Pan-genome of <i>Serratia</i> spp.

<p>Euler diagram displaying the number of clusters found on each subspace of the pan-genome. The pan-genome defined here as the total collection of CDS clusters found in <i>S. symbiotica</i> SCc, <i>S. symbiotica</i> SAp, <i>S. proteamaculans</i> 568, <i>S. odorifera</i> 4R×13 and <i>S. marcescens</i> Db11 (first two obligate and facultative endosymbiont respectively and the rest free-living).</p

<i>S. symbiotica</i> COG profile modification from FLS and between them.

<p><i>S. symbiotica</i> COG profile modification from FLS and between them.</p

Phylogenetic and rearrangements history of the single-copy core genes of the <i>Serratia</i> spp.

<p>On the left side, rooted ML tree with * indicating bootstrap support values of 100 (percent of total). On the middle, pairwise synteny plots of free-living <i>S. marcescens</i>, <i>S. odorifera</i> and <i>S. proteamaculans</i> along with endosymbiotic relatives <i>S. symbiotica</i> SCc and <i>S. symbiotica</i> SAp. On the right side, unrooted minimal number of rearrangements tree as calculated by MGR. On red, branches from the endosymbiotic lineages.</p

Functional profiles of core, pan-genome and selected <i>Serratia</i> and corresponding <i>Buchnera</i> genomes.

<p><b>A.</b> Heatmap showing the two-way clustering of the COG profiles frequency differences from the FLS average. <b>B.</b> Heatmap showing the COG profiles from the selected <i>Serratia</i> and <i>Buchnera</i> genomes. On the right side of each heatmap, COG assignments for each row are displayed. In the bottom left, color key for the COG categories for the first heatmap in relation to the comparison <i>S. symbiotica</i> SCc vs FLS. In the bottom right, COG categories key. <b>BAp</b>:<i> B. aphidicola</i> from <i>A. pisum</i>; <b>BCc</b>: <i>B. aphidicola</i> from <i>C. cedri</i>; <b>Smar</b>: <i>S. marcescens</i> Db11; <b>Sodo</b>: <i>S. odorifera</i> 4R×13; <b>Spro</b>: <i>S. proteamaculans</i> 568; <b>SAp</b>:<i> S. symbiotica</i> from <i>A. pisum</i>; <b>SCc</b>: <i>S. symbiotica</i> from <i>C. cedri</i>.</p

Species, accession numbers and genomic features comparison of <i>Serratia</i> spp. and selected <i>B. aphidicola</i> genomes.

<p>Species, accession numbers and genomic features comparison of <i>Serratia</i> spp. and selected <i>B. aphidicola</i> genomes.</p

High-Frequency Changes in Pilin Glycosylation Patterns during <i>Neisseria meningitidis</i> Serogroup a Meningitis Outbreaks in the African Meningitis Belt

In the meningitis belt of sub-Saharan Africa, there are cyclic meningococcal epidemics that coincide with clonal waves of Neisseria meningitidis carriage and invasive disease. In the framework of longitudinal colonization and disease studies in Ghana and Burkina Faso, meningococcal isolates belonging to the closely related hypervirulent A:ST-5, A:ST-7, and A:ST-2859 clones have been collected from 1998 to 2011 during meningococcal outbreaks. A comparative whole-genome sequencing study with 100 of these isolates identified the pilin glycosylation (pgl) locus as one hot spot of recombination. Frequent exchange of pgl genes in N. meningitidis by lateral gene transfer results in differences in the glycosylation patterns of pilin and other cell surface glycoproteins. In this study, we looked at both recombination and phase variation of the pgl genes of these clinical isolates and analyzed the glycan structures resulting from different pgl alleles and their variable expression. Our results indicate that the basal O-linked sugar of the glycans expressed by these isolates is masked by various additional mono- or disaccharide structures whose expression is highly variable due to the phase-variable expression of pgl genes. We also observed a distinct glycoform in two isolates with pgl loci that were modified by recombination. These data suggest that variation in N. meningitidis protein glycosylation could be crucial for bacterial adaptation to evade herd immunity in semi-immune populations. Investigating pilin glycosylation in N. meningitidis can shed light on the mechanisms by which this pathogen evades the host immune response, and may help identify potential targets for novel therapies and vaccines

High-Frequency Changes in Pilin Glycosylation Patterns during <i>Neisseria meningitidis</i> Serogroup a Meningitis Outbreaks in the African Meningitis Belt

In the meningitis belt of sub-Saharan Africa, there are cyclic meningococcal epidemics that coincide with clonal waves of Neisseria meningitidis carriage and invasive disease. In the framework of longitudinal colonization and disease studies in Ghana and Burkina Faso, meningococcal isolates belonging to the closely related hypervirulent A:ST-5, A:ST-7, and A:ST-2859 clones have been collected from 1998 to 2011 during meningococcal outbreaks. A comparative whole-genome sequencing study with 100 of these isolates identified the pilin glycosylation (pgl) locus as one hot spot of recombination. Frequent exchange of pgl genes in N. meningitidis by lateral gene transfer results in differences in the glycosylation patterns of pilin and other cell surface glycoproteins. In this study, we looked at both recombination and phase variation of the pgl genes of these clinical isolates and analyzed the glycan structures resulting from different pgl alleles and their variable expression. Our results indicate that the basal O-linked sugar of the glycans expressed by these isolates is masked by various additional mono- or disaccharide structures whose expression is highly variable due to the phase-variable expression of pgl genes. We also observed a distinct glycoform in two isolates with pgl loci that were modified by recombination. These data suggest that variation in N. meningitidis protein glycosylation could be crucial for bacterial adaptation to evade herd immunity in semi-immune populations. Investigating pilin glycosylation in N. meningitidis can shed light on the mechanisms by which this pathogen evades the host immune response, and may help identify potential targets for novel therapies and vaccines

Variability at DNA methyltransferase loci.

<p>101 N. meningitidis isolates clustered according to SNP distance, yielding in two sequence type (ST) groups. Each column represents an isolate and rows specify the ORF status of 13 DNA methyltransferases (Rebase geneIDs of Z2491 reference strain). Bars in grey at the bottom represent the number of repeat units determining ON/OFF status of the phase-variable modA12 (M.NmeAORF1589P)</p

Two N. meningitidis serogroup A strains Z2491 and NM1264 display divergent DNA modifications.

<p>DNA modification scores are plotted against the coverage in SMRT sequencing of Tet1 converted samples. Each dot represents a position on either strand with a modification score larger than 20, the color specifying the nucleotide base, on which the modification was detected. Modified adenosines (red dots) are predominantly detected in strain NM1264. The horizontal line indicates the threshold score 50 applied for subsequent motif finding.</p

Methylated nucleotides display higher mutation rates than non-methylated positions.

<p>Positional co-occurrences of (in total 6031) SNPs at positions within (methylation) target motifs. Methylated positions highlighted in red within five target motifs (bold), as detected in the present study, with, each compared to two similar control sequences. Black bars in histogram represent nucleotides in methylated motifs, gray shades represent sequences not known as DNA-methylation targets. For each motif, counts of overlapping SNPs (for 5m-cytosine motifs: C/G in reference →N; or for 6m-adenosine: A/T→N) at each position are normalized by the genome-wide motif occurrences (numbers for methylated motifs in inset box). The dashed lines indicate the corresponding number of SNPs expected from random occurrence (G/C or A/T) across the genome and over-representation was tested with the χ2 statistics (*p value < 10–5).</p