Fig 1.
Electron microscopic images of (a) and (b), bacteriophage pf16 in non-contracted and contracted forms respectively, and (c) and (d) bacteriophage phiPMW.
Scale bar corresponds to 100 nm.
Fig 2.
Comparative genome composition of the Pseudomonas putida phage pf16 and Enterobacteria phage T4.
Predicted ORFs are presented as arrows indicating the direction of transcription. Arrows are coloured by function according to the key presented at the bottom of the figure. Functional annotations (if any) are given alongside respective ORFs. Red shading between phages indicates percentage amino acid identity according to the key given.
Fig 3.
Comparative genome composition of the Pseudomonas putida phage phiPMW and Pseudomonas aeruginosa phage PAK_P1.
Predicted ORFs are presented as arrows indicating the direction of transcription. Arrows are coloured by function according to the key presented at the bottom of the figure. Functional annotations (if any) are given alongside respective ORFs. Red shading between phages indicates percentage amino acid identity according to the key given.
Fig 4.
Molecular models and superimposition of EPS-depolymerase like enzymes from Pseudomonas phage pf16, Erwinia phage phiEaH2, and Fusarium moniliforme.
Pf16 is shown in blue, phiEaH2 in green, and the fungus Fusarium moniliforme in yellow.
Table 1.
Table showing sigma70 promoter elements within Pseudomonas phage pf16.
Table 2.
Table showing sigma70 promoter elements within Pseudomonas phage phiPMW.
Fig 5.
Analysis of Pseudomonas phage pf16 stringent starvation protein B (SspB).
(a): Superimposition of Pseudomonas putida and pf16 SspB molecular models with resulting TM-align score of 0.818 indicating a high level of structural similarity. (b): Sequence alignment of P. putida and pf16 SspB proteins showing a high level of identity. Note the deletion in pf16 of numerous negatively charged residues (aspartate and glutamate). (c): Predicted complex between P. putida sigma factor RpoE, anti-sigma factor RseA, and both P. putida and pf16 SspB protein models highlighting the overlap in binding sites and thus putative competitive inhibitory action by pf16 SspB. The deletion in pf16 SspB compared to P. putida is highlighted in dark blue.
Fig 6.
Sequence alignment of the Pseudomonas phage pf16 and Pseudomonas phage AF tail fibre proteins.
Alignment of the pf16 and AF tail fibre proteins highlighting particular conservation of the C-terminal region.
Fig 7.
Graph showing distribution of putative Tevenvirinae genome sizes.
Phages infecting related hosts are colour coded appropriately with labels provided specifying the phage or group of phages. Pseudomonas phage pf16, Rhodothermus phage RM378 (smallest genome), Prochlorococcus phage P-SSM2 (largest genome), and Enterobacteria phage T4 are circled and labelled in bold. Contour density lines shows clustering of most phages around similar genome sizes. Boxplot at the bottom of the figure summarises the distribution of the phages. The main box and associated lines shows the spread, mean, and quartiles of the main cluster observed within the major contour lines with outliers and the smallest/largest genomes represented as dots.
Fig 8.
Pangenomic analyses of the Tevenvirinae.
(a) Gene presence/absence matrix plot. Blue regions correspond to genes present in a minimum of two phages on the extreme right hand side and increasing to all phages (if applicable) on the extreme left. (b) A plot of unique genes against the number of genomes. Numbers of unique genes rises with genome number highlighting the fact that individual members of the Tevenvirinae contain a significant quantity of novel genes. (c) A plot of the number of pangenomic genes (those not common to any phages) against number of genomes showing a steady rise in the T4-like pangenome and highlighting the wide array of accessory genes present in this group. (d) Graph showing number of completely new genes against genome number in each successive phage highlighting that despite a steady increase in unique genes across the entire Tevenvirinae, the number of new genes with respect to each additional phage steadily declines showing that there is a limit on the novelty and that there is some commonality across a large majority of members.
Fig 9.
Network representations of the BLASTx based core gene analysis of pf16 and the putative Tevenvirinae.
(a) pf16 BLASTx network of genes related to Enterobacteria phage T4 alone. (b) pf16 BLASTx network of genes related to the putative Tevenvirinae following “gene filtration” via BLASTx analysis of all genes against T4 followed by compilation into a new database. T4 is represented as the black dot in the centre of each network. Genes are coloured according to predicted function as per legends provided for Figs 2 and 3. Gene product (gp) labels are provided at each locus. Distance from T4 central dot correlates with relatedness of gp relative to other genes.