Professor, Program Director For Online MSc And Certificate Programs In Neuroscience Graduate Program
About Sue Semple-Rowland
Director of Online Biomedical Neuroscience Certificate and MSc Programs
My current teaching efforts are focused on delivering the highest quality graduate courses online. These graduate courses are an integral part of both the Department’s Biomedical Neuroscience Certificate and Master’s degree programs, both of which are offered to students worldwide in an online format. The certificate program has been running since Fall 2014 and has received glowing reviews from students who have completed this program. I have played an instrumental role in the creation of both of these programs and serve not only as the Director for both programs, but also have created and teach several of the courses that are taken by students enrolled in these programs. I am very excited about the new MSc program that has been approved to begin Fall 2020.
In addition to serving our online certificate and MSc students, our online graduate courses are also very popular among graduate students who are working on MSc or PhD research at UF. UF graduate students who have taken our courses hail from our Neuroscience Graduate program as well as from Biomedical Engineering, BMS programs in COM outside of Neuroscience, Veterinary Medicine, and Health and Human Performance.
My primary research interest has been to understand and develop potential therapies for treatment of inherited retinal photoreceptor diseases. I was fortunate to be able to focus my studies on the avian model of Leber congenital amaurosis – type 1 (LCA1), a disease that causes blindness in newborns. My research on this model began while I was a postdoctoral fellow and has continued throughout my career. My accomplishments include the identification of the genetic mutation underlying the disease in the chicken model (GUCY1B) and restoration of sight to these animals using a lentiviral-based gene therapy that was developed entirely in my laboratory. The results of our studies on the GUCY1B chicken laid the foundation upon which current clinical trials for treatment of LCA1 are based.
When we began our work to develop treatments for LCA1, we were on the forefront of gene therapy vector development. Early on, we made the decision to use lentiviral-based vectors as the platform for our therapies because they could rapidly integrate into the host cell genome and the vectors could carry large, complex transgenes. In addition to working on the types of transgene constructs that could effectively lead to expression of multiple proteins in target cells (e.g. containing IRES, 2A cleavage elements, or multiple promoters), we also focused on identification of minimal promoters whose expression characteristics would make them useful as drivers of photoreceptor-targeted therapies. Many of the vectors that we built are available through Addgene and are requested by investigators interested in expressing multiple proteins in infected cells.
A second major research interest has been to understand how light entrains the circadian clocks located in retinal photoreceptor cells. The GUCY1B chicken carries a null mutation in the gene encoding guanylate cyclase-1 (GC1), an enzyme that is essential for photoreceptors to recover from light stimulation. In the absence of GC1, the rods and cones in avian and human retina are unable to synthesize sufficient cGMP to support phototransduction. By measuring the levels of the transcripts of several genes whose expression is either regulated by photoreceptor clocks or represent components of the clock itself, we were able to determine that the phototransduction cascade that supports vision is not essential for light entrainment of photoreceptor clocks. In our most recent study, we obtained compelling evidence that a G-protein coupled cascade involving activation of phospholipase C in photoreceptors is involved in entraining photoreceptor clocks to light. Identification of a function of this second G-protein signaling cascade in retinal photoreceptors that is likely mediated by visual pigment activation of Gq/11, increases our understanding of the complexity of signaling within these well-studied cells.
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DEPARTMENT OF NEUROSCIENCE
GAINESVILLE FL 32610