Please use this identifier to cite or link to this item: http://hdl.handle.net/2381/15170
Title: The pneumococcal response to oxidative stress includes a role for Rgg
Authors: Terra, Vanessa S.
Hinds, J.
Andrew, Peter W.
Yesilkaya, Hasan
First Published: Dec-2009
Citation: Microbiology, 2009, 155 (Pt 12), pp. 4123-4134
Abstract: Streptococcus pneumoniae resides in the oxygen-rich environment of the upper respiratory tract, and therefore the ability to survive in the presence of oxygen is an important aspect of its in vivo survival. To investigate how S. pneumoniae adapts to oxygen, we determined the global gene expression profile of the micro-organism in aerobiosis and anaerobiosis. It was found that exposure to aerobiosis elevated the expression of 54 genes, while the expression of 15 genes was downregulated. Notably there were significant changes in putative genome plasticity and hypothetical genes. In addition, increased expression of rgg, a putative transcriptional regulator, was detected. To test the role of Rgg in the pneumococcal oxidative stress response, an isogenic mutant was constructed. It was found that the mutant was sensitive to oxygen and paraquat, but not to H(2)O(2). In addition, the absence of Rgg strongly reduced the biofilm-forming ability of an unencapsulated pneumococcus. Virulence studies showed that the median survival time of mice infected intranasally with the rgg mutant was significantly longer than that of the wild-type-infected group, and the animals infected with the mutant developed septicaemia later than those infected intranasally with the wild-type.
DOI Link: 10.1099/mic.0.028282-0
eISSN: 1465-2080
Links: http://hdl.handle.net/2381/15170
http://mic.microbiologyresearch.org/content/journal/micro/10.1099/mic.0.028282-0
Type: Journal Article
Rights: This is an open access article published by the Microbiology Society under the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0/)
Appears in Collections:Published Articles, Dept. of Infection, Immunity and Inflammation

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