Virus–host interaction gets curiouser and curiouser. Part ii: Functional transcriptomics of the e. coli dksa–deficient cell upon phage p1vir infection

Abstract

The virus–host interaction requires a complex interplay between the phage strategy of repro-gramming the host machinery to produce and release progeny virions, and the host defense against in-fection. 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 viru-lence. Interestingly, in a DksA‐deficient host, P1vir genes encoding lysozyme and holin are downregu-lated, 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 respon-sible 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, in-cluding replication and virion assembly, as well as a less efficient lysis.