Dana Shaw, Ph. D.

Personal biography

I have always been fascinated by how a single-celled, microscopic organism can cause extensive disease to a host. After completing a B.S. in Biology (molecular, cellular and developmental) and participating in an undergraduate microbiology research lab, I was inspired to pursue a graduate degree in microbial pathogenesis. My Ph.D., under the guidance of Dr. Jon Skare at the Texas A&M Health Science Center, centered on characterizing pathogenic mechanisms and virulence determinants of the Lyme disease spirochete, Borrelia burgdorferi. During this time, I became intrigued by the versatility of arthropod-borne pathogens, which allows them to survive in drastically different environments throughout a life cycle. I am now completing postdoctoral training with Dr. Joao Pedra to gain experience with the arthropod side of vector-borne disease.

Outside of the lab, I enjoy swimming, the outdoors, trying new restaurants and exploring the East coast with my husband and fellow scientist, Dr. Jason Park.


Publications

Shaw D.K., Wang X., Brown L.J., Chávez A.S., Reif K.E., Smith A.A., Scott A.J., McClure E.E., Boradia V.M., Hammond H.L., Sundberg E.J., Snyder G.A., Liu L., DePonte K., Villar M., Ueti M.W., de la Fuente J., Ernst R.K., Pal U., Fikrig E., Pedra J.H.F Infection-Derived Lipids Elicit a Novel Immune Deficiency Circuitry in Arthropods. Nat. Commun. 2017. 8, 14401 doi: 10.1038/ncomms14401.
Links to media coverage:


Oliva Chávez, A.S., Shaw, D.K., Munderloh, U.G., Pedra, J.H.F. Tick Humoral Responses: Marching to the Beat of a Different Drummer. Front. Microbiol. 2017. 8:223. doi: 10.3389/fmicb.2017.00223.


Shaw, D.K., McClure, E.E., Kotsyfakis, M., Pedra, J.H.F. Tick saliva and microbial effector molecules: two sides of the same coin. Chapter 11 of Arthropod Vector: Controller of Disease Transmission (Volume 2): Vector Saliva-Host-Pathogen Interactions. Elsevier. 2017.

Shaw, D.K., McClure, E.E., Wang, X., Pedra, J.H.F. Deviant behavior: tick-borne pathogens and inflammasome signaling. Vet Sci. 2016, 3(4), 27. doi: 10.3390/vetsci3040027.


Skare J.T., Shaw D.K., Trzeciakowski J.P., Hyde J.AIn vivo imaging demonstrates that Borrelia burgdorferi ospC is uniquely expressed temporally and spatially throughout experimental infection. PLoS One. 2016 Sep 9;11(9):e0162501. doi: 10.1371/journal.pone.0162501.


Wang, X., Shaw, D.K., Sakhon, O.S., Snyder, G.A., Sundberg, E.J., Santambrogio, L., Sutterwala, F.S., Dumler, J.S., Shirey, K.A., Perkins, D.J., Richarda, K., Chagas, A.C., Calvo,E., Kopecký, J., Kotsyfakisi, Pedra, J.H.F. The Tick Protein Sialostatin L2 Binds to Annexin A2 and Inhibits NLRC4-Mediated 2 Inflammasome Activation. Infect Immun. 2016 Apr; IAI.01526-15. 10.1128/IAI.01526-15.


Shaw, D.K., Kotsyfakis, M., Pedra, J.H.F. For whom the bell tolls (and nods): spit-acular saliva. Curr. Trop. Med. Rep. 2016 April;3: 40. doi: 10.1007/s40475-016-0072-4.


Wager, B., Shaw, D.K., Groshong, A.M., Blevins, J.S., Skare, J.T. BB0744 affects tissue tropism and spatial distribution of Borrelia burgdorferi. Infect Immun. 2015 Sep;83(9):3693-703. doi: 10.1128/IAI.00828-15.


Shaw, D.K., Hyde, J.A., J.T. Skare. The Borrelia burgdorferi BB0646 protein is responsible for the lipase and hemolytic activity associated with the etiological agent of Lyme disease. Mol Microbiol. 2012 Jan;83(2):319-34. doi: 10.1111/j.1365-2958.2011.07932.x.


Hyde, J.A., Shaw, D.K., Smith, R. 3rd, Trzeciakowski, J.P., Skare, J.T. Characterization of a conditional bosR mutant in Borrelia burgdorferi. Infect Immun. 2010 Jan;78(1):265-74. doi: 10.1128/IAI.01018-09.


Hyde, J.A., Shaw, D.K., Smith 3rd, R., Trzeciakowski, J.P., Skare, J.T. The BosR regulatory protein in Borrelia burgdorferi interfaces with the RpoS regulatory pathway and modulates both the oxidative stress response and pathogenic properties of the Lyme disease spirochete. Mol Microbiol. 2009 Dec;74(6):1344-55. doi: 10.1111/j.1365-2958.2009.06951.x.


Current Projects

My current project focuses on the immune pathways of Ixodes scapularis in response to the pathogen, Anaplasma phagocytophilum. I. scapularis is unusually permissive to a variety of pathogens (6 total), including A. phagocytophilum, indicating that there is something unique about this tick that allows it to be colonized and not overcome. We are honing in on the immunodeficiency pathway (IMD pathway) which is analogous to the IMD pathway in Drosophila  melanogaster, but with some key differences. Of note, I.  scapularis appears to lack the IMD and FADD proteins and only has a truncated version of Relish, all which are key players in the classically defined IMD pathway of D.  melanogaster. This modified IMD pathway in I. scapularis appears to be modulated by the post-translational modification, ubiquitylation; accomplished through the E3 ubiquitin ligase and X-linked inhibitor of apoptosis (XIAP) in response to A. phagocytophilum infection. Cumulatively, our research has shown that although insects and arachnids are grouped together under the phylum, Arthropoda, there are distinct differences between their immune pathways.


Working in the Pedra lab

The Pedra lab provides a unique research environment that combines three fields: immunology, microbiology and entomology. This combination allows our lab to take into consideration all aspects of the A. phagocytophilum infectious life cycle, providing a powerful platform for advancing tick-borne pathogen research. Furthermore, by focusing on the tick immune response to vector-borne pathogens, it opens up the possibility for controlling the proliferation of these microbes during the vector portion of their life cycle, rather than targeting the mammalian reservoir or deferring to treatment of accidental human infection.

 

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