A polyamorous repressor: deciphering the evolutionary strategy used by the phageinducible chromosomal islands to spread in nature
| Autor: | Ciges-Tomas, J. Rafael, Alite, Christian, Bowring, J., Donderis, Jorge, Penadés, José R., Marina, Alberto |
|---|---|
| Přispěvatelé: | Marina, Alberto, Marina, Alberto [0000-0002-1334-5273] |
| Jazyk: | angličtina |
| Rok vydání: | 2019 |
| Zdroj: | Digital.CSIC. Repositorio Institucional del CSIC instname |
| Popis: | 1 página con el abstract del póster presentado a 44th FEBS Congress Krakow, Poland. July 6-11, 2019 Staphylococcus aureus pathogenicity islands (SaPIs) are a family of related 1517Kb mobile genetic elements that carry and disseminate superantigen and other virulence genes. SaPIs reside passively in the bacterial chromosome, repressed by a master repressor called Stl, encoded by the own SaPI. The key feature of their mobility and spread is the induction by helper phages of their excision, replication, and efficient encapsidation into specific smallheaded phagelike infectious particles. After infection or induction of a resident helper phage, SaPIs are derepressed by the specific proteinprotein interaction of phage proteins with Stl. SaPIs have developed a fascinating mechanism to ensure their promiscuous transfer by targeting with the Stl repressor structurally unrelated phage proteins performing the same conserved function. Combining structural biology approach and functional characterization invivo and invitro we decipher the molecular mechanism of this elegant strategy by which the SaPI hijacks the phage process to sense the starting of the lytic cycle. Our structural studies show that the Stl of the island SaPIbov1 combines a canonic HTH Nterminal domain to bind DNA, and sequentially acquires new domains which act as recognizing modules for the different phage proteins (antirepressors). Our invivo and invitro data deciphers the molecular mechanism that underlies the interaction between the Stl repressor and different phage coded antirepressors, showing how each Stl module mimics the substrate for each antirepressor type. The interaction of Stl with different types of antirepressor always disrupts the Stl dimer, implying the DNA dissociation and SaPI derepression. Our results establish the molecular mechanism of the interaction event that detonates the intra and inter generic transference of the clinically relevant SaPIs. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|