Skip to main content
Fig. 3 | Genome Medicine

Fig. 3

From: Post-vaccine epidemiology of serotype 3 pneumococci identifies transformation inhibition through prophage-driven alteration of a non-coding RNA

Fig. 3

Reduction in transformation efficiency resulting from expression of the serotype 3 capsule. A Transformation efficiency of the Clade I isolate S. pneumoniae 99-4038; the unencapsulated laboratory isolate R6; the mutant R6 cps99-4038 (which carries the cps locus of S. pneumoniae 99-4038); the mutant R6 cps99-4038::Janus (in which the cps locus has been replaced by a resistance marker), and the mutant 99-4038 ΔϕOXC141 (in which the prophage was lost after exposure to mitomycin C). Each point represents an independent experiment, with the overall medians and interquartile ranges summarised by the box plots. A two-tailed Wilcoxon rank-sum test was used to compare the transformation frequencies of the genotypes to that of 99-4038, using a Holm-Bonferroni correction for multiple testing. Significance is coded as: p < 0.05, *; p < 0.01, **; p < 10−3, ***; p < 10−4, ****. B Recombinations inferred within R6 cps99-4038. The annotation of the recipient genome S. pneumoniae R6 is shown as a ring. The red blocks in the inner ring show the positions of inferred recombinations. Genes overlapping with these events are annotated around the edge of the panel. C–H Transmission electron microscopy showing the morphology of S. pneumoniae 99-4038, R6, and R6 cps99-4038. The panels show S. pneumoniae 99-4038 C whole cell and D cell surface morphology; S. pneumoniae R6 E whole cell and F cell surface morphology; and S. pneumoniae R6 cps99-4038G whole cell and H cell surface morphology. The whole cell morphologies are shown at a consistent scale, relative to the indicated 500 nm bar. The cell surface morphologies are each shown relative to the 100 nm bar, with white arrows pointing to the layer likely representing wall teichoic acid

Back to article page