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Assembly and positioning of actomyosin rings by contractility and planar cell polarity.

Sehring IM, Recho P, Denker E, Kourakis M, Mathiesen B, Hannezo E, Dong B, Jiang D - Elife (2015)

Bottom Line: Intriguingly, rings always form at the cells' anterior edge before migrating towards the center as contractility increases, reflecting a novel dynamical property of the cortex.We develop a simple model of the physical forces underlying this tug-of-war, which quantitatively reproduces our results.We thus propose a quantitative framework for dissecting the relative contribution of contractility and PCP to the self-assembly and repositioning of cytoskeletal structures, which should be applicable to other morphogenetic events.

View Article: PubMed Central - PubMed

Affiliation: Sars International Centre for Marine Molecular Biology, University of Bergen, Bergen, Norway.

ABSTRACT
The actomyosin cytoskeleton is a primary force-generating mechanism in morphogenesis, thus a robust spatial control of cytoskeletal positioning is essential. In this report, we demonstrate that actomyosin contractility and planar cell polarity (PCP) interact in post-mitotic Ciona notochord cells to self-assemble and reposition actomyosin rings, which play an essential role for cell elongation. Intriguingly, rings always form at the cells' anterior edge before migrating towards the center as contractility increases, reflecting a novel dynamical property of the cortex. Our drug and genetic manipulations uncover a tug-of-war between contractility, which localizes cortical flows toward the equator and PCP, which tries to reposition them. We develop a simple model of the physical forces underlying this tug-of-war, which quantitatively reproduces our results. We thus propose a quantitative framework for dissecting the relative contribution of contractility and PCP to the self-assembly and repositioning of cytoskeletal structures, which should be applicable to other morphogenetic events.

No MeSH data available.


Ring migration in the aimless case.Parameters are  and DOI:http://dx.doi.org/10.7554/eLife.09206.026
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fig17: Ring migration in the aimless case.Parameters are and DOI:http://dx.doi.org/10.7554/eLife.09206.026

Mentions: To model the dynamic of this situation, we consider small stochastic actin fluxes of the order of . The dynamic of length and contractility remains unchanged from the control case. We show on Appendix figure 10 the resulting anterior and posterior lateral domains positions and average filaments velocity. Observe that as are small, we now start from a nearly homogeneous density. When contractility increases, a ring forms in the middle of the cell as observed experimentally. The duration of the ring formation remains unchanged as it is driven by the contractility increase. However, the average filament velocity is considerably lowered. If and are strictly the same, the dynamic of the anterior and posterior fronts are symmetric but a small imbalance (either to the posterior or anterior side) is sufficient to trigger a side to middle migration as in Appendix figure 10 though the density of actin is much more homogeneous then in the control case.10.7554/eLife.09206.026Appendix figure 10.Ring migration in the aimless case.


Assembly and positioning of actomyosin rings by contractility and planar cell polarity.

Sehring IM, Recho P, Denker E, Kourakis M, Mathiesen B, Hannezo E, Dong B, Jiang D - Elife (2015)

Ring migration in the aimless case.Parameters are  and DOI:http://dx.doi.org/10.7554/eLife.09206.026
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4612727&req=5

fig17: Ring migration in the aimless case.Parameters are and DOI:http://dx.doi.org/10.7554/eLife.09206.026
Mentions: To model the dynamic of this situation, we consider small stochastic actin fluxes of the order of . The dynamic of length and contractility remains unchanged from the control case. We show on Appendix figure 10 the resulting anterior and posterior lateral domains positions and average filaments velocity. Observe that as are small, we now start from a nearly homogeneous density. When contractility increases, a ring forms in the middle of the cell as observed experimentally. The duration of the ring formation remains unchanged as it is driven by the contractility increase. However, the average filament velocity is considerably lowered. If and are strictly the same, the dynamic of the anterior and posterior fronts are symmetric but a small imbalance (either to the posterior or anterior side) is sufficient to trigger a side to middle migration as in Appendix figure 10 though the density of actin is much more homogeneous then in the control case.10.7554/eLife.09206.026Appendix figure 10.Ring migration in the aimless case.

Bottom Line: Intriguingly, rings always form at the cells' anterior edge before migrating towards the center as contractility increases, reflecting a novel dynamical property of the cortex.We develop a simple model of the physical forces underlying this tug-of-war, which quantitatively reproduces our results.We thus propose a quantitative framework for dissecting the relative contribution of contractility and PCP to the self-assembly and repositioning of cytoskeletal structures, which should be applicable to other morphogenetic events.

View Article: PubMed Central - PubMed

Affiliation: Sars International Centre for Marine Molecular Biology, University of Bergen, Bergen, Norway.

ABSTRACT
The actomyosin cytoskeleton is a primary force-generating mechanism in morphogenesis, thus a robust spatial control of cytoskeletal positioning is essential. In this report, we demonstrate that actomyosin contractility and planar cell polarity (PCP) interact in post-mitotic Ciona notochord cells to self-assemble and reposition actomyosin rings, which play an essential role for cell elongation. Intriguingly, rings always form at the cells' anterior edge before migrating towards the center as contractility increases, reflecting a novel dynamical property of the cortex. Our drug and genetic manipulations uncover a tug-of-war between contractility, which localizes cortical flows toward the equator and PCP, which tries to reposition them. We develop a simple model of the physical forces underlying this tug-of-war, which quantitatively reproduces our results. We thus propose a quantitative framework for dissecting the relative contribution of contractility and PCP to the self-assembly and repositioning of cytoskeletal structures, which should be applicable to other morphogenetic events.

No MeSH data available.