Information flow in the presence of cell mixing and signaling delays during embryonic development

Petrungaro, Gabriela; Morelli, Luis G.; Uriu, Koichiro

doi:10.1016/j.semcdb.2018.09.008

Cited by 28 publications

(21 citation statements)

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“…Collisions of velocity fronts are a consequence of uncorrelated motility primarily caused by time delay in cell response to various mechanical and biochemical stimuli. The delay effects are induced by gene expression (6). Often, one gene regulator controls another, and so on, in a gene regulatory network.…”

Section: Stress Accumulation During the Collision Of Migrating Cell Cmentioning

confidence: 99%

“…Often, one gene regulator controls another, and so on, in a gene regulatory network. Post-translational modification of membrane proteins, such as phosphorylation and glycosylation, may only require a few minutes, whereas synthesis of proteins and their transport can take tens of minutes and influence short-time relaxation cycles (6).…”

Section: Stress Accumulation During the Collision Of Migrating Cell Cmentioning

confidence: 99%

“…A more comprehensive account of main features of: (1) collective cell migration, (2) its influence to viscoelasticity of multicellular systems, and (3) feedback impact of viscoelasticity to cell migration are an essential for a wide range of biological processes such as embryo morphogenesis, wound healing, regeneration, and also in pathological conditions, such as cancer (1)(2)(3)(4)(5)(6). Recent studies suggest that the dynamic tuning of the viscoelasticity within a migratory cluster of cells, and the adequate elastic properties of its surrounding tissues, are essential to allow efficient collective cell migration (2)(3).…”

Section: Introductionmentioning

confidence: 99%

“…Cells communicate with each other via direct contact (juxtacrine signalling), over short distances (paracrine signalling), or over large distances (endocrine signalling). Gene expression induces time delay in cell response to various mechanical and biochemical stimulus (6). This time delay might be relevant for cell coupling because what cells acquire at the present time is the information of surrounding cells some time ago.…”

Section: Introductionmentioning

confidence: 99%

“…They estimated stresses values up to 100-150 Pa. Du Roure et al (13) reported that traction stress per single cells is 2.5-3.8 kPa while the maximal traction stress inside the epithelium is ~12.7 kPa. This result is expectable in the context of the fact that cells 6 are able to generate the stress of 1 kPa per single adherens junction (AJs) between two contractile cells (14). However, the residual stress generation could be more intensive in 3D systems (4).…”

Section: Introductionmentioning

confidence: 99%

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Collective cell migration and residual stress accumulation: modeling consideration

Pajić‐Lijaković

Milivojević

2019

Preprint

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Collective cell migration induces a local generation of stress (normal and shear) significant even in . Cells well tolerate compressive stress up to a few kPa. However, shear stress of a few Pa can induce severe damage to vimentin and keratin intermediate filament networks during 1 h, while shear stress of ~60 can cause the inflammation in epithelial cells during 5.5 h. Deeper insight into cell strategy to minimize undesirable shear stress is a priority in order to understand various biological processes. Cell strategy should be connected with the type and distribution of adhesion contacts such as adherens junctions and tight junctions per migrating clusters and surrounding perturbed boundary layers. 3 Abstract Stress generation during collective cell migration represents one of the key factors which influence the configuration of migrating cells, viscoelasticity of multicellular systems and their inter-relation. Local generation of stress (normal and shear) is significant even in 2D (up to ~100 − 150 ). Compressive stress is primarily accumulated (1) within a core region of migrating cell clusters during their movement through the dense environment and (2) during the collisions of migrating cell clusters caused by uncorrelated motility. Shear stress can be significant within perturbed boundary layers around migrating clusters. Cells are more sensitive to the action of shear stress compared with compressive stress. Shear stress of a few Pa significantly influences cell state. Deeper insight into cell strategy to minimize undesirable shear stress is a priority in order to understand various biological processes such as morphogenesis, wound healing and cancer invasion. We pointed out to cause-consequence relations of these complex phenomena based on rheological modeling consideration in order to stimulate further experimental work.Cell strategy should be connected with the type and distribution of adhesion contacts such as adherens junctions and tight junctions per migrating clusters in order to (1) reinforce the cluster structure perpendicular to the direction of cell migration and (2) ensure structural elasticity of cluster in the direction of migration. These conditions lead to the stiffness inhomogeneity per single migrating clusters. Cell strategy should also be related to the state of the perturbed boundary layer around the cluster in the context of its thickness and slip effects.

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Section: Stress Accumulation During the Collision Of Migrating Cell Cmentioning

confidence: 99%

Section: Stress Accumulation During the Collision Of Migrating Cell Cmentioning

confidence: 99%