부산대학교 도서관

To purchase or authenticate to the full-text of this article, please visit this link: http://dx.doi.org/10.1111/j.1574-6968.2008.01438.x Byline: Matthew C. Berry (1), Gayle C. McGhee (2), Youfu Zhao (3), George W. Sundin (1,2) Keywords: fire blight; O-antigen; oxidative burst; reactive oxygen species; Pseudomonas aeruginosa Abstract: Abstract Erwinia amylovora, the causal agent of fire blight, is an enterobacterial pathogen of Rosaceous plants including apple and pear. We have been studying the response of E. amylovora to oxidative stress because, during infection, the bacterium elicits an oxidative burst response in host plants. During the screening of a transposon mutant library for hydrogen peroxide sensitivity, we identified a mutant carrying an insertion in waaL, a gene involved in lipopolysaccharide biosynthesis, that was more sensitive to hydrogen peroxide than the parental wild-type strain. We also confirmed that a waaL mutant of Pseudomonas aeruginosa exhibited an increased sensitivity to hydrogen peroxide compared with the wild-type strain. The E. amylovora waaL mutant was also reduced in virulence, showed a decrease in twitching motility, and was more sensitive to polymyxin B than the wild type. Each of these phenotypes was complemented by the cloned waaL gene. Our results highlight the importance of the lipopolysaccharide layer to virulence in E. amylovora and the unexpected finding of an additional function of lipopolysaccharide in protection from oxidative stress in E. amylovora and P. aeruginosa. Author Affiliation: (1)Program in Genetics, Michigan State University, East Lansing, MI, USA (2)Department of Plant Pathology, Michigan State University, East Lansing, MI, USA (3)Department of Crop Sciences, University of Illinois, Urbana, IL, USA Article History: Received 20 August 2008; accepted 31 October 2008.First published online 8 December 2008. Article note: Correspondence: George W. Sundin, Department of Plant Pathology, Michigan State University, 103 CIPS, East Lansing, MI 48824, USA. Tel.: +1 517 355 4573; fax: +1 517 353 5598; e-mail: sundin@msu.edu