Faculty & Research
- Contact Information
- Contact Melanie Marketon by mmarketo [at] indiana [dot] edu
- By telephone: 812-856-3198/5-6055(lab)
- JH 469A/455 (lab)
- Research Areas
- Microbial Cell Biology and Environmental Responses
- Microbial Interactions and Pathogenesis
Ph.D., University of Texas at Dallas, 2002
Postdoctoral Fellow, University of Chicago, 2003-2006
My research focuses on understanding host-microbe interactions, specifically as related to plague pathogenesis. Yersinia pestis, the causative agent of plague, alternates between two different hosts: mammals and their fleas. We have ongoing projects to study both aspects of the Y. pestis lifestyle.
Y. pestis employs multiple virulence strategies to establish an infection within mammals. One well-studied mechanism is the type III secretion system, effectively a molecular syringe that allows the bacterium to inject cytotoxic proteins (known as Yops) directly into the cytoplasm of target host cells. Type III secretion is essential for virulence, and our research is aimed at understanding the molecular mechanisms that promote proper type III secretion. In particular, we are investigating the mode of action of a novel bi-functional regulator called YopK, which serves to control both the fidelity of type III secretion as well as the rate of secretion. This project involves a combination of genetics, biochemistry, and cell biology as we investigate the role of YopK in both bacteria and the host.
The newest project in the lab is focused on understanding the factors that promote colonization of the flea vector. We have developed a model system for studying this process using Drosophila larvae, and we are currently working to identify the genetic pathways in bacteria and the insect, which participate in colonization. Ultimately, we hope to understand why some fleas are good vectors for plague, while others are not, and simultaneously identify new strategies for biocontrol of plague and other vector-borne diseases.
RfaL is required for Yersinia pestis type III secretion and virulence.
Houppert AS, Bohman L, Merritt PM, Cole CB, Caulfield AJ, Lathem WW, Marketon MM.
Infect Immun. 2013 Apr;81(4):1186-97. doi: 10.1128/IAI.01417-12. Epub 2013 Jan 28.
YopK controls both rate and fidelity of Yop translocation.
Dewoody R, Merritt PM, Marketon MM.
Mol Microbiol. 2013 Jan;87(2):301-17. doi: 10.1111/mmi.12099. Epub 2012 Dec 4.
Identification of chromosomal genes in Yersinia pestis that influence type III secretion and delivery of Yops into target cells.
Houppert AS, Kwiatkowski E, Glass EM, DeBord KL, Merritt PM, Schneewind O, Marketon MM.
PLoS One. 2012;7(3):e34039. doi: 10.1371/journal.pone.0034039. Epub 2012 Mar 30.
YopK regulates the Yersinia pestis type III secretion system from within host cells.
Dewoody R, Merritt PM, Houppert AS, Marketon MM.
Mol Microbiol. 2011 Mar;79(6):1445-61. doi: 10.1111/j.1365-2958.2011.07534.x. Epub 2011 Jan 19.
Immunogenicity and protective immunity against bubonic plague and pneumonic plague by immunization of mice with the recombinant V10 antigen, a variant of LcrV.
DeBord KL, Anderson DM, Marketon MM, Overheim KA, DePaolo RW, Ciletti NA, Jabri B, Schneewind O.
Infect Immun. 2006 Aug;74(8):4910-4.
Rejection of impassable substrates by Yersinia type III secretion machines.
Sorg JA, Miller NC, Marketon MM, Schneewind O.
J Bacteriol. 2005 Oct;187(20):7090-102.
Plague bacteria target immune cells during infection.
Marketon MM, DePaolo RW, DeBord KL, Jabri B, Schneewind O.
Science. 2005 Sep 9;309(5741):1739-41. Epub 2005 Jul 28.