Abstract
Phage-inducible chromosomal island-like elements (PLEs) are bacteriophage satellites found in Vibrio cholerae. PLEs parasitize the lytic phage ICP1, excising from the bacterial chromosome, replicating, and mobilizing to new host cells following cell lysis. PLEs protect their host cell populations by completely restricting the production of ICP1 progeny. Previously, it was found that ICP1 replication was reduced during PLE(+) infection. Despite robust replication of the PLE genome, relatively few transducing units are produced. We investigated if PLE DNA replication itself is antagonistic to ICP1 replication. Here we identify key constituents of PLE replication and assess their role in interference of ICP1. PLE encodes a RepA_N initiation factor that is sufficient to drive replication from the PLE origin of replication during ICP1 infection. In contrast to previously characterized bacteriophage satellites, expression of the PLE initiation factor was not sufficient for PLE replication in the absence of phage. Replication of PLE was necessary for interference of ICP1 DNA replication, but replication of a minimalized PLE replicon was not sufficient for ICP1 DNA replication interference. Despite restoration of ICP1 DNA replication, non-replicating PLE remained broadly inhibitory against ICP1. These results suggest that PLE DNA replication is one of multiple mechanisms contributing to ICP1 restriction.
Highlights
Viral satellites are found in all domains of life and can have a profound impact on their helper viruses and their host cells [1,2,3]
phage inducible chromosomal islands (PICIs)-like elements (PLEs) was previously shown to replicate to high copy during ICP1 infection and reduce ICP1 DNA replication compared to a PLE(-) control [12] (Figure 1), these results were obtained through qPCR and only assessed a single ~100bp target sequence
Samples were prepped for total DNA at each time point and the resulting Illumina sequencing reads were mapped against the V. cholerae, ICP1, and PLE genomes
Summary
Viral satellites are found in all domains of life and can have a profound impact on their helper viruses and their host cells [1,2,3]. Certain details of the life cycles of PLEs and their helper phage, ICP1, distinguish PLEs from other bacteriophage satellites Both P4 and the well characterized subfamily of PICIs referred to as staphylococcal pathogenicity islands (SaPIs) confer partial restriction of their helper phages [14, 15]. The copyright holder for this preprint It is made available under through their replication cycle [12] This allows PLEs to function as effective abortive infection systems: individual ICP1 infected cells die, but since no phage are produced, the population as a whole is protected [12]. ICP1 is only known to produce lytic infections that kill the host cell [16] Both P4 and PICIs parasitize temperate phages which occasionally integrate into the genomes of the cells they infect. If ICP1 kills every cell it can infect, cells that are potential hosts for PLEs, it is to the PLEs’ benefit to completely restrict the production of infectious ICP1 progeny
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
