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

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.

2014 ◽  
Vol 107 (4) ◽  
pp. 998-1010 ◽  
Author(s):  
Oleg Polyakov ◽  
Bing He ◽  
Michael Swan ◽  
Joshua W. Shaevitz ◽  
Matthias Kaschube ◽  
...  

2014 ◽  
Vol 206 (3) ◽  
pp. 435-450 ◽  
Author(s):  
Claudia G. Vasquez ◽  
Mike Tworoger ◽  
Adam C. Martin

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.


2017 ◽  
Vol 372 (1720) ◽  
pp. 20150513 ◽  
Author(s):  
Guy B. Blanchard

Computer-assisted tracking of the shapes of many cells over long periods of development has driven the exploration of novel ways to quantify the contributions of different cell behaviours to morphogenesis. A handful of similar methods have now been published that are used to calculate tissue deformations (strain rates) in epithelia. These methods are further used to quantify strain rates attributable to each of the cell behaviours in the tissue, such as cell shape change, cell rearrangement and cell division, that together sum to the tissue strain rates. In this review, aimed at developmental biologists, I will introduce the general approach, characterize differences in current approaches and highlight extensions of these methods that remain to be fully explored. The methods will make a major contribution to the emerging field of tissue mechanics. Precisely quantified strain rates are an essential first step towards exploring constitutive equations relating stress to strain via tissue mechanical properties. This article is part of the themed issue ‘Systems morphodynamics: understanding the development of tissue hardware’.


2011 ◽  
Vol 22 (14) ◽  
pp. 2491-2508 ◽  
Author(s):  
Jessica K. Sawyer ◽  
Wangsun Choi ◽  
Kuo-Chen Jung ◽  
Li He ◽  
Nathan J. Harris ◽  
...  

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.


eLife ◽  
2017 ◽  
Vol 6 ◽  
Author(s):  
SeYeon Chung ◽  
Sangjoon Kim ◽  
Deborah J Andrew

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.


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