Variation in traction forces during cell cycle progression

Vianay, Benoît; Senger, Fabrice; Álamos, Simón; Anjur-Dietrich, Maya; Bearce, Elizabeth; Cheeseman, Bevan L.; Lee, Lisa; Théry, Manuel

doi:10.1101/212472

Cited by 10 publications

(16 citation statements)

References 49 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Cell adhesion complex area increases as cells progress from G1 into S and subsequently decreases as cells enter G2. These changes are supported by recent observations that cellular contractile forces follow the same trend through the cell cycle (Vianay et al, 2018) and therefore suggest a concerted cell cycledependent regulation of adhesion. A central regulator of this process is CDK1 because perturbation of CDK1 results in a loss of cell cycle-dependent adhesion changes.…”

Section: Discussionsupporting

confidence: 82%

Cell adhesion is regulated by CDK1 during the cell cycle

Jones

Askari

Humphries

2018

Journal of Cell Biology

127

139

View full text Add to dashboard Cite

show abstract

Section: Discussionsupporting

confidence: 82%

Cell adhesion is regulated by CDK1 during the cell cycle

Jones

Askari

Humphries

2018

Journal of Cell Biology

127

139

View full text Add to dashboard Cite

show abstract

“…Interestingly, the mechanisms that mediate TEAD and AP1 activation in response to nuclear flattening appear to be independent, but both occur during G1 and promote G1/S transition. While the molecular mechanisms mediating G1 nuclear flattening remain to be identified, it may result from the increasing contractility developed by cells during G1 [44] and/or by the associated adhesion remodeling [45]. Whereas NE fluctuations were reported during cell cycle progression, their consequences on cell growth are unclear [46].…”

Section: Discussionmentioning

confidence: 99%

Nuclear envelope deformation controls cell cycle progression in response to mechanical force

et al. 2019

View full text Add to dashboard Cite

The shape of the cell nucleus can vary considerably during developmental and pathological processes; however, the impact of nuclear morphology on cell behavior is not known. Here, we observed that the nuclear envelope flattens as cells transit from G1 to S phase and inhibition of myosin II prevents nuclear flattening and impedes progression to S phase. Strikingly, we show that applying compressive force on the nucleus in the absence of myosin II ‐mediated tension is sufficient to restore G1 to S transition. Using a combination of tools to manipulate nuclear morphology, we observed that nuclear flattening activates a subset of transcription factors, including TEAD and AP 1, leading to transcriptional induction of target genes that promote G1 to S transition. In addition, we found that nuclear flattening mediates TEAD and AP 1 activation in response to ROCK‐generated contractility or cell spreading. Our results reveal that the nuclear envelope can operate as a mechanical sensor whose deformation controls cell growth in response to tension.

show abstract

“…Therefore, we have demonstrated a role for an active stress generated during interphase or potentially through non cell autonomous behaviors. Cell cycle dependent processes which impact cell adhesion (53), junction tension and cortical mechanics (54, 66) all could give rise to the active stress generation during interphase. Disentangling these effects will be an interesting avenue for future research on cell shape remodeling in epithelia.…”

Section: Discussionmentioning

confidence: 99%

Cell cycle-dependent active stress drives epithelia remodeling

Devany

Sussman

Yamamoto

et al. 2019

Preprint

View full text Add to dashboard Cite

Epithelia have distinct cellular architectures, which are established in development, re-established after wounding, and maintained during tissue homeostasis despite cell turnover and mechanical perturbations. In turn, cell shape also controls tissue function as a regulator of cell differentiation, proliferation, and motility. Here we investigate cell shape changes in a model epithelial monolayer. After the onset of confluence, cells continue to divide and change shape over time, eventually leading to a final steady state characterized by arrested motion and more regular cell shapes. Such monolayer remodeling is robust, with qualitatively similar changes in cell shape and dynamics observed in a variety of conditions. However, quantitative differences in monolayer remodeling dynamics reveal underlying order parameters controlling epithelial architecture. For instance, for monolayers formed atop extracellular matrix with varied stiffness, the cell density varies significantly but the relationship between cell shape and motility remain similar. In contrast, pharmacological perturbations can alter the cell shape at which their motility is arrested. Remarkably, across all of these experimental conditions the final cell shape is well correlated to the cell division rate. Furthermore, inhibition of the cell cycle immediately arrests both cell motility and shape change, demonstrating that active stress from cell divisions contributes significantly to monolayer remodeling. Thus, the architecture and mechanics of epithelial tissue can arise from an interplay between cell mechanics and stresses arising from cell division. Bi D, LopezJH, Schwarz JM, Manning ML (2015) A density-independent rigidity transition in biological tissues. Nat Phys 11(12):1074-1079. 30. Lecuit T, Lenne P-F (2007) Cell surface mechanics and the control of cell shape, tissue patterns and morphogenesis. Nat Rev Mol Cell Biol 8(8):633-644. 31. Bi D, Yang X, Marchetti MC, Manning ML (2016) Motility-driven glass and jamming transitions in biological tissues. Phys Rev X 6(2). 32. Yang X, et al. (2017) Correlating cell shape and cellular stress in motile confluent tissues. Proc Natl Acad Sci U S A 114(48):12663-12668. 33. Ng MR, Besser A, Danuser G, Brugge JS (2012) Substrate stiffness regulates cadherindependent collective migration through myosin-II contractility. J Cell Biol 199(3):545-563. 34. Trepat X, et al. (2009) Physical forces during collective cell migration. Nat Phys 5:426-430. 35. De Pascalis C, et al. (2018) Intermediate filaments control collective migration by restricting traction forces and sustaining cell-cell contacts. J Cell Biol 217(9):3031-3044. 36. Sussman DM (2017) cellGPU: Massively parallel simulations of dynamic vertex models. Comput Phys Commun 219:400-406. 37. Sussman DM, Paoluzzi M, Cristina Marchetti M, Lisa Manning M (2018) Anomalous glassy dynamics in simple models of dense biological tissue. EPL 121(3):36001. 38. Doyle AD, Carvajal N, Jin A, Matsumoto K, Yamada KM (2015) Local 3D matrix microenvironment regulates cell migrat...

show abstract

Variation in traction forces during cell cycle progression

Cited by 10 publications

References 49 publications

Cell adhesion is regulated by CDK1 during the cell cycle

Cell adhesion is regulated by CDK1 during the cell cycle

Nuclear envelope deformation controls cell cycle progression in response to mechanical force

Cell cycle-dependent active stress drives epithelia remodeling

Contact Info

Product

Resources

About