Abstract:
Chris Macdonald - The Small Multidrug Resistance (SMR) family of prokaryotic and archaean proton-coupled transporters provides a window into the evolutionary events that generated the molecular diversity of membrane protein function today. These small 4-pass integral membrane proteins assemble into functional dimers with an unusual antiparallel architecture. The most well-studied example, EmrE, is a homodimeric member that provides resistance to a broad range of hydrophobic cationic aromatic compounds. This talk will cover recent work in the Stockbridge lab that has fundamentally altered our understanding of this family, including functional characterization through flux measurements and solid-supported membrane (SSM) electrophysiology, in vivo metabolic assays, and phylogenetic analysis. We suggest an evolutionary trajectory for the development of new functions in these small proteins.

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Maral Budak -The information transmission between neurons and brain regions occurs via synapses. Therefore, disruption of synaptic signaling (e.g. synaptic failure or desynchronization of spikes) may have devastating outcomes, such as loss of consciousness or neurodegenerative diseases. First, our objective is understanding the effect of synaptic failure on functional connectivity of different network structures, and we observed that synaptic failure does not always decrease the coherence of neuronal networks, but sometimes promotes the formation of coherent states of activity in the networks. Next, we aim to understand the mechanism of hidden hearing loss caused by myelinopathy. Recently, it’s been hypothesized that disruption of myelination patterns at auditory nerves (AN) causes desynchronization of AN spiking activity. To test this hypothesis, we constructed a reduced biophysical model for a population of inner hair cells with postsynaptic auditory nerve fibers. As a result, our model confirms that heminodal disruption causes desynchronization of AN spikes leading to a loss of temporal resolution.