L3

Thin film flows of nematic liquid crystal will be considered, using the Leslie-Ericksen formulation for nematics. Our model can account for variations in substrate anchoring, which may exert a strong influence on patterns that arise in the flow. A number of simulations will be presented using an "in house" code, developed to run on a GPU. Current modeling directions involving flow over interlaced electrodes, so-called "dielectrowetting", will be discussed.

The dynamics of many physical systems often evolve to asymptotic states that exhibit periodic spatial and temporal variations in their properties such as density, temperature, etc. Such regular patterns look the same when moved by a basic unit and/or rotated by certain special angles. They possess both translational and rotational symmetries giving rise to discrete spatial Fourier transforms. In contrast, an aperiodic crystal displays long range spatial order but no translational symmetry. 

Recently, quasicrystals which are related to aperiodic crystals have been observed to form in diverse physical systems such as metallic alloys (atomic scale) and dendritic-, star-, and block co-polymers (molecular scale). Such quasicrystals lack the lattice symmetries of regular crystals, yet have discrete Fourier spectra. We look to understand the minimal mechanism which promotes the formation of such quasicrystalline structures using a phase field crystal model. Direct numerical simulations combined with weakly nonlinear analysis highlight the parameter values where the quasicrystals are the global minimum energy state and help determine the phase diagram. 

By locating parameter values where multiple patterned states possess the same free energy (Maxwell points), we obtain states where a patch of one type of pattern (for example, a quasicrystal) is present in the background of another (for example, the homogeneous liquid state) in the form of spatially localized dodecagonal (in 2D) and icosahedral (in 3D) quasicrystals. In two dimensions, we compute several families of spatially localized quasicrystals with dodecagonal structure and investigate their properties as a function of the system parameters. The presence of such meta-stable localized quasicrystals is significant as they may affect the dynamics of the crystallisation in soft matter.

The problem of a bubble moving steadily in a Hele-Shaw cell goes back to Taylor and Saffman in 1959.  It is analogous to the well-known selection problem for Saffman-Taylor fingers in a Hele-Shaw channel.   We apply techniques in exponential asymptotics to study the bubble problem in the limit of vanishing surface tension, confirming previous numerical results, including a previously predicted surface tension scaling law.  Our analysis sheds light on the multiple tips in the shape of the bubbles along solution branches, which appear to be caused by switching on and off exponentially small wavelike contributions across Stokes lines in a conformally mapped plane. 

Tensors are higher dimensional analogues of matrices; they are used to record data with multiple changing variables. Interpreting tensor data requires finding low rank structure, and the structure depends on the application or context. Often tensors of interest define semi-algebraic sets, given by polynomial equations and inequalities. I'll give a characterization of the set of tensors of real rank two, and answer questions about statistical models using probability tensors and semi-algebraic statistics. I will also describe work on learning a path from its three-dimensional signature tensor. This talk is based on joint work with Guido Montúfar, Max Pfeffer, and Bernd Sturmfels.

In biological cells, genomic DNA is complexed with proteins, forming so-called chromatin structure, and packed into the nucleus. Not only the nucleotide (A, T, G, C) sequence of DNA but also the 3D structure affects the genomic function. For example, certain regions of DNA are tightly packed with proteins (heterochromatin), which inhibits expression of genes coded there. The structure sometimes changes drastically depending on the state (e.g. cell cycle or developmental stage) of the cell. Hence, the structural dynamics of chromatin is now attracting attention in cell biology and medicine. However, it is difficult to experimentally observe the motion of the entire structure in detail. To combine and interpret data from different modes of observation (such as live imaging and electron micrograph) and predict the behavior, structural models of chromatin are needed. Although we can use molecular dynamics simulation at a microscopic level (~ kilo base-pairs) and for a short time (~ microseconds), we cannot reproduce long-term behavior of the entire nucleus. Mesoscopic models are wanted for that purpose, however hard to develop (there are fundamental difficulties).

In this seminar, I will introduce our recent theoretical/computational studies of chromatin structure, either microscopic (molecular dynamics of DNA or single nucleosomes) or abstract (polymer models and reaction-diffusion processes), toward development of such a mesoscopic model including local "states" of DNA and binding proteins.

References:

T. Kameda, A. Awazu, Y. Togashi, "Histone Tail Dynamics in Partially Disassembled Nucleosomes During Chromatin Remodeling", Front. Mol. Biosci., in press (2019).

Y. Togashi, "Modeling of Nanomachine/Micromachine Crowds: Interplay between the Internal State and Surroundings", J. Phys. Chem. B 123, 1481-1490 (2019).

E. Rolls, Y. Togashi, R. Erban, "Varying the Resolution of the Rouse Model on Temporal and Spatial Scales: Application to Multiscale Modelling of DNA Dynamics", Multiscale Model. Simul. 15, 1672-1693 (2017).

S. Shinkai, T. Nozaki, K. Maeshima, Y. Togashi, "Dynamic Nucleosome Movement Provides Structural Information of Topological Chromatin Domains in Living Human Cells", PLoS Comput. Biol. 12, e1005136 (2016).

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The Weak Gravity Conjecture holds that in any consistent theory of quantum gravity, gravity must be the weakest force. This simple proposition has surprisingly nontrivial physical consequences, which in the case of supersymmetric string/M-theory compactifications lead to nontrivial geometric consequences for Calabi-Yau manifolds. In this talk we will describe these conjectured geometric consequences in detail and show how they are realized in concrete examples, deriving new results about 5d supersymmetric black holes in the process.

In the first part of the talk, I will describe surface colonization strategies of the motile bacteria Pseudomonas aeruginosa. During early stages of biofilm formation, the majority of cells that land on a surface eventually detach. After a prolonged lag time, cells begin to cover the surface rapidly. Reversible attachments provide cells and their descendants with multigenerational memory of the surface that primes the planktonic population for colonization. Two different strains use different surface sensing machinery and show different colonization strategies. We use theoretical modelling to investigate how the hydrodynamics of type IV pili and flagella activity lead to increased detachment rates and show that the contribution from this hydrodynamic effect plays a role in the different colonization strategies observed in the two strains.

In the second part of the talk, I will show that when cells migrate through constricting pores, there is an increase in DNA damage and mutations. Experimental observations show that this breakage is not due to mechanical stress. I present an elastic-fluid model of the cell nucleus, coupled to kinetics of DNA breakage and repair proposing a mechanism by which nuclear deformation can lead to DNA damage. I show that segregation of soluble repair factors from the chromatin during migration leads to a decrease in the repair rate and an accumulation of damage that is sufficient to account for the extent of DNA damage observed experimentally.

Understanding the mechanisms of mutagenesis is important for prevention and treatment of numerous diseases, most prominently cancer. Large sequencing datasets revealed a substantial number of mutational processes in recent years, many of which are poorly understood or of completely unknown aetiology. These mutational processes leave characteristic sequence patterns in the DNA, often called "mutational signatures". We use bioinformatics methods to characterise the mutational signatures with respect to different genomic features and processes in order to unravel the aetiology and mechanisms of mutagenesis. 

In this talk, I will present our results on how mutational processes might be modulated by DNA replication. We developed a linear-algebra-based method to quantify the magnitude of replication strand asymmetry of mutational signatures in individual patients, followed by detection of these signatures in early and late replicating regions. Our analysis shows that a surprisingly high proportion (more than 75 %) of mutational signatures exhibits a significant replication strand asymmetry or correlation with replication timing. However, distinct groups of signatures have distinct replication-associated properties, capturing differences in DNA repair related to replication, and how different types of DNA damage are translated into mutations during replication. These findings shed new light on the aetiology of several common but poorly explained mutational signatures, such as suggesting a novel role of replication in the mutagenesis due to 5-methylcytosine (signature 1), or supporting involvement of oxidative damage in the aetiology of a signature characteristic for oesophageal cancers (signature 17). I will conclude with our ongoing work of wet-lab validations of some of these hypotheses and usage of computational methods (such as genetic algorithms) in guiding the development of experimental protocols.