期刊
INFECTION AND IMMUNITY
卷 69, 期 8, 页码 5037-5045出版社
AMER SOC MICROBIOLOGY
DOI: 10.1128/IAI.69.8.5037-5045.2001
关键词
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资金
- NIAID NIH HHS [R56 AI038424, AI38424, R01 AI038424, N01-AI-75326, R15 AI075326, AI33963] Funding Source: Medline
- NICHD NIH HHS [HD070466] Funding Source: Medline
Group B streptococci (GBS) contain a family of protective surface proteins characterized by variable numbers of repeating units within the proteins. The prototype alpha C protein of GBS from the type la/C strain A909 contains a series of nine identical 246-by tandem repeat units. We have previously shown that deletions in the tandem repeat region of the alpha C protein affect both the immunogenicity and protective efficacy of the protein in animal models, and these deletions may serve as a virulence mechanism in GBS. The molecular mechanism of tandem repeat deletion is unknown. To determine whether RecA-mediated homologous recombination is involved in this process, we identified, cloned, and sequenced the recA gene homologue from GBS. A strain of GBS with recA deleted, A909 Delta recA, was constructed by insertional inactivation in the recA locus. A909 Delta recA demonstrated significant sensitivity to UV light, and the 50% lethal dose of the mutant strain in a mouse intraperitoneal model of sepsis was 20-fold higher than that of the parent strain. The spontaneous rate of tandem repeat deletion in the alpha C protein in vitro, as well as in our mouse model of immune infection, was studied using A909 Delta recA. We report that tandem repeat deletion in the alpha C protein does occur in the absence of a functional recA gene both in vitro and in vivo, indicating that tandem repeat deletion in GBS occurs by a recA-independent recombinatorial pathway.
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