can form outside the embryo, suggesting that tube formation and elongation are intrinsic properties of the SG.

Morphogenetic pattern formation during ascidian notochord formation is regulative and highly robust

Development ◽  
2002 ◽  
Vol 129 (1) ◽  
pp. 1-12 ◽  
Author(s):  
Edwin M. Munro ◽  
Garrett Odell
Keyword(s):  
Confocal Microscopy ◽  
Cell Shape ◽  
Shape Change ◽  
Time Lapse ◽  
Neural Plate ◽  
Convergent Extension ◽  
Complex Interplay ◽  
Cell Stage ◽  
Cell Shape Change ◽  
Global Patterns

The ascidian notochord forms through simultaneous invagination and convergent extension of a monolayer epithelial plate. Here we combine micromanipulation with time lapse and confocal microscopy to examine how notochord-intrinsic morphogenetic behaviors and interactions with surrounding tissues, determine these global patterns of movement. We show that notochord rudiments isolated at the 64-cell stage divide and become motile with normal timing; but, in the absence of interactions with non-notochordal tissues, they neither invaginate nor converge and extend. We find that notochord formation is robust in the sense that no particular neighboring tissue is required for notochord formation. Basal contact with either neural plate or anterior endoderm/lateral mesenchyme or posterior mesoderm are each alone sufficient to ensure that the notochord plate forms and extends a cylindrical rod. Surprisingly, the axis of convergent extension depends on the specific tissues that contact the notochord, as do other patterns of cell shape change, movement and tissue deformation that accompany notochord formation. We characterize one case in detail, namely, embryos lacking neural plates, in which a normal notochord forms but by an entirely different trajectory. Our results show ascidian notochord formation to be regulative in a fashion and to a degree never before appreciated. They suggest this regulative behavior depends on a complex interplay between morphogenetic tendencies intrinsic to the notochord plate and instructive and permissive interactions with surrounding tissues. We discuss mechanisms that could account for these data and what they imply about notochord morphogenesis and its evolution within the chordate phylum.

The role of microtubules in chick blastoderm expansion—a quantitative study using colchicine

Development ◽  
1975 ◽  
Vol 34 (1) ◽  
pp. 265-277
Author(s):  
J. R. Downie
Keyword(s):  
Cell Division ◽  
Cell Shape ◽  
Shape Change ◽  
Cell Sheet ◽  
Cell Movement ◽  
Vitelline Membrane ◽  
General Context ◽  
Chick Blastoderm ◽  
Cell Shape Change ◽  
Cytoplasmic Microtubules

Since their discovery, cytoplasmic microtubules have been much studied in the context of cell movement and cell shape change. Much of the work has used drugs, particularly colchicine and its relatives, which break down microtubules — the so-called anti-tubulins. Colchicine inhibits the orientated movements of many cell types in vitro, and disrupts cell shape change in several morphogenetic situations. The investigation reported here used chick blastoderm expansion in New culture in an attempt to quantify the colchicine effect on orientated cell movement. However, although colchicine could halt blastoderm expansion entirely, a simple interpretation was not possible. (1) Colchicine at concentrations capable of blocking mitosis, and of disrupting all or most of the cytoplasmic microtubules of the cells studied, inhibited blastoderm expansion, often resulting in an overall retraction of the cell sheet. (2) Though blastoderm expansion does normally involve considerable cell proliferation, the colchicine effect could not be ascribed to a block on cell division since aminopterin, which stops cell division without affecting microtubules, did not inhibit expansion. (3) Blastoderm expansion is effected by the locomotion of a specialized band of edge cells at the blastoderm periphery. These are the only cells normally attached to the vitelline membrane — the substrate for expansion. When most of the blastoderm was excised, leaving the band of edge cells, and the cultures then treated with colchicine, expansion occurred normally. The colchicine effect on blastoderm expansion could not therefore be ascribed to a direct effect on the edge cells. (4) An alternative site of action of the drug is the remaining cells of the blastoderm. These normally become progressively flatter as expansion proceeds. If flattening in these cells is even partially dependent on their cytoplasmic microtubules, disruption of these microtubules might result in the inherent contractility of the cells resisting and eventually halting edge cell migration. That cell shape in these cells is dependent on microtubules was demonstrated by treating flat blastoderm fragments with colchicine. On incubation, the area occupied by these fragments decreased by 25–30 % more than controls. The significance of these results in the general context of orientated cell movements and cell shape determination is discussed, with particular emphasis on the analogous system of Fundulus epiboly.

Autonomy and non-autonomy in Drosophila mesoderm determination and morphogenesis

Development ◽  
1994 ◽  
Vol 120 (4) ◽  
pp. 853-859 ◽  
Author(s):  
M. Leptin ◽  
S. Roth
Keyword(s):  
Cell Shape ◽  
Shape Change ◽  
Developmental Program ◽  
Cell Shape Change ◽  
Ventral Furrow ◽  
Large Numbers ◽  
The Individual ◽  
Mutant Cells ◽  
Transplantation Experiments ◽  
Shape Changes

The mesoderm in Drosophila invaginates by a series of characteristic cell shape changes. Mosaics of wild-type cells in an environment of mutant cells incapable of making mesodermal invaginations show that this morphogenetic behaviour does not require interactions between large numbers of cells but that small patches of cells can invaginate independent of their neighbours' behaviour. While the initiation of cell shape change is locally autonomous, the shapes the cells assume are partly determined by the individual cell's environment. Cytoplasmic transplantation experiments show that areas of cells expressing mesodermal genes ectopically at any position in the egg form an invagination. We propose that ventral furrow formation is the consequence of all prospective mesodermal cells independently following their developmental program. Gene expression at the border of the mesoderm is induced by the apposition of mesodermal and non-mesodermal cells.

scholarly journals Tissue tectonics: morphogenetic strain rates, cell shape change and intercalation

2009 ◽  
Vol 6 (6) ◽  
pp. 458-464 ◽  
Author(s):  
Guy B Blanchard ◽  
Alexandre J Kabla ◽  
Nora L Schultz ◽  
Lucy C Butler ◽  
Benedicte Sanson ◽  
...  
Keyword(s):  
Cell Shape ◽  
Shape Change ◽  
Strain Rates ◽  
Cell Shape Change

A dominant inhibitory version of the small GTP-binding protein Rac disrupts cytoskeletal structures and inhibits developmental cell shape changes in Drosophila

Development ◽  
1995 ◽  
Vol 121 (3) ◽  
pp. 903-914 ◽  
Author(s):  
N. Harden ◽  
H.Y. Loh ◽  
W. Chia ◽  
L. Lim
Keyword(s):  
Epidermal Cell ◽  
Cell Shape ◽  
Shape Change ◽  
Yeast Cells ◽  
Cell Shape Change ◽  
Gtp Binding ◽  
Wide Range ◽  
Cell Shape Changes ◽  
Germband Retraction ◽  
Shape Changes

The Rho subfamily of Ras-related small GTP-binding proteins is involved in regulation of the cytoskeleton. The cytoskeletal changes induced by two members of this subfamily, Rho and Rac, in response to growth factor stimulation, have dramatic effects on cell morphology. We are interested in using Drosophila as a system for studying how such effects participate in development. We have identified two Drosophila genes, DRacA and DRacB, encoding proteins with homology to mammalian Rac1 and Rac2. We have made transgenic flies bearing dominant inhibitory (N17DRacA), and wild-type versions of the DRacA cDNA under control of an Hsp70 promoter. Expression of the N17DRacA transgene during embryonic development causes a high frequency of defects in dorsal closure which are due to disruption of cell shape changes in the lateral epidermis. Embryonic expression of N17DRacA also affects germband retraction and head involution. The epidermal cell shape defects caused by expression of N17DRacA are accompanied by disruption of a localized accumulation of actin and myosin thought to be driving epidermal cell shape change. Thus the Rho subfamily may be generating localized changes in the cytoskeleton during Drosophila development in a similar fashion to that seen in mammalian and yeast cells. The Rho subfamily is likely to be participating in a wide range of developmental processes in Drosophila through its regulation of the cytoskeleton.

Sign in / Sign up

Export Citation Format

Share Document