Depletion of m6A-RNA inEscherichia colireduces the infectious potential of T5 bacteriophage

Author:

Saikia Bibakhya,Riquelme-Barrios Sebastian,Carell Thomas,Brameyer Sophie,Jung KirstenORCID

Abstract

AbstractN6-methyladenosine (m6A) 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 m6A RNA modification in prokaryotes, especially in relation to phage replication, is limited. To address this knowledge gap, we investigated the effects of m6A RNA modification on phage replication in two model organisms:Vibrio campbelliiBAA-1116 (previouslyV. harveyiBB120) andEscherichia coliMG1655. An m6A-RNA depletedV. campbelliimutant (ΔrlmFΔrlmJ) 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 m6A-RNA depletedE. colimutant (ΔrlmFΔrlmJ) compared to the wild type. This was shown by a lower efficiency of plaquing and a higher percentage of surviving cells. There were no differences in 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 thatE. colicells with lower m6A RNA levels have a higher chance of surviving T5 phage infection.ImportanceThe 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 m6A-RNA modifications during phage infection. We found that anE. colimutant depleted of m6A-RNA is more resistant 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.

Publisher

Cold Spring Harbor Laboratory

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