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Stacey Gilk, Ph.D.

Assistant Professor

Summary of the focus of the research of Dr. Gilk

The Gilk Lab studies manipulation of host cell lipids and lipid signaling by the intracellular bacterial pathogen Coxiella burnetii

Description and summary of your laboratory's research focus 

Our lab studies the intracellular bacterial pathogen Coxiella burnetii, the causative agent of human Q fever.  Acute disease generally presents as a debilitating flu-like illness, while chronic Q fever manifests as a life-threatening endocarditis.  During infection, Coxiella targets macrophages, where it survives in a unique, lysosomal-like compartment termed the parasitophorous vacuole (PV).  Formation of the PV is essential for bacterial survival, yet we know little about PV biogenesis and maintenance.  We are especially interested in how cholesterol and other lipids contribute to PV formation and the unique properties of the PV membrane. 

We are utilizing a combination of cell biology, biochemistry, and molecular biology techniques to address the role of cholesterol in Coxiella-host cell interactions.  Using a novel cholesterol-free tissue culture system, we found that Coxiella does not require cholesterol for PV formation and growth, and is in fact sensitive to high levels of cholesterol.  Coxiella expresses a unique eukaryotic-like sterol reductase that can modify sterols.  Bacteria lacking this sterol reductase are hypersensitive to cholesterol, leading to the hypothesis that Coxiella enzymatically modifies cholesterol during infection.  In addition, we are addressing mechanisms behind Coxiella manipulation of host cell cholesterol trafficking and homeostasis.

 

Gilk Lab:  http://gilklab.wix.com/home

  • Justis AV, Hansen B, Beare PA, King KB, Heinzen RA, Gilk SD.  Interactions between the Coxiella burnetii parasitophorous vacuole and the endoplasmic reticulum involve the host protein ORP1L. 2016. Cellular Microbiology.
  • Gilk SD, Cockrell DC, Luterbach C, Hansen B, Knodler LA, Ibarra JA, Steele-Mortimer O, Heinzen RA. Bacterial colonization of host cells in the absence of cholesterol. PLoS Pathog. 2013 Jan;9(1):e1003107.
  • Gilk, S.D.  2012.  The role of lipids in C. burnetii infection. Coxiella burnetii: Linking structure to function. Edited by R. Toman, J. L. Mege, R.A. Heinzen, and J.E. Samuel.  Adv Exp Med Biol. 984:199-213.
  • Beare, P.A., Larson, C.L, Gilk, S.D., and R.A. Heinzen.  2012.  Two systems for targeted gene deletion in Coxiella burnetii.Appl Environ Microbiol. Jul;78(13):4580-9.
  • *Beare, P.A., *Gilk, S.D., Larson, C.L., Hill, J, Stead, C.M., Howe, D., Omsland, A., Cockrell, D.C., Voth, D.E., and Heinzen, R.A.  2011.  The Dot/Icm type IVB secretion system requirements for Coxiella burnetii growth in human macrophages.  mBio, 2(4): e00175-11.    *co first-author
  • Gilk, S.D., Beare, P.A, and R.A. Heinzen. 2010. Coxiella burnetii expresses a functional delta24 sterol reductase.  J. Bacteriology, 192(23):6154-6159.
  • Beare, P.A, Unsworth, N., Andoh, M., Voth, D.E.,  Omsland, A., Gilk, S.D., Williams,  K., Sobral, B., Porcella, S.F., Samuel,  J.E.,  and R.A. Heinzen. 2009. Genome sequencing reveals extensive transposon-mediated genomic plasticity within the genus CoxiellaInfection and Immunity 77(2):642-56.
  • B.S., 1998: University of Notre Dame
  • Ph.D., 2004: University of Vermont
  • Postdoctoral, 2004-2007, University of North Carolina, Chapel Hill
  • Postdoctoral, 2007-2012, Rocky Mountain Laboratories, National Institutes of Health

Department of Microbiology and Immunology | IU School of Medicine | 635 Barnhill Drive, MS 420 | Indianapolis, IN 46202 | (317) 274-0506