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Infection and Immunity, May 2005, p. 2881-2890, Vol. 73, No. 5
0019-9567/05/$08.00+0 doi:10.1128/IAI.73.5.2881-2890.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.
Institute of Basic Medical Sciences,1 Departments of Microbiology and Immunology,2 Biochemistry,3 Pediatrics,4 Medical Laboratory Science and Biotechnology, College of Medicine, National Cheng-Kung University, Tainan,5 Department of Laboratory Medicine and Biotechnology,6 Institute of Medical Science, Medical College, Tzu Chi University, Hualien, Taiwan7
Received 28 June 2004/ Returned for modification 28 September 2004/ Accepted 29 December 2004
The oligopeptide permease (Opp) of group A streptococci (GAS) is a membrane-associated protein and belongs to the ATP-binding cassette transporter family. It is encoded by a polycistronic operon containing oppA, oppB, oppC, oppD, and oppF. The biological function of these genes in GAS is poorly understood. In order to understand more about the effects of Opp on GAS virulence factors, an oppA isogenic mutant was constructed by using an integrative plasmid to disrupt the opp operon and confirmed by Southern blot hybridization. No transcript was detected in the oppA isogenic mutant by Northern blot analysis and reverse transcriptase PCR. The growth curve for the oppA isogenic mutant was similar to that for wild-type strain A-20. The oppA isogenic mutant not only decreased the transcription of speB, speX, and rofA but also increased the transcription of speF, sagA (streptolysin S-associated gene A), slo (streptolysin O), pel (pleotrophic effect locus), and dppA (dipeptide permease). No effects on the transcription of emm, sda, speJ, speG, rgg, and csrR were found. The phenotypes of the oppA mutant were restored by the oppA revertant and by the complementation strain. The oppA mutant caused less mortality and tissue damage than the wild-type strain when inoculated into BALB/c mice via an air pouch. Based on these data, we suggest that the opp operon plays an important role in the pathogenesis of GAS infection.
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