arXiv subjects

Cristina Martinez-Torres

Publications and source records attributed to Cristina Martinez-Torres.

5 recordsLinked to original sources

arXiv2025

Nonlinear Filtering and Spatial Asymptotic Consistency for SPDEs Observed via Spatio-Temporal Point Processes

In this paper, we develop the mathematical framework for filtering problems arising from biophysical applications where data is collected from confocal laser scanning microscopy recordings of the space-time evolution of intracellular wave dynamics of biophysical quantities. In these applications, signals are described by stochastic partial differential equations (SPDEs) and observations can be modelled as functionals of marked point processes whose intensities depend on the underlying signal. We derive both the unnormalized and normalized filtering equations for these systems, demonstrate the asymptotic consistency and approximations of finite dimensional observation schemes respectively partial observations. Our theoretical results are validated through extensive simulations using synthetic and real data. These findings contribute to a deeper understanding of filtering with point process observations and provide a robust framework for future research in this area.

math.ST↗

arXiv2025

A mass conserved reaction-diffusion system reveals switching between coexisting polar and oscillatory cell motility states

Motile eukaryotic cells display distinct modes of migration that often occur within the same cell type. It remains unclear, however, whether transitions between the migratory modes require changes in external conditions, or whether the different modes are coexisting states that emerge from the underlying signaling network. Using a simplified mass-conserved reaction-diffusion model of small GTPase signaling with F-actin mediated feedback, we uncover a distinct bistable mechanism (involving gradient-like phase-separation and traveling waves) and a regime where a polarized mode of migration coexists with spatiotemporal oscillations; the latter, in larger domains, including in three-dimensional surface geometry, result in disordered patterns even in the absence of noise or shape deformations. Indeed, experimental observations of D. discoideum show that, upon collision with a rigid boundary, cells may switch from polarized to disordered motion.

nlin.PS↗

arXiv2024

Modelling how lamellipodia-driven cells maintain persistent migration and interact with external barriers

Cell motility is fundamental to many biological processes, and cells exhibit a variety of migration patterns. Many motile cell types follow a universal law that connects their speed and persistency, a property that can originate from the intracellular transport of polarity cues due to the global actin retrograde flow. This mechanism was termed the ``Universal Coupling between cell Speed and Persistency"(UCSP). Here we implemented a simplified version of the UCSP mechanism in a coarse-grained ``minimal-cell" model, which is composed of a three-dimensional vesicle that contains curved active proteins. This model spontaneously forms a lamellipodia-like motile cell shape, which is however sensitive and can depolarize into a non-motile form due to random fluctuations or when interacting with external obstacles. The UCSP implementation introduces long-range inhibition, which stabilizes the motile phenotype. This allows our model to describe the robust polarity observed in cells and explain a large variety of cellular dynamics, such as the relation between cell speed and aspect ratio, cell-barrier scattering, and cellular oscillations in different types of geometric confinements.

physics.bio-ph↗

arXiv2023

A minimal physical model for curvotaxis driven by curved protein complexes at the cell's leading edge

Cells often migrate on curved surfaces inside the body, such as curved tissues, blood vessels or highly curved protrusions of other cells. Recent \textit{in-vitro} experiments provide clear evidence that motile cells are affected by the curvature of the substrate on which they migrate, preferring certain curvatures to others, termed ``curvotaxis". The origin and underlying mechanism that gives rise to this curvature sensitivity are not well understood. Here, we employ a ``minimal cell" model which is composed of a vesicle that contains curved membrane protein complexes, that exert protrusive forces on the membrane (representing the pressure due to actin polymerization). This minimal-cell model gives rise to spontaneous emergence of a motile phenotype, driven by a lamellipodia-like leading edge. By systematically screening the behaviour of this model on different types of curved substrates (sinusoidal, cylinder and tube), we show that minimal ingredients and energy terms capture the experimental data. The model recovers the observed migration on the sinusoidal substrate, where cells move along the grooves (minima), while avoiding motion along the ridges. In addition, the model predicts the tendency of cells to migrate circumferentially on convex substrates and axially on concave ones. Both of these predictions are verified experimentally, on several cell types. Altogether, our results identify the minimization of membrane-substrate adhesion energy and binding energy between the membrane protein complexes as key players of curvotaxis in cell migration.

physics.bio-ph↗

arXiv2019

Disorder protects collagen networks from fracture

Collagen forms the structural scaffold of connective tissues in all mammals. Tissues are remarkably resistant against mechanical deformations because collagen molecules hierarchically self-assemble in fibrous networks that stiffen with increasing strain. Nevertheless, collagen networks do fracture when tissues are overloaded or subject to pathological conditions such as aneurysms. Prior studies of the role of collagen in tissue fracture have mainly focused on tendons, which contain highly aligned bundles of collagen. By contrast, little is known about fracture of the orientationally more disordered collagen networks present in many other tissues such as skin and cartilage. Here, we combine shear rheology of reconstituted collagen networks with computer simulations to investigate the primary determinants of fracture in disordered collagen networks. We show that the fracture strain is controlled by the coordination number of the network junctions, with less connected networks fracturing at larger strains. The hierarchical structure of collagen fine-tunes the fracture strain by providing structural plasticity at the network and fiber level. Our findings imply that structural disorder provides a protective mechanism against network fracture that can optimize the strength of biological tissues.

physics.bio-ph↗