Skip navigation
  • Home
  • Browse
    • Communities
      & Collections
    • Browse Items by:
    • Publication Date
    • Author
    • Title
    • Subject
    • Department
  • Sign on to:
    • My MacSphere
    • Receive email
      updates
    • Edit Profile


McMaster University Home Page
  1. MacSphere
  2. Open Access Dissertations and Theses Community
  3. Open Access Dissertations and Theses
Please use this identifier to cite or link to this item: http://hdl.handle.net/11375/23741
Title: AN ANALYSIS INTO THE FUNCTIONING OF THE S. INTERMEDIUS B196 STREPTOCOCCUS INVASION LOCUS
Other Titles: THE STREPTOCOCCUS INVASION LOCUS IN S. INTERMEDIUS B196
Authors: Wu, Bryan
Advisor: Surette, Michael
Department: Biochemistry and Biomedical Sciences
Keywords: sil;streptococcus invasion locus
Publication Date: 2018
Abstract: The Streptococcus Anginosus Group (SAG) is a group of Gram-positive cocci which require carbon dioxide to grow. They are commensal members of the healthy upper respiratory, gastrointestinal and female urogenital tract; however, they are most commonly known as major pathogens in brain and liver abscesses, forming both mono- and polymicrobial infections. The Streptococcus invasion locus (sil), first identified as a virulence factor in Group A Streptococcus (GAS), has recently been identified in the SAG. The sil locus in GAS is a two component quorum-sensing system composed of three operons: silAB, coding for a two component system; silE/D/CR, coding for an ABC transporter and a signal peptide, and silC, which overlaps silCR on the opposite strand. The presence of exogenous SilCR activates SilA, which in turn upregulates the transcription of the silE/D/CR operon. In the SAG, however, silCR and silED have distinct promoters, and the SAG sil system lacks the silC gene. In this study, I examined the transcriptional dynamics of the sil system in S. intermedius B196. I determined that SilA is the major regulator of the genes in the sil system, being one of the first genes of the system to be expressed, and likely upregulates its own transcription. I also found evidence suggesting that, despite having its own promoter, silCR transcription may still be driven by the silED promoter. I also found evidence that suggests silED may be responsible for the export and/or processing of bacteriocins targeting closely related species or strains.
URI: http://hdl.handle.net/11375/23741
Appears in Collections:Open Access Dissertations and Theses

Files in This Item:
File Description SizeFormat 
Wu_Bryan_finalsubmission201809_Masters.pdf
Access is allowed from: 2019-09-23
1.62 MBAdobe PDFView/Open
Show full item record Statistics


Items in MacSphere are protected by copyright, with all rights reserved, unless otherwise indicated.

Sherman Centre for Digital Scholarship     McMaster University Libraries
©2022 McMaster University, 1280 Main Street West, Hamilton, Ontario L8S 4L8 | 905-525-9140 | Contact Us | Terms of Use & Privacy Policy | Feedback

Report Accessibility Issue