An overview on Vibrio temperate phages: Integration mechanisms, pathogenicity, and lysogeny regulation.

Vibrio species are geographically spread in marine habitats. Their virulence is often associated with the acquisition of mobile genetic elements such as phages. These phages can lysogenize the host cell by stably integrating their genomes into the host genome as prophages using the host or phage-encoded recombinases. Prophage-encoded virulence genes are then transferred to the host cell, which increases the population-level diversity and enhances bacterial survival. Prophages can also switch to a lytic cycle in response to environmental factors or host-quorum sensing. However, despite the importance of prophages as carriers of virulence factors, there are no reviews on the diversity and the lysis regulation of prophages in vibrios. Hence, the aim of this review was to highlight the pathogenicity of Vibrio's temperate phages, study their integration mechanisms, and their lysogeny regulation.

ORF4 of the Temperate Archaeal Virus SNJ1 Governs the Lysis-Lysogeny Switch and Superinfection Immunity.

Recent environmental and metagenomic studies have considerably increased the repertoire of archaeal viruses and suggested that they play important roles in nutrient cycling in the biosphere. However, very little is known about how they regulate their life cycles and interact with their hosts. Here, we report that the life cycle of the temperate haloarchaeal virus SNJ1 is controlled by the product ORF4, a small protein belonging to the antitoxin MazE superfamily. We show that ORF4 controls the lysis-lysogeny switch of SNJ1 and mediates superinfection immunity by repression of genomic DNA replication of the superinfecting viruses. Bioinformatic analysis shows that ORF4 is highly conserved in two SNJ1-like proviruses, suggesting that the mechanisms for lysis-lysogeny switch and superinfection immunity are conserved in this group of viruses. As the lysis-lysogeny switch and superinfection immunity of archaeal viruses have been poorly studied, we suggest that SNJ1 could serve as a model system to study these processes.IMPORTANCE Archaeal viruses are important parts of the virosphere. Understanding how they regulate their life cycles and interact with host cells provide crucial insights into their biological functions and the evolutionary histories of viruses. However, mechanistic studies of the life cycle of archaeal viruses are scarce due to a lack of genetic tools and demanding cultivation conditions. Here, we discover that the temperate haloarchaeal virus SNJ1, which infects Natrinema sp. strain J7, employs a lysis-lysogeny switch and establishes superinfection immunity like bacteriophages. We show that its ORF4 is critical for both processes and acts as a repressor of the replication of SNJ1. These results establish ORF4 as a master regulator of SNJ1 life cycle and provides novel insights on the regulation of life cycles by temperate archaeal viruses and on their interactions with host cells.

CI:Mor interactions in the lysogeny switches of Lactococcus lactis TP901-1 and Staphylococcus aureus φ13 bacteriophages.

Aim: To structurally characterize in detail the interactions between the phage repressor (CI) and the antirepressor (Mor) in the lysis-lysogeny switches of two Gram-positive bacteriophages, the lactococcal TP901-1 and staphylococcal φ13. Methods: We use crystallographic structure determination, computational structural modeling, and analysis, as well as biochemical methods, to elucidate similarities and differences in the CI:Mor interactions for the two genetic switches. Results: By comparing a newly determined and other available crystal structures for the N-terminal domain of CI (CI-NTD), we show that the CI interface involved in Mor binding undergoes structural changes upon binding in TP901-1. Most importantly, we show experimentally for the first time the direct interaction between CI and Mor for φ13, and model computationally the interaction interface. The computational modeling supports similar side chain rearrangements in TP901-1 and φ13. Conclusion: This study ascertains experimentally that, like in the TP901-1 lysogeny switch, staphylococcal φ13 CI and Mor interact with each other. The structural basis of the interaction of φ13 CI and Mor was computationally modeled and is similar to the interaction demonstrated experimentally between TP901-1 CI-NTD and Mor, likely involving similar rearrangement of residue side chains during the formation of the complex. The study identifies one CI residue, Glu69, which unusually interacts primarily through its aliphatic chain with an aromatic residue on Mor after changing its conformation compared to the un-complexed structure. This and other residues at the interface are suggested for investigation in future studies.

Tide driven microbial dynamics through virus-host interactions in the estuarine ecosystem.

Microbes drive ecosystems and their viruses manipulate these processes, yet the importance of tidal functioning on the estuarine viruses and microbes remains poorly elucidated. Here, an integrative investigation on tidal patterns in viral and microbial communities and their inherent interactions over an entire spring-neap tidal cycle was conducted along a macrotidal subtropical estuary. The viral and microbial abundances oscillated significantly over the tidal cycle with relatively higher abundances observed at spring tide compared to neap tide. The distinct tidal dynamic patterns in bacterial production and community composition were tightly associated with the variations in viral infection, production and decay, revealing the tide-driven interactions between viruses and microbes. Concurrent with the higher viral decay but lower bacterial abundance and inhibited bacterial metabolism during the neap tide, lower gross viral production was coupled with a synchronous switching from viral lytic to lysogenic infection induced by the loss of viral infection efficiency and the transition from marine to freshwater bacterial populations triggered by tidal mixing. Our results highlighted the major tidal impact on the microbial dynamics through virus-host interactions, with cascading effects, neglected so far, on estuarine biogeochemical cycles.