Mechanisms and roles of the LuxS system, methyl recycling, and DNA methylation on the physiology of Campylobacter jejuni

Abstract

Introduction iii Materials and Methods Results Discussion Acknowledgements Author Contributions Figures legends Tables CHAPTER 4. CHARACTERIZATION OF THE CJSA_RS00180 DNA METHYLTRANSFERASE IN CAMPYLOBACTER JEJUNI IA3902 Abstract Introduction Materials and Methods Results Discussion Figures legends Tables CHAPTER 5. General Conclusions General Discussion Recommendations for Future Research ix ACKNOWLEDGEMENTS This thesis was made possible by the collective efforts and support of colleagues, friends, and family. First, I would like to express my sincerest gratitude to my major professor, Dr. Paul Plummer, as he has been an invaluable mentor at every step of my graduate studies. I am thankful for his kindness, patience, expertise, and the time he has spent answering all of my questions, challenging me and instilling confidence in myself as a scientist, improving my writing, and helping me gain access to innumerable opportunities, all of which have helped me develop into a successful independent researcher. I am very grateful for the opportunity to work in his laboratory. I would also like to thank my program of study committee: Drs. Qijing Zhang, Michael Yaeger, Lisa Nolan, and Gwyn Beattie for their guidance, suggestions, and encouragement. I thank all the members of the Plummer lab and Zhang lab, whom I have had the privilege to work with, and have invested countless number of hours to help assist me with experiments and training, sharing their wisdom and expertise in all things Campylobacter, and have always been available for me to exchange thoughts and ideas with. My research successes would not have been possible without your support and guidance. I also thank the countless number of former and current employees at the Iowa State University College of Veterinary Medicine and at the Interdepartmental Microbiology program for their support throughout my graduate career. Lastly, I would like to sincerely thank my parents Dach and Sherry, my sister Connie, Alan, Marty, Brent, Anna, and all my friends for their unwavering love and invaluable support network. For without their continuous love and support, I would not be where I am today.

Small Noncoding RNA CjNC110 Influences Motility, Autoagglutination, AI-2 Localization, Hydrogen Peroxide Sensitivity, and Chicken Colonization in Campylobacter jejuni

“…The loss of the ability of ΔluxS to sustain colonization in chickens, as demonstrated in this study, has been previously described in IA3902, but the same phenotype was not observed in the closely related NCTC 11168 (8); the reason for this difference is currently unknown but has been speculated to be related to strain-specific differences in the metabolism of methionine or S-adenosylmethionine (SAM) recycling, which are also affected by the luxS mutation (28). Additional work in our lab has shown that the luxS mutation in IA3902 does disrupt the AMC, which functions to recycle SAM and produce methionine (64); however, DNA methylation in IA3902 was not affected by the luxS mutation (65). Comparative genomics reveals that NCTC 11168 does harbor an additional genomic system for methionine biosynthesis in the form of metAB which is not present in IA3902 and may represent an alternative pathway for synthesis of this required amino acid and an explanation for the observed difference in colonization ability.…”

Investigation of the gallbladder host environment and small RNAs in the pathobiology of Campylobacter jejuni sheep abortion clone IA 3902

“…The LuxS enzyme is critical for the formation of S-adenosylmethionine (SAM), which is a major methyl donor necessary for methylation of DNA, proteins, carbohydrates and other molecules important to the physiology of prokaryotes (Parveen and Cornell, 2011). It is plausible that expression of this methyltransferase is sensitive to decreased availability of products from the activated methyl cycle due to luxS mutation; however, recent data generated within our lab group suggests that this gene does not encode an active methyltransferase (Mou, 2015).…”