Abstract
The phage growth limitation system of Streptomyces coelicolor A3(2) is an unusual bacteriophage defence mechanism. Progeny ϕC31 phage from an initial infection are thought to be modified such that subsequent infections are attenuated in a Pgl+ host but normal in a Pgl− strain. Earlier work identified four genes required for phage resistance by Pgl. Here we demonstrate that Pgl is an elaborate and novel phage restriction system that, in part, comprises a toxin/antitoxin system where PglX, a DNA methyltransferase is toxic in the absence of a functional PglZ. In addition, the ATPase activity of PglY and a protein kinase activity in PglW are shown to be essential for phage resistance by Pgl. We conclude that on infection of a Pgl+ cell by bacteriophage ϕC31, PglW transduces a signal, probably via phosphorylation, to other Pgl proteins resulting in the activation of the DNA methyltransferase, PglX and this leads to phage restriction.
Highlights
University of Strathclyde, 161, Cathedral Street, Glasgow G4 0RE, UK. 2 Current address: Center for Molecular and Translational Human InfectiousDiseases Research, The Methodist Hospital Research Institute, 6565 Fannin St., SM8-073 Houston, TX 77030, USA.the initial round of infection the progeny phage are modified and restricted in the second round of infection
In this work we demonstrated that PglX is a DNA methyltransferase, as predicted by the bioinformatics searches
A strong genetic interaction between pglX and pglZ implies that PglX is toxic and that toxicity is suppressed in strains that are pglZ þ or contain the truncated pglZ1-834 allele in target for the methyltransferase encoded by the B. cereus PglX homologue was elucidated by PacBio sequencing
Summary
The initial round of infection the progeny phage are modified and restricted in the second round of infection This system differs fundamentally from typical R–M systems, where, if the phage DNA becomes modified, there can be an escape from restriction and rapid spread of infection through sensitive bacteria. In Pgl, even if modification fails during the first burst, it is likely that it will occur in subsequent cycles thereby severely limiting spread of infection (Fig. 1; Sumby and Smith, 2002). While the predicted function of PglX as a DNA methyltransferase fits well with the proposed mechanism by Chinenova et al (1982) the Pgl system appears to involve additional activities that are novel to R–M systems, not least the putative kinase activity of PglW
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