@article{21015, abstract = {Early embryo geometry is one of the most invariant species-specific traits, yet its role in ensuring developmental reproducibility and robustness remains underexplored. Here we show that in zebrafish, the geometry of the fertilized egg—specifically its curvature and volume—serves as a critical initial condition triggering a cascade of events that influence development. The embryo geometry guides patterned asymmetric cell divisions in the blastoderm, generating radial gradients of cell volume and nucleocytoplasmic ratio. These gradients generate mitotic phase waves, with the nucleocytoplasmic ratio determining individual cell cycle periods independently of other cells. We demonstrate that reducing cell autonomy reshapes these waves, emphasizing the instructive role of geometry-derived volume patterns in setting the intrinsic period of the cell cycle oscillator. In addition to organizing cell cycles, early embryo geometry spatially patterns zygotic genome activation at the midblastula transition, a key step in establishing embryonic autonomy. Disrupting the embryo shape alters the zygotic genome activation pattern and causes ectopic germ layer specification, underscoring the developmental significance of geometry. Together, our findings reveal a symmetry-breaking function of early embryo geometry in coordinating cell cycle and transcriptional patterning.}, author = {Mishra, Nikhil and Li, Yuting I and Hannezo, Edouard B and Heisenberg, Carl-Philipp J}, issn = {1745-2481}, journal = {Nature Physics}, pages = {139--150}, publisher = {Springer Nature}, title = {{Geometry-driven asymmetric cell divisions pattern cell cycles and zygotic genome activation in the zebrafish embryo}}, doi = {10.1038/s41567-025-03122-1}, volume = {22}, year = {2026}, } @misc{21137, author = {Naik, Suyash}, publisher = {Institute of Science and Technology Austria}, title = {{Data associated with Keratins coordinate tissue spreading }}, doi = {10.15479/AT-ISTA-21137}, year = {2026}, } @article{21275, abstract = {DNA methylation is a primary layer of epigenetic modification that plays a pivotal role in the regulation of development, aging, and cancer. The concurrent activity of opposing enzymes that mediate DNA methylation and demethylation gives rise to a biochemical cycle and active turnover of DNA methylation. While the ensuing biochemical oscillations have been implicated in the regulation of cell differentiation, their functional role and spatiotemporal dynamics are unknown. In this work, we demonstrate that chromatin-mediated coupling between these local biochemical cycles can lead to the emergence of phase-locked domains, regions of locally synchronized turnover activity, whose coarsening is arrested by genomic heterogeneity. We introduce a minimal model based on stochastic oscillators with constrained long-range and nonreciprocal interactions, shaped by the local chromatin organization. Through a combination of analytical theory and stochastic simulations, we predict both the degree of synchronization and the typical size of emergent phase-locked domains. We qualitatively test these predictions using single-cell sequencing data. Our results show that DNA methylation turnover exhibits surprisingly rich spatiotemporal patterns that may be used by cells to control cell differentiation.}, author = {Olmeda, Fabrizio and Gupta, Misha and Bektas, Onurcan and Rulands, Steffen}, issn = {2835-8279}, journal = {PRX Life}, publisher = {American Physical Society}, title = {{Spatiotemporal patterns of active epigenetic turnover}}, doi = {10.1103/89bj-79g5}, volume = {4}, year = {2026}, } @article{21847, abstract = {Analog quantum simulators provide access to many-body dynamics beyond the reach of classical computation. However, extracting physical insights from experimental data is often hindered by measurement noise, limited observables, and incomplete knowledge of the underlying microscopic model. Here, we develop a machine learning approach based on a variational autoencoder (VAE) to analyze interference measurements of tunnel-coupled one-dimensional Bose gases, which realize the sine-Gordon quantum field theory. Trained in an unsupervised manner, the VAE learns a minimal latent representation that strongly correlates with the equilibrium control parameter of the system. Applied to nonequilibrium protocols, the latent space uncovers signatures of frozen-in solitons following rapid cooling, and reveals anomalous postquench dynamics not captured by conventional correlation-based methods. These results demonstrate that generative models can extract physically interpretable variables directly from noisy and sparse experimental data, providing complementary probes of equilibrium and nonequilibrium physics in quantum simulators. More broadly, our work highlights how machine learning can supplement established field-theoretical techniques, paving the way for scalable, data-driven discovery in quantum many-body systems.}, author = {Moller, Frederik Skovbo and Fernández-Fernández, Gabriel and Schweigler, Thomas and De Schoulepnikoff, Paulin and Schmiedmayer, Jörg and Muñoz-Gil, Gorka}, issn = {2643-1564}, journal = {Physical Review Research}, number = {2}, publisher = {American Physical Society}, title = {{Learning minimal representations of many-body physics from snapshots of a quantum simulator}}, doi = {10.1103/r7pj-gl7r}, volume = {8}, year = {2026}, } @article{21899, abstract = {Cell extrusion is an essential mechanism for controlling cell density in epithelial tissues. Another essential element of epithelia is curvature, which is required to achieve complex shapes, like in the lung or intestine. Here, we introduce a three-dimensional bubbly vertex model to study the interplay between extrusion and curvature. We find a generic cellular bulging instability at topological defects, which is much stronger than for standard vertex models. Analyzing cell shapes in three-dimensional imaging data of spherical mouse colon organoids, we infer that pentagonal cells have an increased basal interfacial tension, suggesting that cells at topological defects react to the different force conditions. Using the bubbly vertex model, we show that such basal tensions stabilize against the predicted instability and result in better cell shape control than tissue-scale mechanisms such as lumen pressure and spontaneous curvature. Our theory suggests that epithelial curvature naturally leads to bulged and extrusionlike cell shapes because the interfacial curvature of individual cells at the defects strongly amplifies buckling effected by tissue-scale topological defects in elastic sheets. Our results highlight the complex interplay of forces across scales in three-dimensional tissue organization.}, author = {Drozdowski, Oliver M and Kocameşe-Tamgac𝚤, Büşra and Boonekamp, Kim E. and Boutros, Michael and Schwarz, Ulrich S.}, issn = {2160-3308}, journal = {Physical Review X}, number = {2}, publisher = {American Physical Society}, title = {{Cell bulging and extrusion in a three-dimensional bubbly vertex model for curved epithelial sheets}}, doi = {10.1103/x82g-cq7n}, volume = {16}, year = {2026}, } @unpublished{22276, abstract = {Tissue tension is a key determinant of tissue shape, and its regulation is essential for both morphogenesis and the maintenance of tissue integrity. During zebrafish embryogenesis, the enveloping layer (EVL) – an epithelial monolayer covering the blastoderm – undergoes extensive spreading that is driven by pulling forces exerted at its margin and more than doubles its surface area. Yet whether and how the EVL actively regulates its tissue tension during this process remains unclear. Here, we show that the EVL maintains constant tissue tension while spreading, and that it achieves this by reducing apical cell contractility in response to the same pulling forces that drive its spreading. We identify a mechanosensitive pathway underlying this response, mediated by the scaffold/adaptor protein Kibra regulating the activity of atypical protein kinase C (aPKC) at the apical domain of EVL cells. Under low mechanical stretch, Kibra forms condensates at the base of actin-based apical projections, where it activates Myosin II to increase apical contractility through aPKC downregulation. As mechanical stretch increases, apical projections disassemble, Kibra condensates dissolve, and aPKC activity rises. Elevated aPKC activity in turn reduces apical contractility by reducing Myosin II activity, thereby maintaining constant tissue tension despite increased mechanical stretch. Together, these findings reveal a mechanosensitive mechanism that enables robust adaptation of tissue tension to changing mechanical stretch, ensuring efficient tissue spreading and morphogenesis.}, author = {Hino, Naoya and Kapoor, Tushna and Gubbala, Uday R and Hannezo, Edouard B and Heisenberg, Carl-Philipp J}, keywords = {Epithelial spreading, tissue tension, mechanosensation, aPKC, Kibra, zebrafish}, publisher = {Institute of Science and Technology Austria}, title = {{Apical domain mechanosensation regulates tissue tension homeostasis}}, year = {2026}, } @article{22326, abstract = {In many developmental systems, cells differentiate into a tissue by reading out morphogen concentration fields, a process fundamentally limited by noise. How much can the precision of this process be improved by nonlocal information, e.g., via cell-cell communication? Using a Bayes-optimal framework, we show that positional inference depends crucially on morphogen spatial correlations and on the "structural prior" that encodes the geometry of the cellular lattice performing the readout, thereby determining what a cell can reliably assume about the position of its neighbors when interpreting nonlocal morphogen signals. We derive upper bounds on positional information gain due to nonlocal readout and identify signal processing algorithms that approximate optimal positional inference, as well as simple chemical reaction schemes which implement such algorithms. Our theory suggests that correlational information can be exploited to significantly enhance developmental precision.}, author = {Zhang, Chen Y and Mateu Hoyos, Pablo and Brückner, David and Tkačik, Gašper}, issn = { 1079-7114}, journal = {Physical Review Letters}, publisher = {American Physical Society}, title = {{Nonlocal decoding of positional and correlational information during development}}, doi = {10.1103/mbjk-v4ym}, volume = {137}, year = {2026}, } @article{20670, abstract = {β-Barrel nanopores are involved in crucial biological processes, from ATP export in mitochondria to bacterial resistance, and represent a promising platform for emerging sequencing technologies. However, in contrast to ion channels, the understanding of the fundamental principles governing ion transport through these nanopores remains largely unexplored. Here we integrate experimental, numerical and theoretical approaches to elucidate ion transport mechanisms in β-barrel nanopores. We identify and characterize two distinct nonlinear phenomena: open-pore rectification and gating. Through extensive mutation analysis of aerolysin nanopores, we demonstrate that open-pore rectification is caused by ionic accumulation driven by the distribution of lumen charges. In addition, we provide converging evidence suggesting that gating is controlled by electric fields dissociating counterions from lumen charges, promoting local structural deformations. Our findings establish a rigorous framework for characterizing and understanding ion transport processes in protein-based nanopores, enabling the design of adaptable nanofluidic biotechnologies. We illustrate this by optimizing an aerolysin mutant for computing applications.}, author = {Mayer, Simon and Mitsioni, Marianna Fanouria and Robin, Paul and Van Den Heuvel, Lukas and Ronceray, Nathan and Marcaida, Maria Jose and Abriata, Luciano A. and Krapp, Lucien F. and Anton, Jana S. and Soussou, Sarah and Jeanneret-Grosjean, Justin and Fulciniti, Alessandro and Möller, Alexia and Vacle, Sarah and Feletti, Lely and Brinkerhoff, Henry and Laszlo, Andrew H. and Gundlach, Jens H. and Emmerich, Theo and Dal Peraro, Matteo and Radenovic, Aleksandra}, issn = {1748-3395}, journal = {Nature Nanotechnology}, pages = {116--124}, publisher = {Springer Nature}, title = {{Lumen charge governs gated ion transport in β-barrel nanopores}}, doi = {10.1038/s41565-025-02052-6}, volume = {21}, year = {2026}, } @article{21849, abstract = {The development of complex tissues relies on the precise assignment of cell identity. At the molecular scale, this process depends on the deposition of epigenetic modifications—such as methylation—that are regulated by complex biochemical networks and occur at specific regions on the DNA and chromatin. Here we show that despite the complexity of epigenetic regulation, dynamical scaling and self-similarity of DNA methylation marks emerge in embryonic development. Drawing on single-cell multi-omics experiments, super-resolution microscopy and statistical physics, we demonstrate that these phenomena originate in dynamical feedback between DNA methylation and the formation of nanoscale dynamic chromatin aggregates. These nanoscale processes lead to genome-wide increase in DNA methylation marks following a power law and self-similar correlation functions. Using this framework, we identify methylation patterns that precede gene expression changes in embryonic symmetry breaking. Our work identifies linear sequencing measurements as a laboratory to study mesoscopic biophysical processes in vivo.}, author = {Olmeda, Fabrizio and Lohoff, Tim and Kafetzopoulos, Ioannis and Clark, Stephen J. and Benson, Laura and Santos, Fatima and Krueger, Felix and Walker, Simon and Reik, Wolf and Rulands, Steffen}, issn = {1745-2481}, journal = {Nature Physics}, pages = {931--940}, publisher = {Springer Nature}, title = {{Scaling and self-similarity in the formation of the embryonic epigenome}}, doi = {10.1038/s41567-026-03263-x}, volume = {22}, year = {2026}, } @article{22608, abstract = {For tissues to spread, they must deform while staying intact. How spreading tissues balance flexibility with integrity is not yet well understood. Here, we show that keratin intermediate filaments adapt tissue mechanical resilience to the stresses arising in epithelial tissues during spreading. By analyzing the expansion of the enveloping cell layer (EVL) over the yolk cell in zebrafish embryos in vivo, we find that keratin network maturation in EVL cells is promoted by stresses building up within the spreading tissue. Through genetic interference and tissue rheology experiments, complemented by a vertex model with mechanochemical feedback, we demonstrate that stress-induced keratin network maturation in the EVL increases tissue viscosity, to prevent tissue rupture. Further, keratins are required in the yolk cell for mechanosensitive actomyosin network contraction and flow, the forces pulling the EVL. These dual mechanosensitive functions of keratins enable a balance between pulling force production and EVL mechanical resilience, ensuring uniform and robust tissue spreading.}, author = {Naik, Suyash and Keta, Yann-Edwin and Pranjic-Ferscha, Kornelija and Hannezo, Edouard B and Henkes, Silke and Heisenberg, Carl-Philipp J}, issn = {2041-1723}, journal = {Nature Communications}, publisher = {Springer Nature}, title = {{Keratins coordinate tissue spreading by balancing spreading forces with tissue material properties}}, doi = {10.1038/s41467-026-72366-z}, volume = {17}, year = {2026}, } @misc{22852, abstract = {This Research Data contains supplemental videos for Chapter 4 "Designing bistable nanostructures for target behavior" of my PhD Thesis "Biological functionality without biochemistry: designing nanomachines for target behavior". Supplemental video 1: Video showing the transition pathway of a bistable nanostructure with sphere-based arms, corresponding to the Machine in Scenario 4. Supplemental video 2: Video showing the transition pathway of the Source in Scenario 1. The arm tips change sides during the transition, demonstrating that the arms pass through each other. Supplemental video 3: Video showing the transition pathway of a fully polyhedral hinge structure with unconstrained arms. Note that we only show the ends of the arms. Supplemental video 4: Video showing the transition pathway of the coupled energy-delivery reaction of a Machine (gray) and a Source (blue) nanostructure for the optimized parameters in Scenario 3. Note that we only show the ends of the arms.}, author = {Ehrmann, Andreas}, keywords = {functional nanostructures, bistability, target behavior, transition pathway}, publisher = {Institute of Science and Technology Austria}, title = {{Supplemental videos for Designing bistable nanostructures for target behavior}}, doi = {10.15479/AT-ISTA-22852}, year = {2026}, } @phdthesis{22873, author = {Ehrmann, Andreas}, isbn = {978-3-99078-092-3}, issn = {2663-337X}, keywords = {PhD Thesis, functional nanomachines, biological functionality, nanotechnology, energy delivery, target behavior, dynamics, design principles, optimization, differentiable statistical physics, machine learning}, pages = {168}, publisher = {Institute of Science and Technology Austria}, title = {{Biological functionality without biochemistry: Designing nanomachines for target behavior}}, doi = {10.15479/AT-ISTA-22873}, year = {2026}, } @unpublished{22893, abstract = {Many biological machines function through controlled conformational transitions, yet designing synthetic nanostructures with prescribed dynamical behavior remains a major challenge. Here, we develop a modular inverse-design framework for bistable nanostructures whose function is controlled by an energy profile along a geometric reaction coordinate. Inspired by proteins with rigid domains connected by flexible hinges, we introduce a hinge-arm paradigm in which a small bistable hinge controls the energetics of a conformational transition, while rigid arms map this transition onto the separation between external binding sites. Specifically, we ask which features of a target energy profile can be programmed under different design constraints. We find that the energy barriers and the binding-site separations in the two metastable states can be readily designed, while controlling the location of the transition state or the full shape of the energy profile requires additional design freedom. Using a differentiable design framework, we find that some optimized solutions are numerically inexact but still display the functional behavior for which the target profile was selected, emphasizing the importance of function-based evaluation criteria. These results establish a practical hierarchy of designability for bistable nanostructures and provide a route toward synthetic nanomachines that couple conformational transitions to target behavior.}, author = {Ehrmann, Andreas and Krstić, Marija and Samadzadeh, Sahar and Goodrich, Carl Peter}, booktitle = {arXiv}, title = {{Designing bistable nanostructures for target behavior}}, doi = {10.48550/arXiv.2606.31620}, year = {2026}, } @unpublished{22892, abstract = {Countless biological processes are fueled by energy-rich molecules like ATP and GTP that supply energy with extreme efficiency. However, designing similar energy-delivery schemes from the bottom up, essential for the development of powered nanostructures and other \emph{de novo} machinery, presents a significant challenge: how can an energy-rich structure be stable in solution yet still deliver this energy at precisely the right time? In this paper, we present a purely physical mechanism that solves this challenge, facilitating energy transfer akin to ATP hydrolysis, yet occurring between synthetic nanostructures without any biochemical interactions. This targeted energy delivery is achieved by exploiting a differentiable state-based model to balance the energy profiles that govern the structural transitions in the two nanostructures, creating a coupled relaxation pathway with minimal barriers that facilitates energy delivery. We verify the effectiveness and robustness of this mechanism through Langevin Dynamics simulations, demonstrating that a bath of the high-energy structures can systematically and repeatedly drive the target structure out of equilibrium, enabling it to perform tasks. As the mechanism operates only through explicit physical forces without any biochemistry or internal state variables, our results present generic and far-reaching design principles, setting the stage for the next generation of synthetic nanomachines.}, author = {Ehrmann, Andreas and Goodrich, Carl Peter}, booktitle = {arXiv}, title = {{Controlling energy delivery with bistable nanostructures}}, doi = {10.48550/arXiv.2506.14266}, year = {2026}, } @article{22963, abstract = {Although studies of tumor invasion have mainly emphasized the evolution of genetic and epigenetic heterogeneity, cellular behaviors also depend on the physical microenvironment. Yet, the tumor microenvironment is both complex and continuously remodeled, making it hard to rigorously test its causal influence on tumor dissemination. Here, we adopted a reductionist approach to studying tumor cell invasion in microengineered environments of tunable patterned geometries. We find that not only the presence of obstacles but more unexpectedly their spatial disorder causes a drastic shift from a collective to a single-cell mode of invasion—comparable in strength to loss of cell-cell adhesion. Combining live-imaging and perturbation experiments with minimal biophysical modeling, we demonstrate that cell dissemination results both from local geometrical constraints and a global integration of spatial disorder over time. We identify generic universality classes of invasion dynamics dependent on environmental geometry, enabling us to identify quantitative physical principles for tumor dissemination.}, author = {Dunajova, Zuzana and Tasciyan, Saren and Majek, Juraj and Merrin, Jack and Jenkins, Robert P. and Sahai, Erik and Sixt, Michael K and Hannezo, Edouard B}, issn = {2375-2548}, journal = {Science Advances}, number = {37}, publisher = {AAAS}, title = {{Substrate heterogeneity promotes cancer cell dissemination through interface roughening}}, doi = {10.1126/sciadv.aed0587}, volume = {12}, year = {2026}, } @phdthesis{21423, abstract = {Biological systems, such as cytoskeletal filaments and multicellular collectives, exhibit rich self-organization driven by their intrinsic activity and physical constraints. Across scales, geometry plays a central role: the shape of active units and the structure of their environment strongly influence how order emerges in these far-from-equilibrium systems. In this thesis, we combine minimal active-matter models with bottom-up in vitro experiments to identify the principles by which geometry and activity shape collective behavior in biological matter. At the subcellular scale, we investigate how the physical properties of chiral FtsZ filaments govern their large-scale organization. Using a mesoscopic model validated by reconstituted filament assays, we show that filament shape, intrinsic curvature, and flexibility, together with activity-driven straightening, determine whether filaments form chiral rings, polar bands, or nematic-like states. Our model shows that small changes in filament mechanics produce large shifts in collective structures, revealing how the geometry of individual filaments amplifies through activity to control patterns relevant for bacterial cytokinesis. At the cellular scale, we examine how geometry of the external environment influences collective cancer cell migration. Experiments in controlled microfabricated obstacle environments demonstrate that geometric disorder alone can induce a transition from collective to single-cell invasion. A minimal model of active particles in disordered geometries reproduces these effects, demonstrating that cell dissemination results both from local geometrical constraints and a global integration of spatial disorder over time. Surprisingly, this transition is accompanied by a change in the universality class of interface dynamics, revealing that cell-environment interactions can shift the collective behavior of an invasive front purely through mechanics. In the last system, we study how cell-intrinsic geometry and chirality affect collective motion in confined and unconfined settings. Using a minimal model inspired by in vitro experiments, we analyze motile cells that exhibit persistent rotation due to intrinsic left-right asymmetry. In circular confinement, this simplified chiral model reproduces several experimentally observed features within specific parameter regimes. At high densities in unconfined environments, however, intrinsic chirality becomes masked even before the onset of the jamming transition. These results show that single-cell geometric asymmetry does not necessarily translate into large-scale chiral flows, offering new insight into how forces and symmetries shape collective motion in dense cellular systems. Overall, this work uncovers how geometric constraints – embedded in the intrinsic architecture of an active filament or encoded in the complexity of a microenvironment couple to active forces to generate different classes of complex behaviors. }, author = {Dunajova, Zuzana}, isbn = {978-3-99078-076-3}, issn = {2663-337X}, pages = {110}, publisher = {Institute of Science and Technology Austria}, title = {{Geometry-driven self-organization of migrating cells and chiral filaments}}, doi = {10.15479/AT-ISTA-21423}, year = {2026}, } @misc{21439, abstract = {These files contain supplementary movies accompanying the PhD thesis “Geometry-driven self-organization of migrating cells and chiral filaments” by Zuzana Dunajova (2026). The videos provide additional visual material supporting the experiments and results described in the thesis.}, author = {Dunajova, Zuzana}, publisher = {Institute of Science and Technology Austria}, title = {{Supplementary movies to PhD thesis “Geometry-driven self-organization of migrating cells and chiral filaments”}}, doi = {10.15479/AT-ISTA-21439}, year = {2026}, } @article{21235, abstract = {The condensation of charged polymers is an important driver for the formation of biomolecular condensates. Recent experiments suggest that this mechanism also controls the clustering of eukaryotic chromosomes during the late stages of cell division. In this process, interchromosome attraction is driven by the condensation of cytoplasmic RNA and Ki-67, a charged intrinsically disordered protein that coats the chromosomes as a brush. Attraction between chromosomes has been shown to be specifically promoted by a localized charged patch on Ki-67, although the physical mechanism remains unclear. To elucidate this process, we combine coarse-grained simulations and analytical theory to study the RNA-mediated interaction between charged polymer brushes on the chromosome surfaces. We show that the charged patch on Ki-67 leads to interchromosome attraction via RNA bridging between the two brushes, whereby the RNA preferentially interacts with the charged patches, leading to stable, long-range forces. By contrast, if the brush is uniformly charged, bridging is basically absent due to complete adsorption of RNA onto the brush. Moreover, the RNA dynamics becomes caged in presence of the charged patch while remaining diffusive with uniform charge. Our work sheds light on the physical origin of chromosome clustering, while also suggesting a general mechanism for cells to tune work production by biomolecular condensates via different charge distributions.}, author = {Sorichetti, Valerio and Robin, Paul and Palaia, Ivan and Hernandez-Armendariz, Alberto and Cuylen-Haering, Sara and Šarić, Anđela}, issn = {2835-8279}, journal = {PRX Life}, number = {3}, publisher = {American Physical Society}, title = {{Charge distribution of the coating brush drives interchromosome attraction}}, doi = {10.1103/41fd-r847}, volume = {3}, year = {2025}, } @article{21236, abstract = {The migration behavior of colliding cells is critically determined by transient contact interactions. During these interactions, the motility machinery, including the front-rear polarization of the cell, dynamically responds to surface protein-mediated transmission of forces and biochemical signals between cells. While biomolecular details of such contact interactions are increasingly well understood, it remains unclear what biophysical interaction mechanisms govern the cell-level dynamics of colliding cells and how these mechanisms vary across cell types. Here we develop a phenomenological theory based on 14 candidate contact-interaction mechanisms coupling cell position, protrusion, and polarity. Using high-throughput micropattern experiments, we detect which of these phenomenological contact interactions captures the interaction behaviors of cells. We find that various cell types—ranging from mesenchymal to epithelial cells—are accurately captured by a single model with only two interaction mechanisms: polarity-protrusion coupling and polarity-polarity coupling. Remarkably, the qualitatively different interaction behaviors of distinct cells, as well as cells subject to molecular perturbations of surface protein-mediated signaling, can all be quantitatively captured by varying the strength and sign of the polarity-polarity coupling mechanism. Altogether, our data-driven phenomenological theory of cell-cell interactions reveals polarity-polarity coupling as a versatile and general contact-interaction mechanism, which may underlie diverse collective migration behaviors of motile cells.}, author = {Brandstätter, Tom and Brieger, Emily and Brückner, David and Ladurner, Georg and Rädler, Joachim O. and Broedersz, Chase P.}, issn = {2835-8279}, journal = {PRX Life}, number = {3}, publisher = {American Physical Society}, title = {{Data-driven theory reveals protrusion and polarity interactions governing collision behavior of distinct motile cells}}, doi = {10.1103/3hhj-rt1n}, volume = {3}, year = {2025}, } @article{19279, abstract = {Recent experimental advances in nanofluidics have allowed to explore ion transport across molecular-scale pores, in particular, for iontronic applications. Two-dimensional nanochannels—in which a single molecular layer of electrolyte is confined between solid walls—constitute a unique platform to investigate fluid and ion transport in extreme confinement, highlighting unconventional transport properties. In this work, we study ionic association in 2D nanochannels, and its consequences on non-linear ionic transport, using both molecular dynamics simulations and analytical theory. We show that under sufficient confinement, ions assemble into pairs or larger clusters in a process analogous to a Kosterlitz–Thouless transition, here modified by the dielectric confinement. We further show that the breaking of pairs results in an electric-field dependent conduction, a mechanism usually known as the second Wien effect. However the 2D nature of the system results in non-universal, temperature-dependent, scaling of the conductivity with electric field, leading to ionic coulomb blockade in some regimes. A 2D generalization of the Onsager theory fully accounts for the non-linear transport. These results suggest ways to exploit electrostatic interactions between ions to build new nanofluidic devices.}, author = {Toquer, Damien and Bocquet, Lydéric and Robin, Paul}, issn = {1089-7690}, journal = {Journal of Chemical Physics}, number = {6}, publisher = {AIP Publishing}, title = {{Ionic association and Wien effect in 2D confined electrolytes}}, doi = {10.1063/5.0241949}, volume = {162}, year = {2025}, }