November 1, 2019
Snowbird Ski & Summer Resort
REGISTRATION REQUIRED: Click here to Register for the Symposium (REGISTRATION IS OPEN)
POSTER ABSTRACT SUBMISSION: Abstract deadline: October 25, 2019; 5:00PM; SUBMIT HERE: (ABSTRACT SUBMISSION IS OPEN)
(If you are attending the Symposium, you must also register for the meeting)
9:00AM-12:00PM SCIENTIFIC SESSION I (Cliff Lodge, Ballrooms 1&2)
12:00-1:45PM Lunch (Cliff Lodge, Magpie Room)
12:30-1:45PM Optional Policy Workshop (Sasha Luks- Morgan) (Workshop registration)
1:45-5:00PM SCIENTIFIC SESSION II (Cliff Lodge, Ballrooms 1&2)
5:00-6:30PM Poster session and mixer (Cliff Lodge, Primrose Lobby; Ballroom Mezzanine); sponsored by the SfN Intermountain Chapter; Hard Deadline: October 13, 2017, 5:00PM. ABSTRACT submittal
6:30-8:00PM Dinner, Cliff Lodge, Primrose
8:00-9:00PM Keynote Speaker
9:30-11:00PM Mixer, Cliff Lodge, Primrose
KEYNOTE SPEAKER: Aaron Gitler, Ph.D.; Professor, Department of Genetics, Stanford University
Title: "Simple model systems provide insight into human neurodegenerative diseases"
Research Summary: My goal is to discover the cellular and molecular mechanisms by which protein aggregates contribute to neurodegeneration and to harness these mechanisms to devise novel therapeutic strategies. We use the baker’s yeast, Saccharomyces cerevisiae, as a simple, yet powerful, model system to study the cell biology underpinning protein-misfolding diseases, which include Alzheimer’s disease, Parkinson’s disease, and amyotrophic lateral sclerosis (ALS). We are focusing on the ALS disease proteins TDP-43, FUS/TLS and C9orf72 and have generated yeast models to define mechanisms by which these proteins cause ALS. Because these proteins aggregate and are toxic in yeast, we have used these yeast models to perform high-throughput genomewide modifier screens to discover suppressors and enhancers of toxicity. Launching from the studies in yeast, we have extended our findings into animal models and even recently into human patients. For example, we discovered mutations in one of the human homologs of a hit from our yeast TDP-43 modifier screen in ALS patients. Mutations in this gene are relatively common (~5% of cases) making it one of the most common genetic risk factors for ALS discovered to date. These screens are also providing new and completely unexpected potential drug targets, underscoring the power of such simple model systems to help reveal novel insight into human disease.
Speaker: Samara Reck-Peterson, Ph.D., Professor, Department of Cell and Developmental Biology, University of California, San Diego; Investigator, Howard Hughes Medical Institute
Title: "Trucks, tolls, and traffic jams: mechanisms of intracellular transport"
Research Summary: My lab studies the molecular motors that transport cargo along cellular highways, microtubules. Two types of machines – dynein and kinesin – move in opposite directions along microtubules. Our goal is to understand how dynein, which transports hundreds of different cellular cargos, is regulated and how it teams up with kinesin to coordinate the delivery of cellular cargos. We are also investigating why defects in intracellular transport result in neurodevelopmental and neurodegenerative disease. We use a variety of approaches to address these questions, including single-molecule biophysics, cryo-electron microscopy, live-cell imaging, genetics, and proteomics.
Speaker: Ruth M. Barrientos, Ph.D., Associate Professor, Departments of Psychiatry & Behavioral Health, and Neuroscience, Ohio State University - College of Medicine
Title: "Cognitive declines in aging: Triggers and mechanisms"
Research Summary: Healthy individuals of advanced age are more likely to suffer precipitous memory impairments following an inflammatory insult than are younger adults. With advanced aged, these insults (e.g., infection, surgery, or unhealthy diet) trigger an exaggerated neuroinflammatory response, which impedes normal synaptic plasticity processes necessary for forming long-term memories. Microglia, the immune cells of the brain, become sensitized in the normal aged brain, and this sensitization is a key culprit of the amplified neuroinflammatory response to these challenges. In my talk, I will discuss factors that lead to microglial sensitization, the various insults that evoke exaggerated neuroinflammation and memory impairments in the aged rat, and interventions that confer protection.
Speaker: Craig Montell, Ph.D., Duggan Professor and Distinguished Professor, Department of Molecular, Cellular and Developmental Biology, University of California, Santa Barbara
Title: "Receptors, channels and animal behavior"
Research Summary: A central question in neurobiology is how an animal senses the environment and uses this information to modify behavior and decision making. Using the fruit fly, Drosophila melanogaster, we are deciphering how environmental temperature, light, gustatory and olfactory cues, and mechanical forces influence behavior. One of the key sensory receptors that we are characterizing are TRP channels. We are also deciphering polymodal sensory roles of gustatory receptors and ionotropic receptors, and defining the behaviors that they control. We are unraveling multiple light-independent roles for rhodopsins, and posit that their ancient roles were in chemosensation rather than light sensation. Most recently, we started developing a variety of strategies to control the mosquito vector, Aedes aegypti, which spreads Dengue, Zika and other diseases.
Speaker: Megan Williams, Ph.D., Associate Professor, Department of Neurobiology & Anatomy , University of Utah
Title: "Wiring the brain: elucidating mechanisms driving synapse specificity"
Research Summary: Proper brain function requires that neurons make specific types of synapses with specific types of target neurons. Defects in this process can alter brain activity and may underlie many types of mental illnesses but we know little about the mechanisms by which synapse specificity develops. We recently discovered that the transmembrane molecule Kirrel3, which is a risk factor for autism and intellectual disability, is selectively required for formation of a specific type of hippocampal synapse that excites inhibitory neurons. Accordingly, loss of Kirrel3 leads to unconstrained activity throughout the hippocampus. This discovery established Kirrel3 as a functionally-relevant, target-specific synaptogenic molecule but we still do not know the mechanism of Kirrel3 function or if human mutations in Kirrel3 could cause disease. Our new data suggest that Kirrel3 binds other Kirrel3 molecules in cis and trans, functions directly in pre- and post-synapse formation, and requires yet to be identified neuron-specific binding partner(s). Moreover, we demonstrate that that most disease-associated missense variants of Kirrel3 have impaired function, providing the first evidence that Kirrel3 variants could cause disease. Our research advances our understanding of mechanisms used to wire the brain with extreme specificity and how subtle changes in synapse specificity could lead to neurodevelopmental disorders.
Speaker: Sungjin Park, Ph.D., Assistant Professor, Department of Neurobiology & Anatomy , University of Utah
Title: "Building a Complex Structure Outside of the cell: Morphogenesis of ECM by a 3D printing mechanism"
Research Summary: One of the remaining mysteries in biology is how different tissues and organs acquire their unique and exquisite shapes during development. It is widely accepted that the extracellular matrix (ECM) provides structural and biochemical cues necessary to establish and maintain cellular architecture within organs. However, how individual ECM components assemble outside of cells into the highly-ordered, anisotropic and complex ultrastructure necessary to perform these functions remains a mystery.
The current model for ECM morphogenesis proposes that ECM components are secreted and then self-organize into a complex, layered structure. To better understand the cellular and molecular processes that underlie ECM organization, we focused on the tectorial membrane (TM), an inner ear ECM that mediates auditory transduction. The TM forms facing the luminal space of the cochlear chamber and exhibits stereotyped morphology. We discovered that surface tethering of a-tectorin (Tecta), a GPI-anchored collagen binding protein, is required to prevent diffusion of secreted ECM components away from the cell surface and to organize TM architecture. We generated knock-in mouse lines in which Tecta is either constitutively secreted (Tectasec), or tethered to the cell surface via a transmembrane domain (TectaT). In Tectasec mice, collagen fibrils do not organize into bundles but instead form an irregularly-shaped aggregate in the luminal space. In TectaT mice, a thin collagen network forms on the cell surface that does not grow to generate the normal multi-layered structure. In contrast to the current self-assembly model, our findings support a novel 3D printing model: (1) a surface-tethered structural organizer establishes a layer of ECM on the cell surface and (2) as each successive layer is “printed, the previously-established layer is released along with the surface organizer and this process establishes the higher-order architecture of the complex ECM. The study will provide a novel insight into our understanding of the structure and function of ECM in many systems.
Speaker: Jason Shepherd, Ph.D., Associate Professor, Department of Neurobiology & Anatomy, University of Utah
Title: "Viral-like intercellular communication in the nervous system"
Research Summary: The neuronal gene Arc is essential for long-lasting information storage in the mammalian brain, mediates various forms of synaptic plasticity, and has been implicated in neurodevelopmental disorders. We recently discovered that Arc self-assembles into viral-like capsids that encapsulate RNA. Endogenous Arc protein is released from neurons in extracellular vesicles that mediate the transfer of Arc mRNA into new target cells, where it can undergo activity-dependent translation. Our new findings suggest that Arc has an unanticipated role in intercellular communication in the nervous system, which adds new complexity and implicates non-cell autonomous processes in memory consolidation. There are a number of fundamental questions that we are currently investigating: What cargo does Arc transfer cell-to-cell? Which cells take up Arc vesicles? Where and when does Arc form capsids in neurons?
Speaker: Janet Iwasa, Ph.D., Assistant Professor, Department of Biochemistry, University of Utah
Title: "Animating Molecular Machines"
Research Summary: Janet Iwasa creates accurate animations to help scientists better visualize and communicate the mechanisms they study. Her illustrations and animations have appeared in scientific journals, the New York Times, on television, and in museum exhibits. In her talk, she will discuss how researchers can use molecular animation to further their scientific understanding and engage diverse audiences, providing examples from her animation projects. She will also discuss software projects that focus on enabling researchers to create their own visualizations. Throughout the talk, she will share stories of how she took her career in this novel direction and what she has learned about engaging with the public about science.
Graduate student speakers:
Charlotte Magee: NP graduate student (Fleckenstein lab): "Impact of Bath Salts on Monoamine Transporters"
Michelle Reed: NP graduate student (Baehr lab): "The Role of CEP164 in Photoreceptors"
Anne Gibson: NP graduate student (Keefe lab): "Effects of methamphetamine-induced dopamine toxicity on striatal plasticity"
Lee Leavitt: School of Biological Sciences masters student (Olivera lab): "Assessing Receptor and Ion Channel Function Using an Integrated Molecular, Cellular and Systems Approach (Constellation Pharmacology)"
Robert Coffman: BYU graduate student (Woodbury lab): “Drunken membranes and their potential effects on neurosecretion”