Integrated Calendar

The actin cytoskeleton plays a major role during the initial stages of embryonic development. In particular, the actin cytoskeleton can switch, in a cell-cycle dependent manner, into a contractile state and exhibit large scale flows which are essential for the organization and the establishment of polarity in the early embryo. We developed a reconstituted model system to study cytoskeletal organization and emulate these processes in artificial cells. The actin machinery is encapsulated within water-in-oil emulsions, and actin nucleators are added to induce the formation of various cytoskeletal structures. By controlling the localization and concentration of these nucleators, we can tune the properties of the system, and induce cytoskeletal symmetry breaking which appears remarkably similar to the initial polarization of the embryo in many species, or bulk actin network contraction which can drive directional transport as observed during cell division. Overall, our reconstituted system provides a powerful platform to study important cytoskeletal phenomena in a simplified environment detached from the complexity of the living cell, and explore fundamental aspects of the properties of active matter.

Rational design of efficient solar energy materials is driven by novel insights into non-equilibrium processes of charge and energy transfer, exciton recombination, charge carrier trapping, radiative and non-radiative relaxation of electronic excited states. To gain a better understanding of these processes, a detailed description of coupled electron-nuclear dynamics in complex systems is essential. A direct solution of fully quantal task is prohibitively expensive, and the accurate and efficient semiclassical methodologies for quantum non-adiabatic dynamics are needed.
In this seminar, I will present novel methods and tools for accurate simulation of quantum dynamics for solar energy material applications. Firstly, the second quantized surface hopping (SQUASH) approach will be presented. The method solves the superexchange problem in Auger dynamics, is capable of describing tunneling, and is particularly suitable for calculations in diabatic representation. Secondly, the coherence penalty functional (CPF) approach will be discussed. The method incorporates decoherence effects within the mean-field framework and provides notable improvements in computed scattering probabilities and electron transfer timescales. Thirdly, the PYXAID toolbox for simulating quantum dynamics in atomistic systems will be introduced. Its capabilities will be showcased on a number of molecular and condensed matter systems relevant to solar energy material research.

Mitochondrial DNA (mtDNA) encodes several proteins playing key roles in bioenergetics. Pathological mutations of mtDNA can be inherited or may accumulate following treatment for viral infections or cancer. Furthermore, many organisms, including humans, accumulate significant mtDNA damage during their lifespan, and it is therefore possible that mtDNA mutations can promote the aging process.

There are no effective treatments for most diseases caused by mtDNA mutation. An understanding of the cellular consequences of mtDNA damage is clearly imperative. Toward this goal, we use the budding yeast Saccharomyces cerevisiae as a cellular model of mitochondrial dysfunction. Genetic manipulation and biochemical study of this organism is easily achieved, and many proteins and processes important for mitochondrial biogenesis were first uncovered and best characterized using this experimental system. Importantly, current evidence suggests that processes required for survival of cells lacking a mitochondrial genome are widely conserved between yeast and other organisms, making likely the application of our findings to human health.

I will discuss our most recent work related to the reversal of mitochondrial dysfunction. Specifically, we have found that reducing the acidity of the vacuole, the yeast analog of the mammalian lysosome, provides significant benefits to cells deleted of mtDNA. Moreover, our work demonstrates that perturbation of conserved signaling pathways involved in nutrient sensation can greatly increase the fitness of cells lacking a mitochondrial genome.