Jason Rawlings

Jason Rawlings

Associate Professor of Biology

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Although Dr. Rawlings grew up in Louisville, Kentucky, he received his B.S. in Biology from Furman University. He then returned home to pursue a Ph.D. in Biology from the University of Kentucky, where he used a variety of genetic approaches to study cytokine signal transduction and its role in controlling development in the fruit fly, Drosophila melanogaster.

Following is graduate studies, Dr. Rawlings accepted an HHMI postdoctoral fellowship in the lab of James Ihle at St. Jude Children’s Research Hospital in Memphis, Tennessee. While at St. Jude, Dr. Rawlings continued his work on studying cytokine signaling, this time in the context of the development and differentiation of cells of the immune system using the laboratory mouse, Mus musculus. His work at St. Jude resulted in a seminal publication that describes how chromatin status controls clonal proliferation of T lymphocytes during an immune response. This publication received a landslide of press, including a commentary written by Wendy Bickmore, a pre-eminent scientist in the field of chromatin biology. The Scientist magazine named the paper it’s “Editor’s Choice in Immunology” and ranked it as the #6 paper in the world in the area of molecular biology. It was also reviewed 3 times by the Faculty of 1000 and also reviewed by the British Society of Immunology.

Dr. Rawlings returned to his alma mater in 2010 bringing his research program from St. Jude to Furman, where he utilizes multiple genetic and molecular approaches to continue his work on elucidating the roles of chromatin biology in immune cell development and function. He has also maintained collaborations with Dr. Paul Thomas at St. Jude and Dr. Brian Goess (Furman, Chemistry).  At Furman, Dr. Rawlings teaches courses including Immunology, Developmental Biology, Genetics, and our introductory course for majors. Dr. Rawlings is an active member of the American Association of Immunologists. Dr. Rawlings enjoys mentoring and working alongside undergraduate students and is most proud of his peer-reviewed publications that include student coauthors.​

Education

  • Postdoc, St. Jude Children's Research Hospital
  • Ph.D., University of Kentucky
  • B.S., Furman University

Research

The Rawlings Lab is currently pursuing two distinct research projects:

1. During an immune response, naïve T lymphocytes that encounter their cognate antigen become activated and acquire the ability to proliferate in response to cytokines. Specifically, genes that are required for proliferation remain transcriptionally silent in naïve T lymphocytes that are exposed to cytokines, but are readily transcribed following T lymphocyte activation. We determined that this change in transcriptional competence is due to a reconfiguration of chromatin (the way in which DNA is packaged in the nucleus). Our current research focuses on determining the mechanism(s) for this activation-induced chromatin reconfiguration as well as to determine if this mechanism is conserved among all lymphocyte populations. Students working on this project will utilize the mouse model system and employ a variety of molecular and immunological techniques including flow cytometry, cell sorting, quantitative PCR, immunofluorescence microscopy, and Western blot. This project has broad implications in the areas of cancer biology, autoimmunity, and immunodeficiency.

For more information on this project, see the following publications (student co-authors indicated with an asterisk):

  • J.S. Rawlings, M. Gatzka, P.G. Thomas, and J.N. Ihle. Chromatin condensation via the condensin II complex is required for peripheral T cell quiescence. EMBO J 2011; 30: 263-76.
  • M.D. Lee*†, K.N. Bingham*†, T.Y. Mitchell*, J.L. Meredith*, and J.S. Rawlings. Calcium mobilization is both required and sufficient for initiating chromatin decondensation during activation of peripheral T-cells. Mol Immunol 2015; 63: 540-549. †these authors contributed equally
  • K.N. Bingham*†, M.D. Lee*†, and J.S. Rawlings. The use of Flow Cytometry to assess the state of chromatin in T cells. JoVE 2015; 106: e53533. †these authors contributed equally
  • J.R. Funsten*, K.O. Murillo Brizuela*, H.E. Swatzel*, A.S. Ward*, T.A. Scott*, S.M. Eikenbusch*, M.C. Shields*, J.L. Meredith*, T.Y. Mitchell*, M.L. Hanna*, K.N. Bingham*, J.S. Rawlings, “PKC signaling contributes to chromatin decondensation and is required for competence to respond to IL-2 during T cell activation”, Cell Immunol 2020.

2. Cancer cells are hallmarked by their increased metabolic profile, which allows them to divide rapidly. An enzyme, phosphatidylinositol 3-kinase (PI3K) regulates cellular metabolism via the activation of the downstream molecule Akt. As such, many cancers have been shown to have hyperactive PI3K making it an attractive target for the development of chemotherapeutic drugs. The most widely known inhibitor of PI3K, Wortmannin, is not a good therapeutic option because it is costly to synthesize, unstable in neutral buffers, and has been shown to inhibit many other enzymes causing unwanted off-target effects. The Goess lab (Chemistry) at Furman University has synthesized a molecule called hibiscone C, which shares many of the structural features of wortmannin but is inherently more stable. The Rawlings lab successfully demonstrated that hibiscone C can inhibit PI3K activity, launching an interdisciplinary project between the Rawlings and Goess labs whereby our goal is to synthesize and test derivatives of Hibiscone C in order to find a more potent, stable, and selective PI3K inhibitor. Students working on this project will utilize the mouse model system and employ a variety of molecular techniques including Western blot and ELISA, with the opportunity to engage in organic synthesis of Hibiscone C derivatives.

For more information on this project, see the following publications (student co-authors indicated with an asterisk):

  • S. Ungureanu*, M. Meadows*, J. Smith*, D.B. Duff*, J.M. Burgess*, and B.C. Goess. Total Synthesis of (±)-Hibiscone C. Tetrahedron Lett 2011; 52(13):1509-1511.
  • C. Besley*, D.P. Rhinehart*, T. Ammons*, B.C. Goess, and J.S. Rawlings. Inhibition of phosphatidylinositol-3-kinase by the furanosesquiterpenoid hibiscone C. Bioorg Med Chem Lett 2017; 27: 3087-3091.

Publications

*Denotes undergraduate coauthor
+these authors contributed equally

    • J.R. Funsten*, K.O. Murillo Brizuela*, H.E. Swatzel*, A.S. Ward*, T.A. Scott*, S.M. Eikenbusch*, M.C. Shields*, J.L. Meredith*, T.Y. Mitchell*, M.L. Hanna*, K.N. Bingham*, J.S. Rawlings. PKC signaling contributes to chromatin decondensation and is required for competence to respond to IL-2 during T cell activation. Cell Immunol 2020; 347: 104027.
    • J.S. Rawlings. Primary Literature in the Undergraduate Immunology Curriculum: Strategies, Challenges, and Opportunities. Front Immunol 2019; 10:1857.
    • C. Besley*, D.P. Rhinehart*, T. Ammons*, B.C. Goess, and J.S. Rawlings. Inhibition of phosphatidylinositol-3-kinase by the furanosesquiterpenoid hibiscone C. Bioorg Med Chem Lett 2017; 27: 3087-3091.
    • J.S. Rawlings. Roles of SMC Complexes During T Lymphocyte Development and Function. In Rossen Donev, editor: Chromatin Remodelling and Immunity, Adv Protein Chem Struct Biol 2017; 106; 17-42.
    • K.N. Bingham*†, M.D. Lee*†, and J.S. Rawlings. The use of Flow Cytometry to assess the state of chromatin in T cells. JoVE 2015; 106: e53533
    • M.D. Lee*+, K.N. Bingham*+, T.Y. Mitchell*, J.L. Meredith*, and J.S. Rawlings. Calcium mobilization is both required and sufficient for initiating chromatin decondensation during activation of peripheral T-cells. Mol Immunol 2015; 63: 540-549.
    • D.M. Hollis, Y. Sawa*, A. Wagoner*, J.S. Rawlings, F.W. Goetz. Isolation and molecular characterization of Rem2 isoforms in the rainbow trout (Oncorhynchus mykiss): Tissue and central nervous system expression. Comp Biochem Physiol B Biochem Mol Biol 2012. 161: 93-101.
    • J.S. Rawlings, M. Gatzka, P.G. Thomas, and J.N. Ihle. Chromatin condensation via the condensin II complex is required for peripheral T cell quiescence. EMBO J 2011. 30: 263-76.
    • J.J. Gruber, D.S. Zatechka, L.R. Sabin, J. Yong, J.J. Lum, M. Kong, W. Zong, Z. Zhang, C. Lau, J. Rawlings, S. Cherry, J.N. Ihle, G. Dreyfuss, and C.B. Thompson. Ars2 links the nuclear cap binding complex to RNA interference and cell proliferation. Cell 2009. 132: 328-39.
    • M. Gatzka, R. Piekorz, R. Moriggl, J. Rawlings, and J. Ihle. A role for STAT5A/B in protection of peripheral T-lymphocytes from postactivation apoptosis: Insights from gene expression profiling. Cytokine 2006. 34: 143-154.
    • J.S. Rawlings, G. Rennebeck, and D.A. Harrison. Two Drosophila suppressors of cytokine signaling (SOCS) differentially regulates the JAK and EGFR pathways. BMC Cell Biology 2004. 5: 38.
    • J.S. Rawlings, K.M. Morey, and D.A. Harrison. The JAK/STAT Signaling Pathway. Journal of Cell Science 2004. 117: 1281-1283.

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