count for 80% of the virionsproduced.The SaPI TerS can also package SaPI DNA into full-sized capsids. Since packaging uses a headful mechanism, three copies of the SaPI genome are now packaged instead of one, but nevertheless these large SaPI capsids are infectious.
SaPIbov2 uses yet another tactic to exploit its helper. (The name ‘SaPIbov2’ tells you this was the second SaPI found in an S. aureus strain causing bovine mastitis.) In addition to making its own TerS, SaPI bov2 also disrupts the functioning of the phage’s TerS. The SaPI gene involved is aptly named ppi for phage packaging interference. To explore this, researchers expressed the ppi gene in an S. aureus strain that carried the helper prophage but no SaPI, and then induced the prophage. The phage replicated its genome, made capsid proteins, and lysed the host cell as usual, but the lysate contained mostly proheads and tails instead of intact virions and the number of phage progeny (measured as plaque-forming units) decreased 500-fold.
The researchers suspected that the ppi gene product Ppi disrupted packaging of the phage DNA because during phage assembly the DNA has to be packaged before the tail can be attached to the prohead. They did more experiments and demonstrated that Ppi interfered with the phage TerS. For this they isolated phage mutants that were able to form plaques on Ppi-producing strains, then sequenced the TerS isolated from ten of them. All ten mutants had a single amino acid substitution in the region of the protein known to interact with the large subunit of the terminase. Using a pull-down assay they found that Ppi binds to wild-type phage TerS, but not to any of the ten mutant TerS proteins and not to the SaPI TerS. Clearly, Ppi specifically binds to the phage TerS and prevents it from working. Thus, when SaPIbov2 and its helper phage replicate together, virtually all DNA in capsids is SaPI DNA packaged by the SaPI TerS. So far, all known SaPIs carry a ppi gene, but these genes vary in their effectiveness, playing more important roles in some SaPI-helper phage pairs than others.
These same researchers also presented preliminary evidence of yet another interference tactic that involves neither small capsid production or ppi. This mechanism is as yet unknown. This will be number four. Likely it won’t be the last. Helper exploitation has evolved repeatedly, employing a variety of tactics. Exploitation of phage P2 by satellite phage P4 also involves the assembly of small capsids by P4, but the mechanism here is different. There are also helpers and helpees among the eukaryotic viruses (e.g., the adeno-associated virus and Sputnik). There are bound to be many more out there just waiting to be discovered. Kleptoparasitism pays!
Ram G, Chen J, Kumar K, Ross HF, Ubeda C, Damle PK, Lane KD, Penadés JR, Christie GE, & Novick RP (2012). Staphylococcal pathogenicity island interference with helper phage reproduction is a paradigm of molecular parasitism. Proceedings of the National Academy of Sciences of the United States of America, 109 (40), 16300-5 PMID: 22991467