## 2 Results and Discussion
### The Host Transcriptome Upon Infection
Downregulation of this gene's expression upon P1_vir_ phage infection is a new and interesting discovery raising questions of its role in the process of P1_vir_ taking over the host metabolism [47]. Indeed we did find several cold shock protein-encoding genes to be downregulated (Figure 3C and Appendix A, Table A1). Response to cold shock is a kind of a global reprogramming hub allowing bacterial cells to adapt. Turning down this pathway in the cells seems to provide a metabolic profit for the virus-cold shock regulatory features became a very useful and versatile tool for taking control of the host. The _cspA_ gene expression is also shown to be induced by the addition of chloramphenicol [48; 49]. Moreover, genes encoding multidrug efflux system transporters, such as _mdtl_ and _mdtl_, are downregulated upon infection (Figure 3C and Appendix A, Table A1). We hypothesize that besides preserving energy and substrates, one of the P1_vir_ phage strategies is to alter systems involved in cellular responsiveness to environmental threats. Using global regulators as multipurpose tools seems to be an effective way for taking control of hosts, also dampening the responsiveness of cellular alert systems. We found that the _yjiY_ gene (synonym: _btsT_) is the most upregulated gene at almost each time point and in each host (Figure 3D). This gene encodes a high-affinity, pyruvate/H\({}^{+}\) symporter which mediates the uptake of pyruvate under nutrient limiting conditions [50]. Expression of _btsT_ is induced at the onset of the stationary phase in media containing peptides or amino acids as the source of carbon [51; 52]. Interestingly, _btsT_, among other genes involved in carbon source transport and metabolism, was downregulated in two MG1655 lysogens carrying closely related Stx2a phages--O104 and P8 [53]. It seems that P1_vir_ has an opposite strategy and upregulates this symporter as an energy/carbon source provider. In the wild-type strain, at 30 min of infection, we found _insI_ as one of the most upregulated genes. In contrast, this gene was not present in any set of genes upregulated upon infection in the _dksA_ host. The _insII_ gene encodes a transposase for the IS30 insertion sequence. This transposase interacts with the terminal inverted repeats of the IS30 sequence element, using them as targets for transposition [54; 55]. Why DksA-deprived cells are unable to express this gene remains unclear. We speculate that in the wild-type cells, phage infection stimulates the excision of this mobile genetic element. Cell lysis, as a result of phage infection, may be a mechanism of propagation of the IS30 element in the bacterial population. The lack of DksA, a major global transcriptional regulator, abolishes this process. We found an even more interesting situation in the _dksA_ strain at 10 min post-infection. The pool of the top ten most highly expressed genes is represented mostly by genes involved in the sulfur metabolism--_cysA_, _cysI_, _cysD_, _cysC_, _cysN_, _cysN_, _cysW_ (Figure 3D and Appendix A, Table A1). These genes are not expressed either at 30 min of infection in the _dksA_ mutant or the wild-type cells at any time point. Sulfate assimilation proceeds by consecutive steps of its import (carried out by a protein encoded by _cysA_[56; 57]), adenylation (encoded by _cysD_, _cysN_), and phosphorylation (encoded by _cysC_), prior to sulfate reduction to sulfite coupled to its release (encoded by _cysH_). CysH encodes a 3'-phospho-adenylylsulfate reductase that releases sulfite and adenosine-3,5-bisphosphate (PAP). The _cysI_ encodes a subunit of sulfite reductase which is involved in the assimilation of sulfate and catalyzes the electron transfer from NADPH to sulfite to produce sulfide [58]. Moreover, _cysD_ belongs to a network of genes that facilitate stress-induced mutagenesis (SIM) in _E. coli_ K-12 [59]. Interestingly, _cysD_, as well as other genes involved in the sulfur metabolism, were also significantly upregulated in the MG1655 lysogen carrying the Stx2a phage PA8 [53].