SA_Peptidomics_LFQ_Submit
Ontology highlight
ABSTRACT:
INSTRUMENT(S): Orbitrap Fusion
ORGANISM(S): Staphylococcus Aureus (ncbitaxon:1280)
SUBMITTER: 
David Gonzalez
PROVIDER: MSV000083390 | MassIVE | Fri Feb 01 13:37:00 GMT 2019
SECONDARY ACCESSION(S): PXD012594
REPOSITORIES: MassIVE
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Project description:Peptidomics of cell-free CA-MRSA USA300 strain TCH1516 supernatants stimulated with LPS or LL37 and extracted with butanol or ethyl acetate
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Project description:The SaeRS two-component regulatory system of Staphylococcus aureus is known to affect the expression of many genes. The SaeS protein is the histidine kinase responsible for phosphorylation of the response regulator SaeR. In S. aureus Newman, the sae system is constitutively expressed due to a point mutation in saeS, relative to other S. aureus strains, which results in substitution of proline for leucine at amino acid 18. Strain Newman is unable to form a robust biofilm and we report here that the biofilm-deficient phenotype is due to the saeSP allele. Replacement of the Newman saeSP with saeSL, or deletion of saeRS, resulted in a biofilm-proficient phenotype. Newman culture supernatants were observed to inhibit biofilm formation by other S. aureus strains, but did not affect biofilm formation by S. epidermidis. Culture supernatants of Newman saeSL or Newman ΔsaeRS had no significant effect on biofilm formation. The inhibitory factor was inactivated by incubation with proteinase K, but survived heating, indicating that the inhibitory protein is heat-stable. The inhibitory protein was found to affect the attachment step in biofilm formation, but had no effect on preformed biofilms. Replacement of saeSL with saeSP in the biofilm-proficient S. aureus USA300 FPR3757 resulted in the loss of biofilm formation. Culture supernatants of USA300 FPR3757 saeSP, did not inhibit biofilm formation by other staphylococci, suggesting that the inhibitory factor is produced but not secreted in the mutant strain. A number of biochemical methods were utilized to isolate the inhibitory protein. Although a number of candidate proteins were identified, none were found to be the actual inhibitor. In an effort to reduce the number of potential inhibitory genes, RNA-Seq analyses were done with wild-type strain Newman and the saeSL and ΔsaeRS mutants. RNA-Seq results indicated that sae regulates many genes that may affect biofilm formation by Newman.
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Project description:Staphylococcus aureus TCH1516 constrained COBRA model showing growth in RPMI + 10% LB.
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Project description:Staphylococcus aureus is a leading cause of bloodstream infections worldwide. In the United States, many of these infections are caused by a strain known as USA300. Although progress has been made, our understanding of the S. aureus molecules that promote bacteremia and survival in human blood is incomplete. To that end, we analyzed the USA300 transcriptome during culture in human blood, human serum, and trypticase soy broth (TSB), a standard laboratory culture media. Notably, genes encoding several cytolytic toxins were up-regulated in human blood over time, and hlgA, hlgB, and hlgC (encoding gamma-hemolysin subunits HlgA, HlgB, and HlgC) were among the most highly up-regulated genes at all time points. Culture supernatants derived from a USA300 isogenic hlgABC-deletion strain (LAC?hlgABC) had significantly reduced capacity to form pores in human neutrophils and ultimately cause neutrophil lysis. Compared with the wild-type USA300 strain (LAC), LAC?hlgABC had modestly reduced ability to cause mortality in a mouse bacteremia model. On the other hand, wild-type and LAC?hlgABC strains caused virtually identical disease in a mouse skin infection model, and bacterial survival and neutrophil lysis after phagocytosis in vitro was similar between these strains. Comparison of the cytolytic capacity of culture supernatants from wild-type and isogenic deletion strains lacking hlgABC, lukS/F-PV (encoding PVL), and/or lukDE revealed significant functional redundancy among two-component leukotoxins in vitro. These findings may explain in part the apparent limited contribution of any single two-component leukotoxin to USA300 immune evasion and virulence. S. aureus strain USA300 transcriptome during culture in human blood, human serum, and trypticase soy broth (TSB): time course.
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Project description:Proteomics of Staphylococcus aureus strain TCH1516 with various genetic modifications
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Project description:Staphylococcus aureus is a leading cause of bloodstream infections worldwide. In the United States, many of these infections are caused by a strain known as USA300. Although progress has been made, our understanding of the S. aureus molecules that promote bacteremia and survival in human blood is incomplete. To that end, we analyzed the USA300 transcriptome during culture in human blood, human serum, and trypticase soy broth (TSB), a standard laboratory culture media. Notably, genes encoding several cytolytic toxins were up-regulated in human blood over time, and hlgA, hlgB, and hlgC (encoding gamma-hemolysin subunits HlgA, HlgB, and HlgC) were among the most highly up-regulated genes at all time points. Culture supernatants derived from a USA300 isogenic hlgABC-deletion strain (LACΔhlgABC) had significantly reduced capacity to form pores in human neutrophils and ultimately cause neutrophil lysis. Compared with the wild-type USA300 strain (LAC), LACΔhlgABC had modestly reduced ability to cause mortality in a mouse bacteremia model. On the other hand, wild-type and LACΔhlgABC strains caused virtually identical disease in a mouse skin infection model, and bacterial survival and neutrophil lysis after phagocytosis in vitro was similar between these strains. Comparison of the cytolytic capacity of culture supernatants from wild-type and isogenic deletion strains lacking hlgABC, lukS/F-PV (encoding PVL), and/or lukDE revealed significant functional redundancy among two-component leukotoxins in vitro. These findings may explain in part the apparent limited contribution of any single two-component leukotoxin to USA300 immune evasion and virulence.
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Project description:CodY is a highly conserved global transcriptional factor that regulates the expression of dozens of genes related to metabolism and virulence in Staphylococcus aureus. The S. aureus CodY regulon has been studied in vitro. However, in vivo CodY DNA-binding activity and the identity of the corresponding target genes remain unknown due to lack of a ChIP-grade monoclonal antibody. Using a novel CodY monoclonal antibody that we developed in established ChIP-exo protocols, we report in vivo target genes of CodY in two S. aureus USA300 clinical strains (TCH1516 and LAC). The total number of CodY-binding sites exceeded 110, but their location varied between the two strains. The majority of the identified binding sites were located within the promoter regions. Based on the sequences of the CodY-binding sites, a model of CodY interaction with DNA is proposed. Furthermore, S. aureus CodY protein is highly conserved across a G+C Gram-positive species, including Bacillus subtilis and Listeria monocytogenes, and thus this study paves the way for exploration of the differential binding of CodY among a range of gram-positive species, including pathogenic ones
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