Integrated Calendar

Small molecular weight organic compounds are common across the galaxy and transcend all known biological interactions. Plants, in particular, have evolved a remarkable capacity to produce diverse sets of so-called specialized metabolites from a few simple, inorganic precursors. Already in 1977, Rhoades argued that plant specialized metabolites are likely multifunctional, i.e. that they serve multiple purposes. Multifunctionality may render the production of specialized metabolites more cost effective and may explain their abundance and tight spatiotemporal control in plants. Work over the last decades confirms that specialized metabolites often have a broad range of functions, from growth and development to defense. However, our understanding of how this multifunctionality affects the interactions between plants and higher trophic levels, including herbivores and their natural enemies is limited. In my presentation, I will explore the importance of multifunctional plant metabolites in a multitrophic context by discussing our work on benzoxazinoids, the most abundant specialized metabolites in grasses such as wheat and maize. We find that benzoxazinoids act as direct defenses [1], within-plant defense signaling molecules [2], microbiome modulators [3] and siderophores [4]. At the same time, the western corn rootworm, a specialist maize pest and important agricultural pest, exploits benzoxazinoids as foraging cues [4], protective agents [5] and micronutrient providers [4]. Thus, the multifunctionality of plant specialized metabolites is mirrored in the adaptations of a specialist herbivore, resulting in a tightly interlocked metabolism. We are also starting to unravel how the metabolism of herbivore natural enemies such as entomopathogenic nematodes can be interlocked with the plant and the herbivore to enhance biological control. These findings have implications for our understanding of the ecology and evolution of plant specialized metabolites, and for their use in agricultural pest control.

One of the fundamental functions of the brain is to integrate incoming sensory stimuli, perceive and associate these integrations with internal representations, and make fast and reliable decisions and actions. Although these processes have been extensively studied, we are still missing a comprehensive understanding of the exact spatiotemporal dynamics at a mesoscale level, i.e. at the neuronal population level spanning many cortical and sub-cortical areas. In my opinion, the key to understanding these processes is to measure from large populations of neurons within a single trial as a subject performs a complex behavior. In my talk, I will present a variety of evidence from behaving mice backing up this claim. In one of the projects, we imaged calcium signals from the whole dorsal cortex of mice performing a whisker-based texture discrimination task with a short-term memory component. Mice use different behavioral strategies to solve the task either deploying an active strategy — engaging their body and whiskers towards the approaching texture — or passively awaited the touch. Based on this strategy, short-term memory was located in frontal secondary motor cortex (M2) in active mice whereas in a newly identified posterior area (P) in passive mice. Optogenetic perturbation of these areas impaired performance specifically in the associated strategy. In some cases, mice overcame the perturbation by switching to the alternative strategy. Thus, depending on behavioral strategy within single trials, cortical population activity is routed differentially to hold information either frontally or posteriorly before converging to similar action. Additional projects, using different tasks, neuronal subtypes and during learning highlight the importance of observing and dissecting mesoscale dynamics during complex behaviors.

The talk will describe nonlinear rheology in extreme conditions that change fluid structure and flow mechanisms. Elongational flow of entangled polymers produces near complete molecular alignment but only changes the viscosity by an order of magnitude and does not destroy the confining tube. A transition in the mechanism of shear thinning in lubricants from alignment to thermal activation is shown to be generic and allows simulations to examine whether the viscosity diverges at a finite glass transition temperature.

Exocytosis occurs in all living cells and is essential for many cellular processes including metabolism, signaling, and trafficking. During exocytosis, cargo loaded vesicles dock and fuse with the plasma membrane to release their content. To accommodate different cargos and cellular needs exocytosis must occur across scales; From synaptic vesicles that are only ~50nm in diameter, and neuroendocrine vesicles that are in the ~500nm range to giant secretory vesicles filled with viscous cargo, such as in the acinar cells in the exocrine pancreas, that reach up to a few µm in diameter. Yet, how fusion and content release are adapted to remain function across these scales is not well understood. It is well established that during exocytosis of small vesicles, vesicle fusion can proceed through one of two pathways: The first is complete incorporation, when the vesicular membrane fuses to the target membrane and the fusion pore expand irreversibly, incorporating the vesicular membrane into the target membrane. The second is “kiss-and-run”, when the fusion pore flickers, opening briefly and collapsing rapidly into two separate membranes. I am interested in understanding how exocytosis occurs in giant vesicles witch challenge efficient secretion and membrane homeostasis due to their massive size and viscous content. I am using the salivary gland of D. Melanogaster, as a model system for giant vesicles secretion. The vesicles in the gland measure between 5-8 µm, fuse and secrete viscous content into a preformed lumen. To visualize the secretion process, I adapted a method for super-resolution microscopy to live-gland imaging. I observed that fusion pores of giant vesicles expand to a stable opening of up to 3µm and slowly constricts down to hundreds of nm or less during secretion. Because constricting a membrane pore from “infinity” in molecular terms, back to a very narrow ‘stalk’ demands an investment of energy, I hypothesized that this is mediated by a specialized protein machinery. I am currently screening for the components of the machinery using the enormous power of Drosophila genetics by taking a candidate gene approach. My preliminary results identify the BAR domain containing protein, MIM (missing in metastasis) as a key regulator of pore dynamics, leading to new and exciting insights into the molecular mechanism of cellular secretion and membrane homeostasis in live tissues.