Virus-Host Interaction Gets Curiouser and Curiouser. PART II: Functional Transcriptomics of the E. coli DksA-Deficient Cell upon Phage P1vir Infection.

Grzegorz M Cech,Agnieszka Szalewska-Pałasz,Katarzyna Potrykus,Anna Kloska

doi:10.3390/ijms22116159

Grzegorz M Cech, Agnieszka Szalewska-Pałasz + Show 2 more

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https://doi.org/10.3390/ijms22116159

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Abstract

The virus–host interaction requires a complex interplay between the phage strategy of reprogramming the host machinery to produce and release progeny virions, and the host defense against infection. Using RNA sequencing, we investigated the phage–host interaction to resolve the phenomenon of improved lytic development of P1vir phage in a DksA-deficient E. coli host. Expression of the ant1 and kilA P1vir genes in the wild-type host was the highest among all and most probably leads to phage virulence. Interestingly, in a DksA-deficient host, P1vir genes encoding lysozyme and holin are downregulated, while antiholins are upregulated. Gene expression of RepA, a protein necessary for replication initiating at the phage oriR region, is increased in the dksA mutant; this is also true for phage genes responsible for viral morphogenesis and architecture. Still, it seems that P1vir is taking control of the bacterial protein, sugar, and lipid metabolism in both, the wild type and dksA− hosts. Generally, bacterial hosts are reacting by activating their SOS response or upregulating the heat shock proteins. However, only DksA-deficient cells upregulate their sulfur metabolism and downregulate proteolysis upon P1vir infection. We conclude that P1vir development is enhanced in the dksA mutant due to several improvements, including replication and virion assembly, as well as a less efficient lysis.

Highlights

Infection of the cell by a virus triggers a sequence of events that may lead to the virus development, multiplication, and release from the host
That kind of strategy is general for many viruses, including phages, it may differ in details and execution [1,53,60]. Another important phage strategy upon infection is the downregulation of cellular response to DNA damage stimulus which we found in both hosts (Figure 4A)— this may result from phage DNA maintenance and protection
We investigated the virus-host interaction to resolve the phenomenon of improved lytic development of P1vir phage in a DksA-deficient E. coli host

Summary

Introduction

Infection of the cell by a virus triggers a sequence of events that may lead to the virus development, multiplication, and release from the host. The bacterial viruses, bacteriophages, serve as a safe model to study the virus-host interactions. The wide knowledge of the life strategies, genetics as well as its complete genome [1] placed the P1 phage among the best-known models of prokaryotic viruses. The P1 phage can infect many bacterial species from Enterobacteriaceae, the deepest knowledge of its development was obtained from the studies on Escherichia coli. P1 chooses one of the two life cycles: lysis, leading to phage particle multiplication and propagation, or lysogeny when the P1 genome becomes an integral part of a bacterium in a form of a circular plasmid. An additional C1 anti-repressor function is achieved via the action of the Ant protein, whose expression is in turn regulated by C1 and other products of the imm region, namely the C4 antisense RNA and Icd [4,5]

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