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B.S., University of Minnesota, Twin Cities, Minneapolis, MN, 2009
Honors and Awards:
Our lab studies the bacterial pathogen Mycobacterium tuberculosis (Mtb), which is the causative agent of the pulmonary infection tuberculosis. Mtb remains a global health issue today due to the ability of the bacterium to persist in a latent state in immune-competent individuals before re-activating to cause disease. It is estimated that up to a third of world’s population is latently infected with Mtb. I am interested in identifying mechanisms utilized by Mtb to persist in the face of a robust immune response. Previous data from our lab suggests that Mtb requires a phosphate-responsive signal transduction system, Pst/SenX3-RegX3, to resist host immune responses in a mouse model of infection. However, it is unknown which specific bacterial factors, whose expression is controlled by the DNA binding regulatory protein RegX3, contribute to persistence. We have evidence that RegX3 controls the activity of a specialized mycobacterial protein secretion system, ESX-5. Although ESX-5 has been implicated in Mtb virulence, there is little known about its regulation or function. My thesis research will involve identifying the regulation mechanism of the ESX-5 secretion system, as well as characterizing the biological function of this system.
Elliott, SR. Tischler, AD. (2016). Phosphate Starvation: a Novel Signal that Triggers ESX-5 Secretion in Mycobacterium tuberculosis. Mol Micro. May;100(3):510-26.
Elliott, SR. Tischler, AD. (2016). Phosphate responsive regulation provides insights for ESX-5 function in Mycobacterium tuberculosis. Curr Genet. 2016 Apr 22.