A regulatory cascade controls Staphylococcus aureus pathogenicity island activation

2021 ◽  
Author(s):  
Andreas F. Haag ◽  
Magdalena Podkowik ◽  
Rodrigo Ibarra-Chávez ◽  
Francisca Gallego del Sol ◽  
Geeta Ram ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Pathogenicity Island ◽  
Regulatory Cascade

scholarly journals Characterization of a Putative Pathogenicity Island from Bovine Staphylococcus aureus Encoding Multiple Superantigens

2001 ◽  
Vol 183 (1) ◽  
pp. 63-70 ◽  
Author(s):  
J. Ross Fitzgerald ◽  
Steven R. Monday ◽  
Timothy J. Foster ◽  
Gregory A. Bohach ◽  
Patrick J. Hartigan ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
T Cells ◽  
Integration Site ◽  
Random Amplified Polymorphic Dna ◽  
Molecular Genetic ◽  
Pathogenicity Island ◽  
Molecular Genetic Analysis ◽  
Deletion Event ◽  
Allele Replacement

ABSTRACT Previous studies have demonstrated that a proportion ofStaphylococcus aureus isolates from bovine mastitis coproduce toxic shock syndrome toxin (TSST) and staphylococcal enterotoxin C (SEC). In this study, molecular genetic analysis of one such strain, RF122, revealed the presence of a 15,891-bp putative pathogenicity island (SaPIbov) encoding the genes for TSST (tst), the SEC bovine variant (sec-bovine), and a gene (sel) which encodes an enterotoxin-like protein. The island contains 21 open reading frames specifying hypothetical proteins longer than 60 amino acids including an integrase-like gene. The element is bordered by 74-bp direct repeats at the left and right junctions, and the integration site lies adjacent to the 3′ end of the GMP synthase gene (gmps) in the S. aureuschromosome. SaPIbov contains a central region of sequence identity with the previously characterized tst pathogenicity island SaPI1 (J. A. Lindsay et al., Mol. Microbiol. 29:527–543, 1998). A closely related strain, RF120, of the same multilocus enzyme electrophoretic type, random amplified polymorphic DNA type, and ribotype, does not contain the island, implying that the element is mobile and that a recent insertion/deletion event has taken place. TSST and TSST/SEC-deficient mutants of S. aureus strain RF122 were constructed by allele replacement. In vitro bovine Vβ-specific lymphocyte expansion analysis by culture supernatants of wild-type strains and of tst and sec-bovine allele replacement mutants revealed that TSST stimulates BTB13-specific T cells whereas SEC-bovine stimulates BTB93-specific T cells. This suggests that the presence of SaPIbov may contribute to modulation of the bovine immune response.

scholarly journals In Vitro Analysis of Predicted DNA-Binding Sites for the Stl Repressor of the Staphylococcus aureus SaPIBov1 Pathogenicity Island

PLoS ONE ◽  
2016 ◽  
Vol 11 (7) ◽  
pp. e0158793 ◽  
Author(s):  
Veronika Papp-Kádár ◽  
Judit Eszter Szabó ◽  
Kinga Nyíri ◽  
Beata G. Vertessy
Keyword(s):  
Staphylococcus Aureus ◽  
Dna Binding ◽  
Binding Sites ◽  
Pathogenicity Island ◽  
Dna Binding Sites ◽  
Vitro Analysis ◽  
In Vitro Analysis

scholarly journals Non-canonical Staphylococcus aureus pathogenicity island repression

2021 ◽  
Author(s):  
Laura Miguel-Romero ◽  
Mohammed Alqasmi ◽  
Julio Bacarizo ◽  
Jason A. Tan ◽  
Richard J. Cogdell ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Dna Binding ◽  
Virulence Factors ◽  
Pathogenicity Island ◽  
Mobile Genetic Elements ◽  
Life Cycles ◽  
Genetic Elements ◽  
Dna Binding Domains ◽  
Binding Domains ◽  
Induction System

ABSTRACTMobile genetic elements (MGEs) control their life cycles by the expression of a master repressor, whose function must be disabled to allow the spread of these elements in nature. Here we describe an unprecedented repression-derepression mechanism involved in the transfer of the Staphylococcus aureus pathogenicity islands (SaPIs). Contrary to the classical phage and SaPI repressors, which are dimers, the SaPI1 repressor StlSaPI1 presents a unique tetrameric conformation, never seen before. Importantly, not just one but two tetramers are required for SaPI1 repression, which increases the novelty of the system. To derepress SaPI1, the phage-encoded protein Sri binds to and induces a conformational change in the DNA binding domains of StlSaPI1, preventing the binding of the repressor to its cognate StlSaPI1 sites. Finally, our findings demonstrate that this system is not exclusive to SaPI1 but widespread in nature. Overall, our results characterise a novel repression-induction system involved in the transfer of MGE-encoded virulence factors in nature.SignificanceWhile most repressors controlling the transfer of mobile genetic elements are dimers, we demonstrate here that the Staphylococcal pathogenicity island 1 (SaPI1) is repressed by two tetramers, which have a novel structural fold in their body that has never been seen before in other proteins. Moreover, by solving the structure of the SaPI1 repressor in complex with its inducing protein Sri, we have demonstrated that Sri forces the SaPI1 repressor to adopt a conformation that is incompatible with DNA binding, explaining how SaPI1 is induced. Finally, our results demonstrate that this repression system is not exclusive of the SaPIs but widespread in nature. Our studies provide important insights understanding how SaPIs spread in nature.

scholarly journals The Staphylococcus aureus Pathogenicity Island 1 Protein gp6 Functions as an Internal Scaffold during Capsid Size Determination

2011 ◽  
Vol 412 (4) ◽  
pp. 710-722 ◽  
Author(s):  
Altaira D. Dearborn ◽  
Michael S. Spilman ◽  
Priyadarshan K. Damle ◽  
Jenny R. Chang ◽  
Eric B. Monroe ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Pathogenicity Island ◽  
Size Determination

scholarly journals Molecular genetics of SaPI1 - a mobile pathogenicity island in Staphylococcus aureus

2001 ◽  
Vol 41 (2) ◽  
pp. 365-377 ◽  
Author(s):  
Alexey Ruzin ◽  
Jodi Lindsay ◽  
Richard P. Novick
Keyword(s):  
Staphylococcus Aureus ◽  
Molecular Genetics ◽  
Pathogenicity Island

scholarly journals Capsid Size Determination by Staphylococcus aureus Pathogenicity Island SaPI1 Involves Specific Incorporation of SaPI1 Proteins into Procapsids

2008 ◽  
Vol 380 (3) ◽  
pp. 465-475 ◽  
Author(s):  
Anton Poliakov ◽  
Jenny R. Chang ◽  
Michael S. Spilman ◽  
Priyadarshan K. Damle ◽  
Gail E. Christie ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Pathogenicity Island ◽  
Size Determination

The tst gene associated Staphylococcus aureus pathogenicity island facilitates its pathogenesis by promoting the secretion of inflammatory cytokines and inducing immune suppression

2020 ◽  
Vol 138 ◽  
pp. 103797
Author(s):  
Yi Zheng ◽  
Chenhao Qin ◽  
Xianfeng Zhang ◽  
Yifan Zhu ◽  
Aiqing Li ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Inflammatory Cytokines ◽  
Immune Suppression ◽  
Pathogenicity Island

scholarly journals Investigations into σB-Modulated Regulatory Pathways Governing Extracellular Virulence Determinant Production in Staphylococcus aureus

2006 ◽  
Vol 188 (17) ◽  
pp. 6070-6080 ◽  
Author(s):  
Lindsey N. Shaw ◽  
Joanne Aish ◽  
Jessica E. Davenport ◽  
Melanie C. Brown ◽  
James K. Lithgow ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Genetic Manipulation ◽  
Hot Spot ◽  
Laboratory Strain ◽  
Transcriptional Analysis ◽  
Extracellular Proteases ◽  
Phenotypic Analysis ◽  
Regulatory Pathways ◽  
Regulatory Cascade ◽  
Exoprotein Secretion

ABSTRACT The commonly used Staphylococcus aureus laboratory strain 8325-4 bears a naturally occurring 11-bp deletion in the σB-regulating phosphatase rsbU. We have previously published a report (M. J. Horsburgh, J. L. Aish, I. J. White, L. Shaw, J. K. Lithgow, and S. J. Foster, J. Bacteriol. 184:5457-5467, 2002) on restoring the rsbU deletion, producing a σB-functional 8325-4 derivative, SH1000. SH1000 is pleiotropically altered in phenotype from 8325-4, displaying enhanced pigmentation, increased growth yields, and a marked decrease in secreted exoproteins. This reduction in exoprotein secretion appears to result from a sixfold reduction in agr expression. In this study we have undertaken transposon mutagenesis of SH1000 to identify components involved in the modulation of extracellular proteases and α-hemolysin compared to 8325-4. In total, 13 genes were identified displaying increased α-hemolysin transcription and extracellular proteolysis. Phenotypic analysis revealed that each mutant also had decreased pigmentation and a general increase in protein secretion. Interestingly this phenotype was not identical in each case but was variable from mutant to mutant. None of the genes identified encoded classic regulatory proteins but were predominantly metabolic enzymes involved in amino acid biosynthesis and transport. Further analysis revealed that all of these mutations were clustered in a 35-kb region of the chromosome. By complementation and genetic manipulation we were able to demonstrate the validity of these mutations. Interestingly transcriptional analysis revealed that rather than being regulated by σB, these genes appeared to have a role in the regulation of σB activity. Thus, we propose that the loss of individual genes in this chromosomal hot spot region results in a destabilization of cellular harmony and disruption of the σB regulatory cascade.

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