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SpxB is a suicide gene of Streptococcus pneumoniae and confers a selective advantage in an in vivo competitive colonization model.

SpxB is a suicide gene of Streptococcus pneumoniae and confers a selective advantage in an in vivo competitive colonization model. Research Abstract Details 

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  • SpxB is a suicide gene of Streptococcus pneumoniae and confers a selective advantage in an in vivo competitive colonization model. Abstract Text:

    gili regev-yochayGili Regev-Yochay,krzysztof trzcinskiKrzysztof Trzcinski,claudette m thompsonClaudette M Thompson,marc lipsitchMarc Lipsitch,richard malleyRichard Malley,

    The human bacterial pathogen Streptococcus pneumoniae dies spontaneously upon reaching stationary phase. The extent of S. pneumoniae death at stationary phase is unusual in bacteria and has been conventionally attributed to autolysis by the LytA amidase. In this study, we show that spontaneous pneumococcal death is due to hydrogen peroxide (H(2)O(2)), not LytA, and that the gene responsible for H(2)O(2) production (spxB) also confers a survival advantage in colonization. Survival of S. pneumoniae in stationary phase was significantly prolonged by eliminating H(2)O(2) in any of three ways: chemically by supplementing the media with catalase, metabolically by growing the bacteria under anaerobic conditions, or genetically by constructing DeltaspxB mutants that do not produce H(2)O(2). Likewise, addition of H(2)O(2) to exponentially growing S. pneumoniae resulted in a death rate similar to that of cells in stationary phase. While DeltalytA mutants did not lyse at stationary phase, they died at a rate similar to that of the wild-type strain. Furthermore, we show that the death process induced by H(2)O(2) has features of apoptosis, as evidenced by increased annexin V staining, decreased DNA content, and appearance as assessed by transmission electron microscopy. Finally, in an in vivo rat model of competitive colonization, the presence of spxB conferred a selective advantage over the DeltaspxB mutant, suggesting an explanation for the persistence of this gene. We conclude that a suicide gene of pneumococcus is spxB, which induces an apoptosis-like death in pneumococci and confers a selective advantage in nasopharyngeal cocolonization.

    SpxB is a suicide gene of Streptococcus pneumoniae and confers a selective advantage in an in vivo competitive colonization model. Publishing Authors By Initials

    g regev-yochayG Regev-Yochay,k trzcinskiK Trzcinski,cm thompsonCM Thompson,m lipsitchM Lipsitch,r malleyR Malley,

    For similar bacteria: gram-positive bacteria: gram-positive cocci: streptococcaceae: streptococcus: streptococcus pneumoniae research abstracts see: bacteria: gram-positive bacteria: gram-positive cocci: streptococcaceae: streptococcus: streptococcus pneumoniae research

    PUBMED ID PMID:

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    SpxB is a suicide gene of Streptococcus pneumoniae and confers a selective advantage in an in vivo competitive colonization model. Journal Published:

    PUBLICATION TYPE: Research Support, Non-U.S. Gov

    Journal: Journal of bacteriology

    VOLUME: 189

    Page Numbers: 6532-9

    Journal Abbreviation: J. Bacteriol.

    ISSN: 0021-9193

    DAY: 13

    MONTH: 07

    YEAR: 2007

    SpxB is a suicide gene of Streptococcus pneumoniae and confers a selective advantage in an in vivo competitive colonization model. Information

    Number of References:

    LANGUAGE: eng

    NlmUniqueID: 2985120

    SpxB is a suicide gene of Streptococcus pneumoniae and confers a selective advantage in an in vivo competitive colonization model. Keywords Mesh Terms:

    KEYWORDS: Streptococcus pneumoniae

    MESH TERMS: growth & development

    Chemical & Substance for Abstract: SpxB is a suicide gene of Streptococcus pneumoniae and confers a selective advantage in an in vivo competitive colonization model. Information

    Substance Name: Pyruvate Oxidase

    Registry Number: EC 1.2.3.3

    Grant and Affiliation Information for SpxB is a suicide gene of Streptococcus pneumoniae and confers a selective advantage in an in vivo competitive colonization model.

    AFFILIATION: Department of Epidemiology and Department of Immunology and Infectious Diseases, Harvard School of Public Health, 677 Huntington Ave., Boston, MA 02115, USA. gregev@hsph.harvard.edu

    Country: United States

    United States Research PublicationUnited States Research Publication

    AGENCY: United States NIAID

    GRANT: R01AI067737

    ACRONYM: AI

    MEDLINETA: J Bacteriol

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