The 2019 keynote address will be given at 7:15 p.m. Friday, October 25th, at the Fayetteville Town Center.
Invited faculty talks will be given from 1:30-3:00 p.m. Friday, October 25th, in the Chancellor Hotel, Eureka Springs Ballroom, on the Fayetteville Square. Abstracts and titles will be posted when available.
Invited student talks will be given from 3:15-5:00 p.m. Friday, October 25th, in the Chancellor Hotel, assigned rooms, on the Fayetteville Square. (Please see the link to “Invited Student Speakers.”)
2019 Keynote Speaker (Friday Evening – Town Center – 7:15 pm)
TITLE: Short clocks and morning larks: a structural switch in Casein Kinase 1δ controls circadian timing in humans
ABSTRACT: Organisms adapt to the 24-hour solar cycle with molecular clocks that coordinate cellular functions with the external cue of sunlight to generate circadian rhythms of behavior and physiology. The timekeeping of these genetically encoded molecular clocks is driven by a transcription-translation feedback loop that leads to daily changes in the abundance of PERIOD (PER) proteins. Inherited mutations in PER2 lead to its premature turnover and a shorter clock, giving rise to Familial Advanced Sleep Phase Syndrome (FASPS), which is characterized by an early sleep onset and waking time (i.e., extreme morning larks). PER2 stability is largely determined by its phosphorylation state at two distinct regions within the protein, the Degron and FASP region; phosphorylation of PER2 by Casein Kinase 1 delta (CK1δ) at the Degron recruits the E3 ubiquitin ligase, β-TrCP, to induce PER2 degradation, while phosphorylation of the latter region somehow stabilizes PER2 to lengthen the clock. Understanding how CK1δ regulates these two sites on PER2 is key to understanding the molecular basis for clock periodicity. The CK1 Tau mutation (R178C), first identified in rodents with a 20-hour period, has been mapped to an anion-binding pocket near the activation loop on the kinase. We solved several high-resolution crystal structures of the wild-type CK1δ and Tau mutant to discover a two-state conformational switch in the activation loop that is coupled to anion occupancy. This conformational switch controls substrate preference, as the Tau mutant exhibits a gain of function toward the Degron and a loss of function at the FASP region using in vitro and cell-based kinase assays. MD simulations support experimental observations that the Tau mutation changes the dynamics of the kinase near the activation loop and suggest a mechanism by which other short period mutants from Drosophila to humans leverage this conformational switch in CK1 to control circadian period.
PHYSICS (1:35 pm Friday):
Dr. Jin Hu, Ph. D.
Department of Physics,
University of Arkansas
TITLE: Exploring the World Using Materials
Awarded Nobel Prize in 2016, the theory of topological phase and topological phase transition have bridged a few scientific disciplines including topology, material science, and high energy physics. Taking into account of the topological properties of electrons leads to the theoretical predictions and experimental demonstrations of a few exotic particles such as Dirac, Weyl, and Majorana fermions in a group of emergent “topological quantum materials”. A Weyl fermion can be viewed as a half of a Dirac fermion, while a Majorana fermion is the anti-particle of itself. These particles have been predicted in high energy physics for almost a century, and now they are finally discovered in crystalline solids. In this talk, I will show how we synthesis the single crystals of these topological quantum materials, use them to explore the exciting phenomena in high energy physics and material science, and explore their promising applications in next generation technology.
BIOLOGY (2:05 pm Friday):
TITLE: Exosomes Modify the Cell Microenvironment and the Classroom
My lab at Ouachita is a member of the Extra Cellular Matrix (ECM) division of the Center for Advanced Surface Engineering (CASE). The ECM is investigating mechanisms for neuronal differentiation and repair. Unlike other cells in our body, when neurons are damaged, they cannot be replaced, and the result is loss of feeling or in some cases, paralysis. By taking a multi-disciplinary and collaborative approach that uses bioinformatics to drive wet lab experiments, we have shown how cells use exosomes to modify their microenvironment. Exosomes are small extracellular membrane-bound vesicles that have a role in cell-to-cell communication. My lab has completed four RNA sequencing projects, each showing exosome specific changes in gene expression and cell morphology. Research has now expanded into cell culture experiments. Our results show that exosomes isolated from differentiating neurites (neuron-like) can cause cell differentiation in the absence of neural growth regulators. Research in my lab begins as a Course Embedded Undergraduate Research Experience (CURE). The ECM-exosome project (NSF-AR-EPSCoR) and an AR-INBRE funded project (Lori Hensley-CoPI), was the foundation for the Cell Biology Education Consortium (CBEC – www.cellbioed.com). The CBEC is an NSF funded undergraduate research collaborative network focusing on incorporating cell tissue culture into the classroom. Created in August of 2018, the CBEC now represents over 100 undergraduate institutions and has funded ~ $60,000 in student projects. I will present my lab’s data and how collaboration has changed how I approach both education and research. Support is provided by NSF /AR-EPSCoR and the Center For Advance Surface Engineering (CASE), the Cell Biology Education Consortium (NSF-RCN-UBE), the AR-CURE project (NSF-EPSCoR), the Ouachita Paterson Summer Research Fellowship, and AR-INBRE.
CHEMISTRY (2:35 pm Friday):
TITLE: Toward a cost-efficient treatment for Chagas disease: The development of novel anti-parasitics from a common core
Neglected tropical diseases (NTDs), which include Chagas disease, are classified as a worldwide health crisis which affect over a billion people in the world’s poorest nations. NTDs are typically associated with populations in developing countries, however, Chagas diseases is now being reported in the United States. This illness is known to infect nearly 8 million people in over 20 Central and South American countries along with an additional 300,000 cases a year reported in the U.S. Chagas disease is a public health problem in these nations. Current effective therapeutic treatments for most NTDs are often plagued by horrific side effects and alarming rates in drug resistance. In general, the mechanism of action for these drugs is largely unknown. The development of alternative medications that circumvent resistance with decreased side effects and defining the mechanism of action of these compounds has not been a priority for the pharmaceutical industry because there is little profit-motive in treating the world’s poorest citizens.
Our research goal is to produce cost-effective, safe, and potent drug candidates that target Trypanosoma cruzi, the parasite responsible for Chagas disease. It is the leading cause of heart disease in Central and South America. Currently, there is no vaccine for Chagas disease and the only treatment is the drug benznidazole, which has seen an alarming increase in treatment failures. In order to identify new therapeutic targets for Chagas disease, the development of a disquaramide-based drug library was undertaken. The synthesized short-chain disquaramides are ideal for making cost-effective anti-Chagastic drug targets due to their short synthetic pathways (three steps), relatively inexpensive syntheses, and known anti-parasitic properties for T. cruzi. To date, a comprehensive library of over 75 of these compounds have been successfully synthesized and are awaiting testing for their anti-Chagastic properties.