Orchestrating morphogenesis: building the body plan by cell shape changes and movements

Perez-Vale, Kia Z.; Peifer, Mark

doi:10.1242/dev.191049

Cited by 58 publications

(51 citation statements)

References 211 publications

(241 reference statements)

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“…Adherens junctions play a critical role in supporting many physiological processes, including collective cell migration (51) and morphogenesis (52). Clearly, such biological systems could be analyzed using our framework to provide mechanistic insight into their dependence on the crosstalk between active contractility and actin polymerization.…”

Section: Discussionmentioning

confidence: 99%

Modeling the three-way feedback between cellular contractility, actin polymerization, and adhesion turnover resolves the contradictory effects of RhoA and Rac1 on endothelial junction dynamics

McEvoy

Sneh

Moeendarbary

et al. 2021

Preprint

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The formation and recovery of gaps in the vascular endothelium governs a wide range of physiological and pathological phenomena, from angiogenesis to atherosclerosis and tumor cell extravasation. However, the interplay between the mechanical and signaling processes that drive dynamic behavior in vascular endothelial cells is not well understood. In this study, we propose a chemo-mechanical model to investigate the maintenance of endothelial junctions as dependent on the crosstalk between actomyosin contractility, VE-cadherin bond turnover, and actin polymerization, which mediate the forces exerted on the cell-cell interface. Our theoretical model reveals that active cell tension can stabilize cadherin bonds within an adhesion, but excessive RhoA signaling can drive bond dissociation and junction failure. While Rac1-mediated actin polymerization aids gap closure, high levels of Rac1 may also facilitate junction weakening. Combining the modeling framework with novel experiments, we identify how dynamic rupture and heal cycles emerge and, further, describe why gaps tend to localize at multi-cell contacts. Beyond, our analysis also indicates that a critical balance between RhoA and Rac1 expression is required to maintain junction stability and limit endothelial dysfunction. The model predicts how pharmacological modulation of actin polymerization and cell contractility impacts junction stability, with predictions subsequently validated experimentally. Our proposed framework can help guide the development of therapeutics that target the Rho family of GTPases and downstream active mechanical processes.

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Section: Discussionmentioning

confidence: 99%

Modeling the three-way feedback between cellular contractility, actin polymerization, and adhesion turnover resolves the contradictory effects of RhoA and Rac1 on endothelial junction dynamics

McEvoy

Sneh

Moeendarbary

et al. 2021

Preprint

View full text Add to dashboard Cite

show abstract

“…The decreasing area is compensated or promoted by the movement of the adjacent epidermis. Given several recent excellent reviews on the role of the amnioserosa cells ( Hayes and Solon, 2017 ; Kiehart et al, 2017 ; Perez-Vale and Peifer, 2020 ), we will focus on the surrounding epidermis for the closure process in the following paragraphs.…”

Section: Dorsal Closurementioning

confidence: 99%

Planar Cell Polarity and E-Cadherin in Tissue-Scale Shape Changes in Drosophila Embryos

Kong

Großhans

2020

Front. Cell Dev. Biol.

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Planar cell polarity and anisotropic cell behavior play critical roles in large-scale epithelial morphogenesis, homeostasis, wound repair, and regeneration. Cell–Cell communication and mechano-transduction in the second to minute scale mediated by E-cadherin complexes play a central role in the coordination and self-organization of cellular activities, such as junction dynamics, cell shape changes, and cell rearrangement. Here we review the current understanding in the interplay of cell polarity and cell dynamics during body axis elongation and dorsal closure in Drosophila embryos with a focus on E-cadherin dynamics in linking cell and tissue polarization and tissue-scale shape changes.

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“…Apical constriction is a cell shape change in which a cell reduces the size of its apical domain in the epithelium (Perez-Vale and Peifer, 2020;Sawyer et al, 2010). One consequence of apical constriction is cell ingression from the epithelium, a step that is sometimes required for epithelial-to-mesenchymal transition (EMT) (Martin and Goldstein, 2014;Ramkumar et al, 2016;Williams et al, 2012).…”

Section: Introductionmentioning

confidence: 99%

Lmo7 recruits myosin II heavy chain to induce apical constriction in Xenopus ectoderm

Matsuda

Chu

Sokol

2021

Preprint

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The reduction of the apical domain, or apical constriction, is a process that occurs in a single cell or is coordinated in a group of cells in the epithelium. Coordinated apical constriction is particularly important when the epithelium is undergoing dynamic morphogenetic events such as furrow or tube formation. However, the underlying mechanisms remain incompletely understood. Here we show that Lim only protein 7 (Lmo7) is a novel activator of apical constriction in the Xenopus superficial ectoderm, which coordinates actomyosin contractility in a group of cells during epithelial morphogenesis. Like other apical constriction regulators, Lmo7 requires the activation of the Rho-Rock-Myosin II pathway to induce apical constriction. However, instead of increasing the phosphorylation of myosin light chain (MLC), Lmo7 binds muscle myosin II heavy chain A (NMIIA) and increases its association with actomyosin bundles at adherens junctions (AJs). Lmo7 overexpression modulates the subcellular distribution of Wtip, a tension marker at AJs, suggesting that Lmo7 generates mechanical forces at AJs. We propose that Lmo7 increases actomyosin contractility at AJs by promoting the formation of actomyosin bundles.

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Orchestrating morphogenesis: building the body plan by cell shape changes and movements

Cited by 58 publications

References 211 publications

Modeling the three-way feedback between cellular contractility, actin polymerization, and adhesion turnover resolves the contradictory effects of RhoA and Rac1 on endothelial junction dynamics

Modeling the three-way feedback between cellular contractility, actin polymerization, and adhesion turnover resolves the contradictory effects of RhoA and Rac1 on endothelial junction dynamics

Planar Cell Polarity and E-Cadherin in Tissue-Scale Shape Changes in Drosophila Embryos

Lmo7 recruits myosin II heavy chain to induce apical constriction in Xenopus ectoderm

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