ArticlePloS one2016
In Vitro Analysis of Predicted DNA-Binding Sites for the Stl Repressor of the Staphylococcus aureus SaPIBov1 Pathogenicity Island.
Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
8 citing papers in PubMed, 9 citations in OpenAlex.
- Detection of Genomic Uracil Patterns.International journal of molecular sciences · 2021Review
- Article
- The structure of a polygamous repressor reveals how phage-inducible chromosomal islands spread in nature.Nature communications · 2019Article
- Mobilisation Mechanism of Pathogenicity Islands by Endogenous Phages in Staphylococcus aureus clinical strains.Scientific reports · 2018Article
- Article
- Structural model of human dUTPase in complex with a novel proteinaceous inhibitor.Scientific reports · 2018Article
- The Stl repressor fromFEBS open bio · 2018Article
- Derepression of SaPIbov1 Is Independent of φNM1 Type 2 dUTPase Activity and Is Inhibited by dUTP and dUMP.Journal of molecular biology · 2017Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The regulation model of the Staphylococcus aureus pathogenicity island SaPIbov1 transfer was recently reported. The repressor protein Stl obstructs the expression of SaPI proteins Str and Xis, latter which is responsible for mobilization initiation. Upon Φ11 phage infection of S. aureus. phage dUTPase activates the SaPI transfer via Stl-dUTPase complex formation. Our aim was to predict the binding sites for the Stl repressor within the S. aureus pathogenicity island DNA sequence. We found that Stl was capable to bind to three 23-mer oligonucleotides, two of those constituting sequence segments in the stl-str, while the other corresponding to sequence segment within the str-xis intergenic region. Within these oligonucleotides, mutational analysis revealed that the predicted binding site for the Stl protein exists as a palindromic segment in both intergenic locations. The palindromes are built as 6-mer repeat sequences involved in Stl binding. The 6-mer repeats are separated by a 5 oligonucleotides long, nonspecific sequence. Future examination of the interaction between Stl and its binding sites in vivo will provide a molecular explanation for the mechanisms of gene repression and gene activation exerted simultaneously by the Stl protein in regulating transfer of the SaPIbov1 pathogenicity island in S. aureus.
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