INBRE 3 (2015-2020) introduced the Developmental Research Project (DRP) program that allows individual faculty at SC INBRE network institutions to submit competitive proposals for biomedical research. Of nine DRP awards conveyed statewide to PUIs in 2015, two were received by Furman faculty (Prof. Jason Rawlings and Prof. Renee Chosed). In 2016, Prof Alison Roark received this award.  In 2017, Prof. Adi Dubash received this award and in 2018 Prof. Linnea Freeman received this award.  Each of these researchers will receive over $75K/year in research support. A brief overview of their research focus is provided below.


Control of T cell proliferation is essential to proper immune function; lack of proper control can lead to pathologies such as autoimmunity, immunodeficiency, and cancer. STAT5 is a transcription factor that is absolutely essential for peripheral T cell proliferation. Following T cell receptor (TCR) engagement, activated T cells produce IL-2 which induces proliferation via STAT5. Naïve T cells, for which TCR engagement has not occurred, are refractory to IL-2 stimulation, remaining quiescent during an immune response. This ensures a clonal expansion of antigen specific T cells. Recently, we demonstrated that IL-2 induces STAT5 activation and nuclear localization in naïve T cells; however, STAT5 cannot engage DNA due to the condensed nature of chromatin in these cells. This condensation is not due to global modification of histones as previously thought, but to a higher-order chromatin condensation that is dependent on the activity of the condensin II complex. In this proposal we will determine the signaling pathway(s) downstream of the TCR that are responsible for chromatin decondensation during T cell activation. We will also determine if chromatin condensation is a conserved mechanism to regulate proliferation in other lymphocyte populations. These studies will provide important insight into the epigenetic control of lymphocyte proliferation and function.


Cnidarians are evolutionarily ancient animals including jellyfish, anemones, and corals, many of which form symbioses with intracellular, photosynthetic algae in the genus Symbiodinium. The goal of the proposed project is to determine the extent to which and the mechanism by which algal symbionts regulate development and reproduction of their cnidarian hosts. My hypothesis is that algal symbionts produce compounds that directly modulate host performance. Given their evolutionarily ancient origins, simple body plans, well established life histories, and mutualistic interactions with photosymbionts, cnidarians are particularly appropriate models for studying the impacts of interspecific cell signaling processes. In particular, studying the effects of exogenous compounds on reproductive function of anthozoans can provide information about conserved signaling pathways that are relevant to all animals. Phytochemicals such as flavonoids are increasingly recognized as endocrine-active compounds that influence reproductive capacity of animals including humans. My proposed work using the sea anemone Aiptasia pallida thus provides insight into the effects of plant-derived compounds on reproductive performance and the mechanisms underlying these effects in all animals, not just cnidarians. 


The desmosome is a highly specialized cell-cell junctional complex responsible for strong mechanical adhesion between cells, a characteristic required for normal tissue structure and resistance to mechanical stress. In addition, a growing body of evidence suggests that desmosomal proteins control many other fundamental biological processes such as cell proliferation, differentiation and migration. Therefore, it is not surprising that expression of protein members of the desmosome complex are altered in many different types of cancer. Loss of desmosome-mediated adhesion has been linked to tumorigenic phenotypes such as increased proliferation and migratory ability. The current proposal will investigate the role played by the desmosomal protein Desmoplakin (DP) in coordinating cell migration. Our preliminary evidence indicates that loss of DP (via siRNA-mediated knockdown) results in an increase in motility of human skin cancer cells. We hypothesize that DP coordinates the migratory properties of cancer cells via regulation of the Rho GTPase and p38 MAPK signaling pathways, both of which have been shown to play important roles in this process. To investigate this, we propose to determine if levels of active Rho GTPases and p38 MAPK are elevated upon loss of DP, and determine if abrogation of these signaling pathways can rescue the elevated motility observed in DP-deficient cells. Analysis of the signaling pathways involved will be achieved by biochemical pulldowns, immunofluorescence, and western blots/quantitative PCR. In addition, we will further investigate the migratory characteristics of control and DP knockdown cells, such as changes in cytoskeletal protrusions, alterations in focal adhesion size and number, and differences in production of extracellular matrix. By identifying the mechanistic signaling links responsible for DP-mediated migration, this work will provide significant insight into the function of desmosomes in this fundamental cellular process. Additionally, this work has the potential to uncover novel therapeutic targets to regulate both normal biological processes requiring cell migration (such as wound healing), as well as abrogation of pathological outcomes (such as cancer metastasis and invasion).

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