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About the Authors:
Lisa M. Parsons
Affiliation: Food and Drug Administration, Center for Biologics Evaluation and Research, Bethesda, Maryland, United States of America
Rahman M. Mizanur
Current address: US Army Medical Research Institute of Infectious Diseases, Division of Molecular and Translational Sciences, Fort Detrick, Frederick, Maryland, United States of America
Affiliation: Food and Drug Administration, Center for Biologics Evaluation and Research, Bethesda, Maryland, United States of America
Ewa Jankowska
Affiliation: Food and Drug Administration, Center for Biologics Evaluation and Research, Bethesda, Maryland, United States of America
Jonathan Hodgkin
Affiliation: Genetics Unit, Department of Biochemistry, University of Oxford, Oxford, United Kingdom
Delia O′Rourke
Affiliation: Genetics Unit, Department of Biochemistry, University of Oxford, Oxford, United Kingdom
Dave Stroud
Affiliation: Genetics Unit, Department of Biochemistry, University of Oxford, Oxford, United Kingdom
Salil Ghosh
Affiliation: Food and Drug Administration, Center for Biologics Evaluation and Research, Bethesda, Maryland, United States of America
John F. Cipollo
* E-mail: [email protected]
Affiliation: Food and Drug Administration, Center for Biologics Evaluation and Research, Bethesda, Maryland, United States of America
Introduction
Caenorhabditis elegans can be infected by over forty microbial pathogens [1]. Among these are the nematode specific pathogen, Microbacterium nematophilum, and the human pathogens Yersinia pestis and Yersinia pseudotuberculosis. M. nematophilum infects the anus, rectum and surrounding cuticle of the nematode causing localized swelling and constipation [2]. Y. pestis and Y. psudotuberculosis do not directly infect C. elegans. Rather these bacteria secrete an exopolysaccharide that adheres to the head region of the nematode, causing starvation [3]. The bus and bah genetic screens have isolated mutants resistant to M. nematophilum and Yersinia spp. respectively, and there is significant genetic overlap between the screens demonstrating that a series of the same genes are required for both pathogenic processes.
The bus screens have yielded more than 20 complementation groups [4], [5]. These were characterized by an absence of swelling in the tail region when exposed to the M. nematophilum leading to the bacterially unswollen (bus) phenotype. Included among the genes that have been cloned six (bus-2, bus-4, bus-8, bus-12, bus-17 and srf-3) encode a distinct gene required for, glycoconjugate biosynthesis [6]-[8]. The bus-2, bus-4 and bus-17 genes encode homologs of glycosyltransferases...