SaPI operon I is required fpr SaPI packaging and is controlled by LexA
Transfer of Staphylococcus aureus pathogenicity islands (SaPls) is directly controlled by the cellular repressor LexA. We have found that transcription of the SaPIbov1 operon I is repressed by LexA and is therefore SOS-induced. Two copies of the LexA binding site consensus (Cheo box) are present in...
| Autores principales: | , , , , , , , |
|---|---|
| Formato: | article |
| Lenguaje: | Inglés |
| Publicado: |
2017
|
| Acceso en línea: | http://hdl.handle.net/20.500.11939/4617 |
Ejemplares similares: SaPI operon I is required fpr SaPI packaging and is controlled by LexA
- SaPI mutations affecting replication and transfer and enabling autonomous replication in the absence of helper phage
- Adaptation of Staphylococcus aureus to ruminant and equine hosts involves SaPI-carried variants of von Willebrand factor-binding protein
- Molecular mapping of Asian soybean rust resistance in soybean landraces PI 594767A, PI 587905 and PI 416764
- Clp-dependent proteolysis of the LexA N-terminal domain in Staphylococcus aureus
- Structure-function analysis of the SaPIbov1 replication origin in Staphylococcus aureus
- A super-family of transcriptional activators regulates bacteriophage packaging and lysis in Gram-positive bacteria