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A locus of group A streptococcus involved in invasive disease and DNA transfer
Author(s) -
HidalgoGrass Carlos,
Ravins Miriam,
DanGoor Mary,
Jaffe Joseph,
Moses Allon E.,
Hanski Emanuel
Publication year - 2002
Publication title -
molecular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.857
H-Index - 247
eISSN - 1365-2958
pISSN - 0950-382X
DOI - 10.1046/j.1365-2958.2002.03127.x
Subject(s) - biology , virulence , complementation , mutant , transposon mutagenesis , transposable element , streptococcus pneumoniae , gene , genetics , microbiology and biotechnology , pneumolysin , plasmid , bacteria
Summary Group A streptococcus (GAS) causes diseases ranging from benign to severe infections such as necrotizing fasciitis (NF). The reasons for the differences in severity of streptococcal infections are unexplained. We developed the polymorphic‐tag‐lengths‐transposon‐mutagenesis (PTTM) method to identify virulence genes in vivo . We applied PTTM on an emm 14 strain isolated from a patient with NF and screened for mutants of decreased virulence, using a mouse model of human soft‐tissue infection. A mutant that survived in the skin but was attenuated in its ability to reach the spleen and to cause a lethal infection was identified. The transposon was inserted into a small open reading frame (ORF) in a locus termed sil , s treptococcal i nvasion l ocus. sil contains at least five genes ( sil A‐E) and is highly homologous to the quorum‐sensing competence regulons of Streptococcus pneumoniae . sil A and sil B encode a putative two‐component system whereas sil D and sil E encode two putative ABC transporters. sil C is a small ORF of unknown function preceded by a combox promoter. Insertion and deletion mutants of sil had a diminished lethality in the animal model. Virulence of a deletion mutant of sil C was restored when injected together with the avirulent emm 14‐deletion mutant, but not when these mutants were injected into opposite flanks of a mouse. DNA transfer between these mutants occurred in vivo but could not account for the complementation of virulence. DNA exchange between the emm 14‐deletion mutant and mutants of sil occurred also in vitro, at a frequency of ∼ 10 ‐8 for a single antibiotic marker. Whereas sil C and sil D mutants exchanged markers with the emm 14 mutant, sil B mutant did not. Thus, we identified a novel locus, which controls GAS spreading into deeper tissues and could be involved in DNA transfer.