Departmental Seminars

Spring Semester 2020: 12:00 pm - 12:50 pm in RITA 102

Monday, February 24, 2020
Deborah Bidwell, Senior Instructor, College of Charleston

Biomimicry – emulating nature’s adaptations to foster optimized human enterprise.

Join me to explore how the biomimicry design process translates time-tested strategies and mechanisms

from the natural world into engineering and design principles for well-adapted entrepreneurial solutions to economic, social, and environmental challenges. I’ll describe my recent research examining biomimetic applications for deterring bat attraction at wind turbines and designing burrowing robots, as well as highlighting current opportunities in undergraduate biomimicry education at CofC.

Monday, February 3, 2020
Dr. Courtney Murren, Professor, College of Charleston

Sabbatical Report:

Getting to the root of it: ecological genetics of Arabidopsis wild populations and mutants.

Roots of weedy annual plant species have critical functional roles for the plant. In this seminar, I will share the culmination of several multi-year studies with Arabidopsis thaliana in which we investigated natural variation among populations of in the wild, responses of roots and shoots to multiple field common gardens, and the effects of mutant response to experimental manipulations. Together, these examinations of the perturbation of ecology and genetics of this system highlight the importance of examining belowground traits together with aboveground traits to understand plant performance of wild plants and to inform crop improvement. I will also highlight the collaborative REEU program, and an orchid project that launched during my sabbatical.

Monday, January 27, 2020
Dr. Carissa James '14, Translational Scientist at FirstString Research, Inc

Alternative Translation as a Novel Cellular Regulator of Gap Junctional Coupling

Gap junctions, comprised of connexin proteins,are essential for direct intercellular electrical, metabolic, and immunological coupling. Connexin43 (Cx43, gene name GJA1) is the most ubiquitously expressed gap junction protein, and Cx43 gap junctions are altered in pathological states including cardiac disease and cancer. The GJA1 mRNA undergoes alternative translation initiation to yield a truncated Cx43 isoform, GJA1-20k, that can regulate gap junction formation. Using epithelial-mesenchymal transition (EMT) as a cellular model of gap junction remodeling, we have demonstrated altered translation initiation of Gja1 as a mechanism by which cellular Cx43 gap junctions can be dynamically regulated. Suppression of Gja1 alternative translation is necessary for Cx43 gap junction loss, and stable expression of GJA1-20k rescues gap junction formation during EMT. To identify regulatory factors acting on the Gja1 mRNA, an MS2 RNA aptamer tagging system was adapted to isolate Gja1 with associated RNA binding proteins. We find the RNA binding protein IMP1 is sensitive to hypoxic stress and complexes with Gja1 mRNA, where it is necessary for alternative translation to generate GJA1-20k. We have demonstrated alterations in translation initiation of the Gja1 mRNA as a critical mechanism by which cells modulate Cx43 gap junctional coupling in changing conditions and identified a novel regulator of this process in mammalian cells.



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