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Brinas-Pascual, N.

Publications and source records attributed to Brinas-Pascual, N..

2 recordsLinked to original sources

Emergence of travelling wave patterns in resource-mediated tissue competition

The study of tissue dynamics has been stimulated during the last decades thanks to the use of quantitative descriptions, with the development of several theoretical and computational frameworks, many of them revolving around the notion of reaction-diffusion systems, eventually with additional structure variables beyond time and space. The use of structure variables can accommodate phenotypic traits. In this work, we study a family of competition models, where a given population depends on a resource (e.g. oxygen) and several populations are competing for it. Our quantitative description incorporates phenotypic traits and heterogeneity at the level of cell cycle variations, which influence replication rates via oxygen consumption. This enables us to replicate the fitness of specific subpopulations to environmental conditions (e.g. oxygen shortage or external influences). Using numerical simulations, we show that such models display dynamical pattern formation in the form of coupled travelling wave profiles that expand or retreat at the same wave speed. The full theoretical analysis of such dynamics is quite involved; to circumvent this difficulty, we introduce a quasi-stationary approximation for the resource dynamics. We find that this approximation can reproduce the overall behaviour very accurately, with the additional benefit of allowing theoretical treatment of the reduced model. In this way, we provide estimates on the wave speed which are numerically shown to be robust across a wide range of macroscopic parameters of the full model. The wave speeds are thus found to depend strongly on the proliferation rate of the fittest population, resembling a winner-takes-all dynamics.

biophysics↗

Spatial clustering of adhesion-deficient cells controlsepithelial rigidity transitions

Epithelial tissues maintain mechanical integrity through a balance between cell-cell adhesion and cortical contractility. Disruption of E-cadherin-mediated adhesion is a hallmark of epithelial-mesenchymal transition and cancer progression; yet how local adhesion defects propagate to tissue-scale mechanical changes remains poorly understood. Here, we use a two-dimensional vertex model (varying mutant cell fraction, spatial arrangement, and initial tissue disorder) to investigate how adhesion-deficient cells regulate epithelial mechanics. We show that increasing the fraction of mutant cells drives the tissue towards geometric signatures associated with reduced mechanical rigidity, characterised by elevated cellular shape index and increased prevalence of non-hexagonal cells. Crucially, spatial organisation acts as an independent structural variable that modulates tissue mechanics beyond mutant fraction alone. For identical mutant fractions, randomly distributed mutants undergo rapid, spatially isolated T2-mediated removal events producing only transient shape-index perturbations. Clustered mutants, by contrast, undergo sequential boundary removal, delaying elimination and sustaining elevated shape index in the surrounding tissue. This persistent elevation induces topological disorder within the local neighbourhood that outlasts mutant clearance itself. Our results establish spatial organisation as a key determinant of epithelial rigidity transitions, with implications for understanding early-stage cancer progression.

biophysics↗