Depletion of m 6 A-RNA in Escherichia coli reduces the infectious potential of T5 bacteriophage

• Published in: Microbiology spectrum 2024-10, p.e0112424
• Main Authors: Saikia, Bibakhya, Riquelme-Barrios, Sebastian, Carell, Thomas, Brameyer, Sophie, Jung, Kirsten
• Format: Article
• Language: English
• ISSN: 2165-0497; 2165-0497
• DOI: 10.1128/spectrum.01124-24

-Methyladenosine (m A) is the most abundant internal modification of mRNA in eukaryotes that plays, among other mechanisms, an essential role in virus replication. However, the understanding of m A-RNA modification in prokaryotes, especially in relation to phage replication, is limited. To address this knowledge gap, we investigated the effects of m A-RNA modifications on phage replication in two model organisms: BAA-1116 (previously BB120) and MG1655. An m A-RNA-depleted mutant (Δ Δ ) did not differ from the wild type in the induction of lysogenic phages or in susceptibility to the lytic Virtus phage. In contrast, the infection potential of the T5 phage, but not that of other T phages or the lambda phage, was reduced in an m A-RNA-depleted mutant (Δ Δ ) compared to the wild type. This was shown by a lower plaquing efficiency and a higher percentage of surviving cells. There were no differences in the T5 phage adsorption rate, but the mutant exhibited a 5-min delay in the rise period during the one-step growth curve. This is the first report demonstrating that cells with lower m A-RNA levels have a higher chance of surviving T5 phage infection. The importance of RNA modifications has been thoroughly studied in the context of eukaryotic viral infections. However, their role in bacterial hosts during phage infections is largely unexplored. Our research delves into this gap by investigating the effect of host -methyladenosine (m A)-RNA modifications during phage infection. We found that an mutant depleted of m A-RNA is less susceptible to T5 infection than the wild type. This finding emphasizes the need to further investigate how RNA modifications affect the fine-tuned regulation of individual bacterial survival in the presence of phages to ensure population survival.