Pirating conserved phage mechanisms promotes promiscuous staphylococcal pathogenicity island transfer

Abstract

Targeting conserved and essential processes is a successful strategy to combat enemies. Remarkably, the clinically important Staphylococcus aureus pathogenicity islands (SaPIs) use this tactic to spread in nature. SaPIs reside passively in the host chromosome, under the control of the SaPI-encoded master repressor, Stl. It has been assumed that SaPI de-repression is effected by specific phage proteins that bind to Stl, initiating the SaPI cycle. Different SaPIs encode different Stl repressors, so each targets a specific phage protein for its de-repression. Broadening this narrow vision, we report here that SaPIs ensure their promiscuous transfer by targeting conserved phage mechanisms. This is accomplished because the SaPI Stl repressors have acquired different domains to interact with unrelated proteins, encoded by different phages, but in all cases performing the same conserved function. This elegant strategy allows intra- and inter-generic SaPI transfer, highlighting these elements as one of nature’s most fascinating subcellular parasites.

Cleavage and Structural Transitions during Maturation of Staphylococcus aureus Bacteriophage 80α and SaPI1 Capsids

“…Phage 80α is able to mobilize several SaPIs, including SaPI1, SaPI2, SaPIbov1 and SaPIbov2 [ 15 , 16 ]. Conversely, some SaPIs, such as SaPIbov1, can respond to more than one phage derepressor, thereby maximizing their survival upon infection with a range of phages [ 17 , 18 , 19 ]. After excision and replication, the SaPI genomes are packaged into transducing particles made from phage-encoded structural proteins.…”

Viral satellites exploit phage proteins to escape degradation of the bacterial host chromosome

“…SF1B-type helicases are implicated in activities ranging from replication and genome maintenance to transcriptional regulation (Byrd & Raney 2017). Additionally, the S. aureus phage parasites, SaPIs, make use of dUTPases as anti-repressors to initiate the transcriptional program of the island, suggesting that these genomic islands can evolve to respond to phage-encoded proteins independent of their biological function for the phage (Tormo-Más et al 2010; Bowring et al 2017). As such, we next wanted to determine if helA has a direct role in PLE 1 replication or if it is necessary to transcriptionally activate the island to allow for production of PLE 1-encoded proteins, such as repA , that are essential for PLE 1 replication.…”

“…The ability of PLE to replicate using several dissimilar helicases implicates strong evolutionary pressures for maintenance of PLE replication in response to ICP1 evolution. While helA is only one of the seemingly wide variety of ICP1 inputs that contribute to PLE activity, SaPIs have similarly evolved to overcome variability in helper phage induction cues (Bowring et al 2017). The apparent promiscuity of the SaPI master repressor allows for recognition of structurally dissimilar but functionally conserved phage proteins to ensure SaPI excision, replication and spread, despite their helper phage’s attempts to avoid SaPI induction.…”

Verificação Da Temperatura De Distribuição De Refeições Quentes Ofertadas Em Uma Instituição De Longa Permanência Para Idosos E a Correlação Com O Crescimento Microbiológico

“…As SaPIs são ilhas cromossômicas que residem quiescentes em locais específicos no cromossomo de S. aureus e são induzidas por fagos auxiliares a se replicar e disseminar para outras linhagens e espécies, desempenhando papéis importante na patogenicidade bacteriana (MARTINEZ-RUBIO et al, 2017; NGUYEN, S. V.; MCSHAN, 2014). SaPIs espalham genes codificadores de toxinas entre bactérias (enterotoxinas e toxinas do choque tóxico, estando relacionadas a contaminação alimentar (BOWRING et al, 2017;SATO'O et al, 2013;SUZUKI et al, 2015).…”