## 2 Results and Discussion
### The Host Transcriptome Upon Infection
In addition, the fact that we observed the inhibition of expression of genes involved in the by P1_vir_ only in the _dksA\({}^{-}\)_ host supports our gentle lysis hypothesis--less efficient protein degradation in the host cell may support more enhanced phage development. Figure 4: Gene Ontology (GO) terms analysis of the host genes upon P1\(\ddot{o}\)_ir_ infection. Panel (**A**) shows downregulated biological processes in the wild-type strain and the _dh_s_A mutant. Panel (**B**) shows upregulated biological processes in both tested hosts. The horizontal line indicates a border between the host sets of GO terms. Descriptions in gray represent GO terms that are common to both hosts. Descriptions in black represent biological processes that are uniquely up- or downregulated in a given host. We used the GSAn algorithm exploiting the semantic of concepts in Gene Ontology which provided a reduced and synthetic number of GO terms resuming the biological role of the gene set input. The Information Content (IC) is a score associated with the terms explaining how much they are informative (the bigger the IC is, the more specific the term is); log(IC) is used for visualization purposes. Term depth (number of GO terms united together after semantic analysis) and covered genes (the number of genes whose expression has been up- or downregulated) are also provided. _Upregulated biological processes in the host cell._ Just like for the downregulated processes, we found many similarities in the upregulation of metabolic processes between both hosts upon P1_vir_ infection. In both hosts, we found upregulation of the organic substance catabolic process, cellular amino acid catabolic process, cellular protein modification process, peptide transport, protein-containing complex assembly, cellular carbohydrate metabolic process, lipid metabolic process, nucleotide biosynthetic process, purine ribonucle-cleotide metabolic process, transcription (DNA-templated), response to heat, and the SOS response (Figure 4B). In general, phage P1_vir_ controls the hosts by upregulating their protein, sugar, and lipid metabolism, while the hosts try to take action by activating the SOS response or upregulating their response to heat. Unique to the wild-type strain, we observed upregulation of inorganic cation transmembrane transport, phosphate ion transmembrane transport, phosphate-containing compound metabolic process, cellular amino acid biosynthetic process, peptide metabolic process, and general cellular response to stress (Figure 4B). Unique to the _dk_s_A strain, we observed upregulation of amino acid transport, anion transmembrane transport, carbohydrate transport, carboxylic acid transmembrane transport, proton transmembrane transport. Besides stimulation of the resources-gaining processes, we also observed upregulation of the monocarboxylic acid catabolic process, monosaccharide catabolic process, nucleobase-containing compound catabolic process, carboxylic acid biosynthetic process, and phosphorelay signal transduction system (Figure 4B). Moreover, upon P1 infection _dk_s_A cells promote the DNA metabolic process, cellular response to DNA damage stimulus, and DNA replication (Figure 4B). Indeed, we observed stimulated DNA replication of the mini-P1 replicon in the _dk_s_A mutant (see accompanying paper [30]). We have found that expression of the _repA_ gene, the phage _ori_R replication initiation protein, is increased in the _dk_s_A mutant when compared to the wild-type strain [30]. Thus, if DNA replication is stimulated in the _dk_s_A mutant, more phages can be produced. Even more interesting and striking is the upregulation of the hydrogen sulfide biosynthetic process that we found unique to the _dk_s_A host (Figure 4B). This biological process appears in Gene Ontology analysis as a result of the upregulation of many sulfur-metabolism-linked genes, which were discussed in a previous section.