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Professor of Microbiology
Office: 540B Eckstein Medical Research Building431 Newton RdIowa City, IA 52242
Office Phone: 319-335-9688
Lab: 540 Eckstein Medical Research Building431 Newton RdIowa City, IA 52242
Email: email@example.comWeb: Yahr Lab WebsiteWeb: Carver College of Medicine InterviewWeb: Google Scholar Page
BS, Biology, University of Wisconsin, Stevens PointMS, Microbiology, Medical College of WisconsinPhD, Microbiology, Medical College of Wisconsin
Post Doctoral, Biochemistry, Dartmouth Medical School
Biosciences Graduate ProgramDepartment of Microbiology Graduate ProgramInterdisciplinary Graduate Program in Translational BiomedicineMedical Scientist Training Program
My laboratory studies regulation of the Pseudomonas aeruginosa type III secretion system (T3SS). T3SS's are unique to Gram-negative bacteria and function to deliver toxins into eukaryotic host cells. The secretion machinery consists of ~30 proteins which span both the inner and outer membranes of the bacterial cell. Following contact of the bacterium with a eukaryotic cell, the type III machinery functions like a molecular syringe to inject toxins into the host cell. Expression of the P. aeruginosa T3SS is highly regulated and induced by at least two environmental cues; contact of the bacteria with eukaryotic cells and growth in the presence of low Ca2+ concentrations. In the absence of these cues, low amounts of the type III secretion channels are assembled within the cell membranes. The channels, however, are inactive and expression of the T3SS is repressed. Expression of the T3SS genes is coupled to type III secretory activity by a cascade of interacting regulatory proteins (ExsA, ExsD, ExsC, and ExsE). ExsA is an activator of type III gene transcription, ExsD binds ExsA to inhibit transcription, ExsC inhibits ExsD activity, and ExsE inhibits ExsC activity. The entire process is coupled to secretion by virtue of the fact that ExsE is a secreted substrate of the T3SS. Changes in the intracellular concentration of ExsE are thought to govern formation of the ExsC-ExsE, ExsC-ExsD, and ExsD-ExsA complexes. Whereas formation of the ExsC-ExsE complex allows ExsD to bind ExsA and transcription of the T3SS is repressed, formation of the ExsC-ExsD complex sequesters ExsD from ExsA and transcription of the T3SS is induced. The major efforts in my lab involve testing the above model and determining how this regulatory cascade interfaces with a number of additional regulatory mechanisms also controlling T3SS gene expression.
Center for Biocatalysis and BioprocessingCenter for Gene Therapy of Cystic Fibrosis and other Genetic Diseases
The AlgZR Two-Component System Recalibrates the RsmAYZ Posttranscriptional Regulatory System To Inhibit Expression of the Pseudomonas aeruginosa Type III Secretion System.
2014 January. 196(2):357-66.
Schesser Bartra S,
ExsA and LcrF recognize similar consensus binding sites, but differences in their oligomeric state influence interactions with promoter DNA.
2013 December. 195(24):5639-50.
Pseudomonas aeruginosa Utilizes the Type III Secreted Toxin ExoS to Avoid Acidified Compartments within Epithelial Cells.
2013 September 18. 8(9):e73111.
An unusual CsrA family member operates in series with RsmA to amplify posttranscriptional responses in Pseudomonas aeruginosa.
Proc Natl Acad Sci U S A.
2013 September 10. 110(37):15055-60.
Sialic Acid Catabolism in Staphylococcus aureus.
2013 April. 195(8):1779-88.
Self-trimerization of ExsD limits inhibition of the Pseudomonas aeruginosa transcriptional activator ExsA in vitro.
2013 February. 280(4):1084-94.
Orientation of Pseudomonas aeruginosa ExsA monomers bound to promoter DNA and base-specific contacts with the P(exoT) promoter.
2012 May. 194(10):2573-85.
The distal ExsA-binding site in Pseudomonas aeruginosa type III secretion system promoters is the primary determinant for promoter-specific properties.
2012 May. 194(10):2564-72.
The transiently ordered regions in intrinsically disordered ExsE are correlated with structural elements involved in chaperone binding.
Biochem Biophys Res Commun.
2012 January 6. 417(1):129-34.
Glucose depletion in the airway surface liquid is essential for sterility of the airways.
2011 January 20. 6(1):e16166.
Date Last Modified: 06/07/2014 -
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