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Role of Phosphorylation and Evidence of Mgla/ Sspa

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Role of Phosphorylation and Evidence of Mgla/ Sspa Regulation of Virulence Gene Transcripts by the Francisella Orphan Response Regulator PmrA: Role of Phosphorylation and Evidence of MglA/ SspA Interaction DISSERTATION Presented in Partial Fulfillment of the Requirements for the Degree Doctor of Philosophy in the Graduate School of The Ohio State University By Brian Len Bell, B.S. Integrated Biomedical Science The Ohio State University 2009 Dissertation Committee: John Gunn, Ph.D., Advisor Chad Rappleye, Ph.D. Larry Schlesinger, M.D. Mark Wewers, M.D. ABSTRACT Francisella tularensis subspecies tularensis is the etiologic agent of tularemia and has been designated a category A biothreat agent by the CDC. Tularemia is characterized by replication and dissemination within host phagocytes. Intramacrophage growth is dependent upon the regulation of Francisella Pathogenicity Island (FPI) virulence genes, which is poorly understood. Two-component regulatory systems (TCS) are widely employed by Gram negative bacteria to monitor and respond to environmental signals. Virulent strains of F. tularensis are devoid of classical, tandemnly arranged TCS, but orphaned members, such as the response regulator PmrA, have been identified. In the F. novicida model system, previous work has shown that a pmrA mutant is deficient for intramacrophage growth and is avirulent in the mouse model. Here we determine that phosphorylation aids PmrA binding to regulated promoters pmrA and the FPI encoded pdpD, and KdpD is the histidine kinase primarily responsible for phosphorylation of PmrA at the aspartic acid at position 51 (D51). A strain expressing PmrA D51A retains some DNA binding but exhibits reduced expression of the PmrA-regulon, is deficient for intramacrophage replication and is attenuated in the mouse model. PmrA co- precipitates with the FPI transcription factors MglA and SspA, which bind RNA ii polymerase. Together this data suggests a model of Francisella gene regulation that includes a TCS consisting of KdpD and PmrA. Once phosphorylated, PmrA binds to regulated gene promoters recruiting free or RNA polymerase bound MglA and SspA to initiate FPI gene transcription. iii DEDICATION To Erin, whose belief and support have made this possible. iv ACKNOWLEDGEMENTS I have been blessed with many excellent mentors: Janet Staab started my career as a bench scientist. Dave Brown taught me to see the big picture. Richard Warren gave me an important nudge into graduate school. Mick Arthur and Tom Dreier showed me how to do the job well. John Gunn helped me become a real student of science and patiently corrected my scientific errors. I have shared laboratories with many talented scientists. The long hours, piles of disappointing data, and the struggle to find meaning were all made bearable by experiencing them together. I hope you have all enjoyed working together as much as I have. This work has been positively affected by every member of the Gunn lab and the Center for Microbial Interface Biology. I would like to thank Denise Monack of Stanford University for generously providing the F. novicida His-SspA strain and Daniel Wozniak for supplying purified CheA. This work was sponsored by the NIH/NIAID Regional Center of Excellence for Bio-defense and Emerging Infectious Diseases Research (RCE) Program and by the CMIB fellowship through NIH Grant T32AI065411. v VITA May 12, 1971 ............................... Born – Columbus, Ohio 1995 ............................................ B.S. Zoology, The Ohio State University 1995 – 1998................................. Research Associate Department of Microbiology The Ohio State University Columbus, Ohio 1998 – 2000................................. Project Scientist Life Sciences Test Facility Dugway Proving Ground Dugway, Utah 2000 – 2006................................. Principal Research Scientist Biotechnology Battelle Memorial Institute Columbus, Ohio 2006-2008 ................................... Graduate Research Associate Molecular Virology, Immunology and Medical Genetics The Ohio State University Medical Center Columbus Ohio 2008 – present ............................. Graduate Research Fellow Center for Microbial Interface Biology The Ohio State University Medical Center Columbus, Ohio vi PUBLICATIONS Identification of an orphan response regulator required for the virulence of Francisella spp. and transcription of pathogenicity island genes. Nrusingh P. Mohapatra, Shilpa Soni, Brian L. Bell, Richard Warren, Robert K. Ernst, Artur Muszynski, Russell W. Carlson, John S. Gunn. Infection and Immunity, July 2007;75(7):3305-14 Final Report for the Joint Vaccine Acquisition Program (JVAP) for the Francisella tularensis Vaccine Project. Brian L. Bell, Robert M. Miceli, Lisa M. Moore, Sheri L. Schanaman, Katie Liljestand, Jennifer Thermos, Jeff Varelman, Stephen Parker, John D. Wright, Richard Warren, and Bruce Harper. West Desert Test Center, Life Sciences Division, U.S. Army Dugway Proving Ground. October 1999. Effects of Decontamination Solutions on Traditional and Molecular Detection Methodologies: TaqMan LightCycler PCR, ORIGEN Electrochemiluminescent, Hand-Held (HHA) and Colony-Forming Unit (cfu) Assays. Sheri L. Schanaman, Jeff Varelman, Brian L. Bell, Lloyd Larsen, Bruce G. Harper, David H. Brown, Michael Glass, Robert M. Miceli. West Desert Test Center, Life Sciences Division, U.S. Army Dugway Proving Ground. May 1999. Biological Weapons Convention Treaty Reference Guide. Daniel D. Martin, Brian L. Bell, and Stephen J. Parker. West Desert Test Center; Life Sciences Division; U.S. Army Dugway Proving Ground. February 1999. Biological Sampling Protocols for Use During On-Site Visits (1992 Biological Weapons Trilateral Agreement). Daniel D. Martin, Brian L. Bell, and Lester J. Richoux. West Desert Test Center; Life Sciences Division; U.S. Army Dugway Proving Ground. December 1998. Molecular Probe for Typing Strains of Candida albicans. Pamela Postlethwait, Brian L. Bell, W. Todd Oberle, and Paula Sundstrom. Journal of Clinical Microbiology, Feb. 1996, p. 474-476. FIELDS OF STUDY Major Field: Integrated Biomedical Science vii TABLE OF CONTENTS ABSTRACT ...........................................................................................................ii DEDICATION .......................................................................................................iv ACKNOWLEDGEMENTS ..................................................................................... v VITA .....................................................................................................................vi LIST OF TABLES .................................................................................................xi LIST OF FIGURES .............................................................................................. xii INTRODUCTION .................................................................................................. 1 1.1. Nomenclature ............................................................................................... 2 1.2. Ecology ......................................................................................................... 4 1.3. Disease ......................................................................................................... 5 1.4. Diagnosis ...................................................................................................... 6 1.5. Treatment ..................................................................................................... 7 1.6. Animal models of tularemia ........................................................................... 8 1.7. Epidemiology ................................................................................................ 9 1.8. Laboratory safety .........................................................................................10 1.9. Biological Warfare ........................................................................................11 1.10. Vaccines ......................................................................................................12 1.11. Pathogenesis ...............................................................................................14 1.12. Virulence Factors .........................................................................................18 1.13. The Francisella Pathogenicity Island (FPI) ...................................................19 1.14. Regulation of the FPI ...................................................................................24 viii 1.15. Other Francisella Virulence Factors .............................................................26 1.16. Two Component Regulatory Systems and Francisella .................................27 PmrA Regulates Francisella Virulence Factors by an Independent Pathway from other Virulence Determinants ............................................................................. 32 2.1. Introduction ........................................................................................................32 2.2. Results ...............................................................................................................35 2.3. Discussion ..........................................................................................................38 2.4. Materials and Methods .......................................................................................66 The Francisella Orphan Response Regulator PmrA Binds to Regulated Gene Promoters and Binding is Mediated by Phosphorylation. ..................................
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