Virus-Host Interaction Gets . PART II: Functional Transcriptomics of the DksA-Deficient Cell upon Phage P1 Infection.

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 P1 phage in a DksA-deficient host. Expression of the and P1 genes in the wild-type host was the highest among all and most probably leads to phage virulence. Interestingly, in a DksA-deficient host, P1 genes encoding lysozyme and holin are downregulated, while antiholins are upregulated. Gene expression of RepA, a protein necessary for replication initiating at the phage region, is increased in the mutant; this is also true for phage genes responsible for viral morphogenesis and architecture. Still, it seems that P1 is taking control of the bacterial protein, sugar, and lipid metabolism in both, the wild type and 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 P1 infection. We conclude that P1 development is enhanced in the mutant due to several improvements, including replication and virion assembly, as well as a less efficient lysis.