L3

The ability of biological matter to move and deform itself is facilitated by microscopic out-of-equilibrium processes that convert chemical energy into mechanical work. In many cases, this mechano-chemical activity takes place on effectively two-dimensional domains formed by, for example, multicellular structures like epithelial tissues or the outer surface of eukaryotic cells, the so-called actomyosin cortex.
We will show in the first part of the talk, that the large-scale dynamics and self-organisation of such structures can be captured by the theory of active fluids. Specifically, using a minimal model of active isotropic fluids, we can rationalize the emergence of asymmetric epithelial tissue flows in the flower beetle during early development, and explain cell rotations in the context of active chiral flows and left-right symmetry breaking that occurs as the model organism C. elegans sets up its body plan.
To develop a more general understanding of such processes, specifically the role of geometry, curvature and interactions with the environment, we introduce in the second part a theory of active fluid surfaces and discuss analytical and numerical tools to solve the corresponding momentum balance equations of curved and deforming surfaces. By considering mechanical interactions with the environment and the fully self-organized shape dynamics of active surfaces, these tools reveal novel mechanisms of symmetry breaking and pattern formation in active matter.

Malignant transformation of somatic tissues is an evolutionary process, driven by selection for oncogenic mutations. Understanding when these mutations occur, and how fast mutant cell clones expand can improve diagnostic schemes and therapeutic intervention. However, clonal dynamics are not directly accessible in humans, posing a need for inference approaches to reconstruct the division history in normal and malignant cell clones, and to predict their future evolution. Inspired from population genetics theory, we develop mathematical models to detect imprints of clonal selection in the variant allele frequency distribution measured in a single tissue sample of a homeostatic tissue. I will present the theoretical basis of our approach and inference results for the tissue dynamics in physiological and clonal hematopoiesis, obtained from variant allele frequencies measured by snapshot bulk whole genome sequencing of human bone marrow samples.

Unraveling the intricacies of intracellular signalling through predictive mathematical models holds great promise for advancing precision medicine and enhancing our foundational comprehension of biology. However, navigating the labyrinth of biological mechanisms governing signalling demands a delicate balance between a faithful description of the underlying biology and the practical utility of parsimonious models.
In this talk, I will present methods that enable training of large ordinary differential equation models of intracellular signalling and showcase application of such models to predict sensitivity to anti-cancer drugs. Through illustrative examples, I will demonstrate the application of these models in predicting sensitivity to anti-cancer drugs. A critical reflection on the construction of such models will be offered, exploring the perpetual question of complexity and how intricate these models should be.
Moreover, the talk will explore novel approaches that meld machine learning techniques with mathematical modelling. These approaches aim to harness the benefits of simplistic and unbiased phenomenological models while retaining the interpretability and biological fidelity inherent in mechanistic models.
 

Motile cells inside living tissues often encounter junctions, where their path branches into several alternative directions of migration. We present a theoretical model of cellular polarization for cells migrating along one-dimensional lines, exhibiting diverse migration modes. When arriving at a symmetric Y-junction and extending protrusions along the different paths that emanate from the junction. The model predicts the spontaneous emergence of deterministic oscillations between competing protrusions, whereby the cellular polarization and growth alternates between the competing protrusions. These predicted oscillations are found experimentally for two different cell types, noncancerous endothelial and cancerous glioma cells, migrating on patterned network of thin adhesive lanes with junctions. Finally we present an analysis of the migration modes of multicellular "trains" along one-dimensional tracks.

I will discuss logarithmic corrections to various CFT partition functions in the context of the AdS4/CFT3 correspondence for theories arising on the worldvolume of M2-branes. I will use four-dimensional gauged supergravity and heat kernel methods and present general expressions for the logarithmic corrections to the gravitational on-shell action or black hole entropy for a number of different supergravity backgrounds. I will outline several subtleties and puzzles in these calculations and contrast them with a similar analysis of logarithmic corrections performed directly in the eleven-dimensional uplift of a given four-dimensional supergravity background. This analysis suggests that four-dimensional supergravity consistent truncations are not the proper setting for studying logarithmic corrections in AdS/CFT. These results have important implications for the existence of scale-separated AdS vacua in string theory and for effective field theory in AdS more generally.

I will show that the massless irreducible representations of the Poincare group are precisely Corrolian field living on I^+. I will also show that the analogous massless irreducible representation of E11 are just the degrees of freedom of maximal supergravity. Finally I will speculate how spacetime could emerge from an underlying fundamental theory.

In this talk I will review how the BV formalism is used in quantizing theories with local gauge symmetries within the framework of perturbative algebraic quantum field theory. The latter is a mathematically rigorous approach to QFT that combines the locality idea going back to Haag and Kastler with Epstein-Glaser renormalization. In my talk I will also show how these methods can also lead to the construction of a factorization algebra.

I will recall the Zilber-Pink conjecture for Shimura varieties and give my perspective on current progress towards a proof.

Consider the following "controlled" random graph process: edges of the complete graph are revealed one by one in random order to an online algorithm, which immediately decides whether to retain each observed edge. The algorithm's objective is to construct a graph property within specified constraints on the total number of observed edges ("time") and the total number of retained edges ("budget").

During this talk, I will present results in this model for natural graph properties, such as connectivity, Hamiltonicity, and containment of fixed-size subgraphs. Specifically, I will describe a strategy to construct a Hamilton cycle at the hitting time for minimum degree 2 by retaining a linear number of edges. This extends the classical hitting time result for Hamiltonicity originally established by Ajtai–Komlós–Szemerédi and Bollobás.

The talk is based on joint work with Alan Frieze and Michael Krivelevich.