Programme
time | speaker | title and abstract |
---|---|---|
9:00-9:50 | Registration and coffee | |
9:50-10:00 | Welcome | |
10:00-11:00 | Erwin Frey |
Protein pattern formation is essential for the spatial organization of many intracellular processes like cell division, flagellum positioning, and chemotaxis. A prominent example of intracellular patterns are the oscillatory pole-to-pole oscillations of Min proteins in E. coli whose biological function is to ensure precise cell division. Cell polarization, a prerequisite for processes such as stem cell differentiation and cell polarity in yeast, is also mediated by a diffusion-reaction process. More generally, these functional modules of cells serve as model systems for self-organization, one of the core principles of life. Under which conditions spatio-temporal patterns emerge, and how these patterns are regulated by biochemical and geometrical factors are major aspects of current research. In this talk we will present a new theoretical framework to characterize pattern forming systems arbitrarily far from global equilibrium. We will show that reaction-diffusion systems that are driven by locally mass-conserving interactions can be understood in terms of local equilibria of diffusively coupled compartments. Diffusive coupling generically induces lateral redistribution of the globally conserved quantities, and the variable local amounts of these quantities determine the local equilibria in each compartment. We find that, even far from global equilibrium, the system is well characterized by its moving local equilibria. These insight lead to the identification of general design principles of cellular pattern forming systems. We will show how they are implemented for the respective specific biological function in cell division of E. coli and cell polarization in yeast. More broadly, these results reveal conceptually new principles of self-organized pattern-formation that may well govern diverse dynamical systems. |
11:00-12:00 | Nathan Goehring |
Patterning of early embryos requires specification of positional information. This includes definition of developmental axes, orientation and migration of cells in response to direction cues, and asymmetric cell divisions which generate cellular diversity. Each of these cases requires symmetry-breaking by molecular networks. Our work focuses on the PAR cell polarity network - a system for generating functional asymmetry in animal cells. This process of cell polarization by PAR proteins plays key roles in symmetry-breaking during early animal development. Our lab and others have shown that this network bears hallmarks of a self-organizing reaction-diffusion network, comprising two antagonistic sets of so-called PAR proteins that regulate one another’s conversion between slowly diffusing, active, membrane-associated states, and rapidly mixing, inactive cytoplasmic states. I will describe our recent investigations into the relationship between the mobility states of PAR proteins and symmetry-breaking in the C. elegans embryo as a model for thinking about how polarity networks are tuned to enable efficient cell polarization. |
12:00-13:00 | Lunch | |
13:00-14:00 | Michael Cates |
The physics of phase separation is described by a diffusive scalar field theory known as Model B. This respects Time Reversal Symmetry (TRS). Adding leading-order terms to break TRS gives new theories capable of describing phase separations in active matter, including 'motility-induced' phase separation. I will report what we have so far learned about these theories, called Active Model B and Active Model B+. |
14:00-15:00 | Frédéric van Wijland |
Collective effects in active matter are fascinating in that they often challenge our equilibrium-based intuition. I will discuss the ingredients necessary for Motility-Induced Phase Separation to occur in a system of interacting active particles. Field-theoretic methods will be used to come up of with educated guesses. |
15:00-15:30 | Coffee break | |
15:30-16:30 | Guillaume Salbreux |
The shape of a biological tissue is determined by mechanical stresses acting within the tissue cells, which are generated by an active network of actin polymers and myosin molecular motors. During embryonic morphogenesis, forces generated in the actomyosin cytoskeleton of epithelial cells result in deformation and 3D bending of the epithelium. To understand tissue morphogenesis, one needs to relate force generation at the cellular scale to deformation occurring at the tissue scale. Here I will discuss how this relation can be captured by vertex models which describe the tissue detailed geometry, or by a continuum, hydrodynamic theory of active surfaces which is a coarse-grained description on the scale larger than a cell. Deformation of an active surface arise from internal active stresses or from internal active bending moments. In an epithelium, active bending moments result from apico-basal asymmetric forces. I will discuss application of this framework to understand how patterned force generation in an epithelium can drive biological tissue folding in the Drosophila wing disc and in pancreatic duct cancerous lesions in mice. |
16:30-17:30 | Kay Jörg Wiese |
Contrary to DNA, RNA folds back onto itself, forming cactus-like structures. At large temperatures these structures are well described by the homopolymer solution of deGennes, predicting the pairing probability to decay algebraically with distance, with an exponent of 3/2. While for a disordered sequence at zero temperature there is no analytical solution, numerical simulations show that this exponent changes from 3/2 to about 4/3. One expects a phase transition between the two regimes, induced by a change in temperature. We construct a field theory for this transition, and calculate the critical exponents. A numerical validation is difficult, since the specific heat and other classical observables vary smoothly across the transition for all system sizes reachable despite the use of a polynomial algorithm. Measuring pairing probability distributions, we construct several observables in which this thermodynamic transition is visible. Curiously, we observe a second transition at a lower temperature, which does not seem to come with any thermodynamic singularity. |
17:30- | Closing, discussions & drinks |