Ryanodine receptors (RyRs) are intracellular ion channels that mediate the release of calcium from intracellular stores. RyR1 and RyR2 are the predominate isoforms in skeletal and cardiac muscle, respectively where they play a central role in excitation-contraction coupling. RyRs are the largest known ion channels and are regulated by a multitude of endogenous effectors including ions, small molecules, and accessory proteins. An area of interest is the regulation of these channels by endogenous effectors, especially as it relates to altered contractile function associated with cardiac ischemia, skeletal muscle fatigue and aging. 

Because of their central role in cellular calcium regulation, defects in RyR channels can lead to potentially fatal disorders. Mutations in RyR1 give rise to the pharmacogenetic skeletal muscle disorder, malignant hyperthermia (MH). RyR2 mutations have been identified in catecholaminergic polymorphic ventricular tachycardia. We are interested in determining the molecular mechanisms by which these mutations alter RyR channel function. 

We analyze channel function on multiples levels of organization. Sarcoplasmic reticulum vesicle [3H]ryanodine binding is used to examine large populations of channels. We incorporate channels into artificial lipid bilayers in order to record single channel currents and assess channel kinetics. Calcium release from permeabilized muscle fibers provides a method of examining RyR function in situ. My research has two long-range goals. The first is to understand how intracellular calcium is regulated and how alterations in the regulation effects cell function. The second goal is to understand the RyR regulatory sites that might be exploited for the development of pharmacological compounds to treat disorders of cellular calcium regulation.

Dr. Whiteley received his B.S. degree in Zoology in 1995 from the University of Texas at Austin and his Ph.D. in Microbiology from the University of Iowa in 2001. His doctoral research involved quorum sensing and biofilm formation in the bacterium Pseudomonas aeruginosa. Following a Postdoctoral Fellowship at Stanford University in 2002, Dr. Whiteley accepted a position as an assistant professor at the University of Oklahoma/Oklahoma Health Sciences Center. In 2006, Dr. Whiteley moved to the University of Texas at Austin where he was promoted to Professor of Molecular Biosciences and Director of the LaMontagne Center for Infectious Disease. In 2017, he accepted the Bennie H. & Nelson D. Abell Chair and Georgia Research Alliance Eminent Scholar in Molecular and Cellular Biology at Georgia Institute of Technology. He also serves as Associate Director of the CF-Air Center at Emory Medical School. Dr. Whiteley has garnered numerous awards for his work including the Merck Irving S. Sigal Memorial Award for national research excellence, the Burroughs Wellcome Investigators in Pathogenesis of Infectious Disease award, recognition as a Kavli fellow of the National Academy of Sciences, the Dean’s teaching excellence award from UT-Austin, and election to the American Academy of Microbiology.

My research interests center on control of movement by sensorimotor integration in the mammalian spinal cord. Using predominantly electrophysiological methods applied in vivo, we study neural signaling by spinal motoneurons, somatosensory neurons, and their central synapses. Our primary analyses include electrical properties, synaptic function, and firing behavior of single neurons. We are actively examining how these neurons and synapses respond soon and long after peripheral nerve injury and regeneration. Our recent findings demonstrate that successful regeneration of damaged sensory axons does not prevent complex reorganization of their synaptic connections made within the spinal cord. In separate studies, we are examining novel mechanisms of sensory encoding and their impairment which recently discovered in rodents treated with anti-cancer drugs. Both nerve regeneration and chemotherapy projects are driven by the long-term goal of accurately identifying the neural mechanisms behind movement disorders. We also continue to explore fundamental operations of the normal adult nervous system. Our most recent studies focus on synaptic modulation of motoneuron firing and on interspecies comparisons of spinal circuits.

Yury O. Chernoff is a professor in the School of Biology and Institute for Bioengineering and Bioscience and Editor-in-Chief of the scientific journal Prion. He received his undergraduate and graduate training and Ph.D. degree in biology from St. Petersburg (then Leningrad) State University (Russia) and performed postdoctoral research at Okayama University (Japan) and University of Illinois at Chicago. 

Major topics of Dr. Chernoff’s research include yeast models for the protein aggregation disorders with an emphasis on the cellular control of protein aggregation and prion propagation, sequence-specificity of amyloid formation, and evolution of prion properties. 

Dr. Chernoff’s work provided the first experimental evidence for the chaperone role in prion phenomena.

Throughout my career, my laboratory has studied sphingolipids, a category of lipids that are important in cell structure, signal transduction and cell-cell communication. For more information about what we found, please refer to the Google Scholar or PubMed links below. 

As an Emeritus Professor, I am working on a project that has interested me for a long time--the fact that the active agent in the venom of the brown recluse spider is a sphingomyelinase D that produces a novel product, ceramide 1,3-cyclic phosphate. This activity has also been found in other spiders, bacteria and fungi. With the help of collaborators, I hope to learn more about the organisms that produce and degrade this novel sphingolipid, and possibly find ways to reduce the injury caused by the enzyme when humans encounter it in the environment.

Dr. Lewis A. Wheaton received his Ph.D. in Neuroscience and Cognitive Sciences from the University of Maryland, College Park in 2005. He was a fellow at the National Institutes of Health (Medical Neurology Branch, 2001-2005) studying neural function and recovery of motor control after stroke. In mid-2005 he was awarded a post-doctoral fellowship at the Baltimore Veterans Affairs Medical Center (Maryland) where he performed neuroscience research in aging and stroke motor control in Veterans.

In 2008, Dr. Wheaton joined the School of Applied Physiology at Georgia Tech as an Assistant Professor. He became tenured in 2014 and is currently an Associate Professor in Biological Sciences. Dr. Wheaton is the Director of the Cognitive Motor Control Laboratory at Georgia Tech, engaged in over $1 million in state and federal research funding focused on understanding aspects of human motor control rehabilitation in aging, stroke and amputation. His lab has employed numerous high school, undergraduate, graduate, and post-doctoral fellows. He is the course director for 4 courses in the School of Biological Sciences (Human Neuroimaging, Movement Disorders, Human Neuroanatomy, and the History of Neuroscience). He has Chaired/Co-Chaired 3 international conferences focused on motor control research and clinical outcomes, obtaining funding by federal and private sources. His research has yielded several manuscript publications in the field of motor control neuroscience, several focused expert reviews, and numerous conference presentations both in the US and abroad.

Dr. Wheaton is also an adjunct Associate Professor in the Department of Rehabilitation at Emory School of Medicine and a Member of the Children’s Center for Neurosciences Research at the Emory Children’s Pediatric Research Center.

Dr. Wheaton earned a BS (Biology) degree at Radford University (VA). He is an active parent volunteer at his children's schools and in the local community.

The research focus of Boris Prilutsky's laboratory is Neural Control and Biomechanics of Movement. They study how the nervous system controls hundreds of muscles and kinematic degrees of freedom of the body to produce purposeful motor behaviors and how the neural control of motor behaviors is affected by neural and musculoskeletal injuries.

I am an evolutionary biologist broadly interested in the evolution of complex life. My Ph.D. training focused on the evolutionary stability of cooperation in the legume-rhizorium symbiosis. Here I developed new experimental methods to study how among-organism genetic conflict arises and can be mitigated. A similar evolutionary tension lies at the heart of all key events in the origin of complex life, termed the ‘Major Transitions in Evolution’: namely, how do new organisms arise and evolve to be more complex without succumbing to within-organism conflict? Studying the early evolution of multicellular organisms has been particularly difficult because these transitions occurred deep in the past, and transitional forms have largely lost to extinction. As a postdoc, I circumvented this constraint by creating a new approach to study the evolution of multicellularity: we evolved it de novo. Since founding my own research group at Georgia Tech in 2014, I have combined this approach with mathematical modeling and synthetic biology to examine how simple clumps of cells evolve into multicellular organisms. Our research has shown how classical constraints in the origin of multicellularity — e.g., the origin of life cycles, multicellular development, cellular differentiation, and cellular interdependence — can be solved by Darwinian evolution. At home, I raise two kids on a hobby farm (really just a big garden) with bees, chickens, rabbits, goats, a dog, and lots of edible plants.

Michael Goodisman is interested in understanding how evolutionary processes affect social systems and how sociality, in turn, affects the course of evolution. His research explores the molecular basis underlying sociality, the nature of selection in social systems, the breeding biology of social animals, the process of self-organization in social groups, and the course of development in social species. His teaching interests are centered on the importance of behavior, genetics, and ethics in biological systems. Goodisman also works to improve and advance undergraduate education.