Mireille Ansaldi (Laboratoire de Chimie Bactérienne, Institut de Microbiologie de la Méditerranée, CNRS, Aix-Marseille Université) - Nitric-oxide controls phage-mediated horizontal gene transfer in Enterobacteria ¬
4:00pm - 5:00pm /
Tuesday 17th October 2017
/ Venue: Lecture Theatre 1 Life Sciences Building
- Kelly Welburn
- Suitable for: Anyone with an interest in Behaviour, Evolution, Ecology and Microbiology
- Admission: Free
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Bacterial genomes contain large amounts of proviruses also called prophages, either functional or defective for infectious propagation. All these prophages contribute to bacterial genome evolution by providing an additional pool of genes that sometimes accommodate new properties to the host, a phenomenon called lysogenic conversion. Prophages usually highjack the host stress response signalisation to resume a lytic cycle when conditions become threatening for the host and therefore for the integrated prophage. This is typically the case in the presence of DNA damages that induce the SOS-response and therefore prophage induction.
We recently developed a genetic screen to identify host genes that are involved in prophage maintenance by preventing the excision mechanism under prophage inducing conditions. Unexpectedly, we identified the nitric oxide reductase NorV, but not its canonical activity, as a prophage maintenance factor. In agreement with these results, the sole addition of nitric oxide under anaerobiosis, proved sufficient to counteract prophage induction even in the presence of mitomycine C, a classical and potent prophage inductor.
Thus, nitric oxide serves as a maintenance signal and induces the production of NorV that in turn prevents prophage induction independently of its usual activity. Surprisingly, nitric oxide, which is a potent nitrosative agent responsible for many cellular damages, does not promote prophage excision but rather counteracts the SOS-response outcome. These results make particularly sense for enterobacteria and their prophages when exposed to nitric oxide produced in the gut during inflammation or through their own anaerobic respiration.
We recently developed a genetic screen to identify host genes that are involved in prophage maintenance by preventing the excision mechanism under prophage inducing conditions. Unexpectedly, we identified the nitric oxide reductase NorV, but not its canonical activity, as a prophage maintenance factor. In agreement with these results, the sole addition of nitric oxide under anaerobiosis, proved sufficient to counteract prophage induction even in the presence of mitomycine C, a classical and potent prophage inductor.
Thus, nitric oxide serves as a maintenance signal and induces the production of NorV that in turn prevents prophage induction independently of its usual activity. Surprisingly, nitric oxide, which is a potent nitrosative agent responsible for many cellular damages, does not promote prophage excision but rather counteracts the SOS-response outcome. These results make particularly sense for enterobacteria and their prophages when exposed to nitric oxide produced in the gut during inflammation or through their own anaerobic respiration.