Disease relevance of Prophages

• As further evidence that the proteolytic activity of recA protein is responsible for its regulatory function, we show here that the ability of two mutationally altered recA proteins to cleave phage lambda repressor correlates with the ability of the mutant cells to induce prophage [1].
• Thermoinduction of cells of E. coli carrying prophage lambdacI857 within the bfe gene brings about not only "escape synthesis" of core subunits of the DNA-dependent RNA polymerase (RNA nucleotidyltransferase, nucleosidetriphosphate:RNA nucleotidyltransferase, EC 2-7-7-6), but also a striking stimulation of sigma factor synthesis [2].
• The tum gene of coliphage 186, encoded on a LexA controlled operon, is essential for UV induction of a 186 prophage [3].
• The product of the cloned recA+ gene of Proteus mirabilis substitutes for a defective recA protein in Escherichia coli recA- mutants and restores recombination, repair, and prophage induction functions to near normal levels (Eitner, G., Adler, B., Lanzov, V. A., and Hofemeister, J. (1982) Mol. Gen. Genet. 185, 481-486) [4].
• With the exception of Mem and other minor ORFs, the striking similarity between the deduced proteomes of phiMFV1 and the recently described phiMAV1 of arthritogenic strains of Mycoplasma arthritidis, along with the prominent gene synteny between these elements, provides the taxonomic basis for a new family of prophage [5].

High impact information on Prophages

• In lambda lysogens, cleavage of lambda Cl repressor in a similar but far slower reaction results in prophage induction [6].
• Lambda cII expression from an induced prophage is increased twofold in the presence of a large excess of anti-OOP RNA [7].
• Induction of a lambda E-W-S-cI857 prophage in which the pseT gene can be transcribed from the late lambda promoter, PR1, leads to greater than 100-fold amplification of pnk activity; pnk comprises approximately 7% of the total soluble cell protein [8].
• Repression of cI by the lytic repressor was not required for prophage induction to occur [9].
• Strain persistence or extinction between epidemics was strongly associated with presence or absence, respectively, of the prophage encoding streptococcal pyrogenic exotoxin A [10].

Chemical compound and disease context of Prophages

• Plasmid R6-5 contains a locus whose product inhibits induction of sfiA and prophage lambda in a recA441 mutant at 42 degrees C and in a recA+ host after treatment with nalidixic acid [11].
• Similar characteristics of induction were observed when the lactose genes were fused to a prophage lambda promoter by using Mud(ApR, lac) [12].
• Of the dinucleotides tested, only d(A-G), d(G-G), and d(I-G) induced prophage [13].
• Maintenance of the prophage state requires the continuous expression of two repressors: (i) C1 is a protein which negatively regulates the expression of lytic genes including the C1 inactivator gene coi, and (ii) C4 is an antisense RNA which specifically inhibits the synthesis of an anti-repressor Ant [14].
• Since the Fels prophages are inducible by aflatoxin B1, by daunorubicin, and by other agents, it seems that mutagenesis and Fels prophage induction occur in separate subpopulations of cells; this situation had previously been reported to occur for mutagenesis and prophage lambda induction in Escherichia coli [15].

Biological context of Prophages

• Stable maintenance of the plasmid prophage of bacteriophage P1 requires the P1 ParB protein, which acts on a DNA site termed parS [16].
• Induction of prophage P2sig5 at 42 degrees caused replication of the bacterial chromosome in a dnaA mutant of Escherichia coli [17].
• A mutation of the ssb gene, lexC113, imparts to the cells UV sensitivity and inability to induce lambda prophage and to amplify recA protein, indicating participation of SSB in DNA repair and viral induction processes [18].
• Promotor activity in turn was regulated by a thermolabile repressor specified by a defective lambda prophage contained in the host chromosome [19].
• Both the lambda and CTXphi phages have repressor systems that maintain their respective prophages in a quiescent state, and in both types of prophages this repressed state is abolished when the host cell SOS response is activated [20].

Anatomical context of Prophages

• Both H2O2 and neutrophils were found to augment Stx2 production, raising the possibility that these agents may lead to prophage induction in vivo and thereby contribute to EHEC pathogenesis [21].

Gene context of Prophages

• The addiction module of plasmid prophage P1 consists of a pair of genes called phd and doc [22].
• We have purified the TraJ protein, using an Flac::lambda traJ lysogen that overproduces the protein after heat induction of the prophage [23].
• Here, we show that thermal induction of the prophage accelerated araB-lacZ fusion formation, confirming that derepression is a rate-limiting step in the fusion process [24].
• The upstream sequences include functional phd and doc genes, which encode an addiction system that stabilizes the P1 prophage state, and extend to and beyond pac, the site at which phage DNA packaging begins [25].
• E. coli sbcA mutants and lambda reverse both express genes of the Rac prophage, and we have located the lar gene immediately downstream of recT in this element [26].

Analytical, diagnostic and therapeutic context of Prophages

• Molecular epidemiologic studies showed clonal diversity among the O139 strains and continuous emergence of new epidemic clones, reflected by changes in the structure, organization, and location of the CTX prophages in the V. cholerae O139[27]
• Southern blot analyses revealed that V. mimicus strain PT5 contains two CTX prophages integrated at different sites within the V. mimicus genome whereas V. mimicus strains PT48, 523-80, and 9583 each contain tandemly arranged copies of CTXPhi [28].
• Complementation tests demonstrated that the deletions in all three strains removed both att P and the int gene, i,e., DNA from both prophage ends [29].
• Genotyping based on pulsed-field gel electrophoresis (PFGE), PCR ribotyping, enterobacterial repetitive intergenic consensus motif (ERIC2)-PCR, and prophage content analysis was carried out in 45 toxic shock syndrome toxin-1 (TSST-1)-positive Staphylococcus aureus strains isolated in 19 cities of the Czech Republic between 1986 and 2004 [30].
• PCR walking, starting from the int gene of phage varphi297, demonstrated that the varphi297 prophage integrated in the yecE gene of a lysogenic E. coli K12 strain [31].

References