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.
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Author details
Funding
Wellcome (201531/Z/16/Z)
- Jose R Penades
Biotechnology and Biological Sciences Research Council (BB/N002873/1)
- Jose R Penades
Medical Research Council (MR/M003876/1)
- Jose R Penades
Ministerio de Economía y Competitividad (BIO2013-42619-P)
- Alberto Marina
Ministerio de Economía y Competitividad (BIO2016-78571-P)
- Alberto Marina
ERC Advanced Grant 2014 (Proposal n{degree sign} 670932 Dut-signal)
- Jose R Penades
The funders had no role in study design, data collection and interpretation, or the decision to submit the work for publication.
Copyright
© 2017, Bowring et al.
This article is distributed under the terms of the Creative Commons Attribution License permitting unrestricted use and redistribution provided that the original author and source are credited.
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