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Published on: February 19, 2019
Moonlighting bacteriophage proteins derepress staphylococcal pathogenicity islands
María Angeles Tormo-Más1, Ignacio Mir, Archana Shrestha
1Centro de Investigación y Tecnología Animal, Instituto Valenciano de Investigaciones Agrarias (CITA-IVIA), Apdo. 187, Segorbe, Castellón 12400, Spain.
Nature
|May 18, 2010
Summary
Staphylococcal superantigen-carrying pathogenicity islands (SaPIs) use specific phage proteins to activate their replication and transfer. This interaction ensures SaPI mobilization, highlighting a unique evolutionary adaptation for spreading.
Area of Science:
- Microbiology
- Molecular Biology
- Genetics
Background:
- Staphylococcal superantigen-carrying pathogenicity islands (SaPIs) are mobile genetic elements.
- SaPIs integrate into bacterial chromosomes and can be transferred between bacteria.
- A repressor protein, Stl, maintains SaPIs in a quiescent state.
Purpose of the Study:
- To investigate the mechanism of SaPI derepression and mobilization.
- To identify the phage-encoded factors involved in SaPI activation.
- To understand the evolutionary relationship between SaPIs and helper phages.
Main Methods:
- Analysis of SaPI gene expression and regulation.
- Identification of specific protein-protein interactions between SaPI and phage proteins.
- Experimental induction of SaPIs using helper phages.
Main Results:
- A specific, non-essential phage protein binds to the SaPI repressor (Stl).
- This binding disrupts the Stl-DNA complex, initiating SaPI excision, replication, and packaging.
- Different SaPIs utilize distinct phage proteins for derepression, demonstrating specific interactions.
Conclusions:
- SaPI mobilization is triggered by specific phage antirepressors that target the SaPI repressor.
- This mechanism ensures SaPI transfer only when helper phage proteins are available.
- The specific interactions between SaPI repressors and phage antirepressors represent a significant evolutionary adaptation for pathogenicity island transfer.
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