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Selective Sweeps and Parallel Pathoadaptation Drive Pseudomonas aeruginosa Evolution in the Cystic Fibrosis Lung.

Diaz Caballero J, Clark ST, Coburn B, Zhang Y, Wang PW, Donaldson SL, Tullis DE, Yau YC, Waters VJ, Hwang DM, Guttman DS - MBio (2015)

Bottom Line: Our functional analysis of these alleles shows that they provide differential fitness benefits dependent on the antibiotic under selection.Pseudomonas aeruginosa is a bacterial opportunistic pathogen responsible for significant morbidity and mortality in cystic fibrosis (CF) patients.We show that diversity of P. aeruginosa is driven by recurrent clonal emergence and expansion within this patient and identify potential adaptive variants associated with these events.

View Article: PubMed Central - PubMed

Affiliation: Department of Cell and Systems Biology, University of Toronto, Toronto, Ontario, Canada.

No MeSH data available.


Related in: MedlinePlus

Distribution of pbpB alleles in clade A (A) and clade (B) over the 12 sampling time points. Clades A and B share an ancestral major allele. A minor allele is observed specifically in clade A, and two others segregate only in clade B.
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fig5: Distribution of pbpB alleles in clade A (A) and clade (B) over the 12 sampling time points. Clades A and B share an ancestral major allele. A minor allele is observed specifically in clade A, and two others segregate only in clade B.

Mentions: Given the relatively large number of variants that distinguish clades A and B, it is impossible to conclusively identify the beneficial mutation that initially gave rise to clade B. Nevertheless, it may be possible to identify SNPs that helped maintain one or both populations. As discussed above, three independent nonsynonymous mutations arose during the course of this study in the pbpB locus, encoding PBP3. Two derived alleles are found exclusively in clade B isolates (one at very low frequency), and one derived allele is found exclusively in clade A isolates (Fig. 5; see Fig.  S5 and S6 in the supplemental material). The ancestral PBP3 allele is found in both clades.


Selective Sweeps and Parallel Pathoadaptation Drive Pseudomonas aeruginosa Evolution in the Cystic Fibrosis Lung.

Diaz Caballero J, Clark ST, Coburn B, Zhang Y, Wang PW, Donaldson SL, Tullis DE, Yau YC, Waters VJ, Hwang DM, Guttman DS - MBio (2015)

Distribution of pbpB alleles in clade A (A) and clade (B) over the 12 sampling time points. Clades A and B share an ancestral major allele. A minor allele is observed specifically in clade A, and two others segregate only in clade B.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4556809&req=5

fig5: Distribution of pbpB alleles in clade A (A) and clade (B) over the 12 sampling time points. Clades A and B share an ancestral major allele. A minor allele is observed specifically in clade A, and two others segregate only in clade B.
Mentions: Given the relatively large number of variants that distinguish clades A and B, it is impossible to conclusively identify the beneficial mutation that initially gave rise to clade B. Nevertheless, it may be possible to identify SNPs that helped maintain one or both populations. As discussed above, three independent nonsynonymous mutations arose during the course of this study in the pbpB locus, encoding PBP3. Two derived alleles are found exclusively in clade B isolates (one at very low frequency), and one derived allele is found exclusively in clade A isolates (Fig. 5; see Fig.  S5 and S6 in the supplemental material). The ancestral PBP3 allele is found in both clades.

Bottom Line: Our functional analysis of these alleles shows that they provide differential fitness benefits dependent on the antibiotic under selection.Pseudomonas aeruginosa is a bacterial opportunistic pathogen responsible for significant morbidity and mortality in cystic fibrosis (CF) patients.We show that diversity of P. aeruginosa is driven by recurrent clonal emergence and expansion within this patient and identify potential adaptive variants associated with these events.

View Article: PubMed Central - PubMed

Affiliation: Department of Cell and Systems Biology, University of Toronto, Toronto, Ontario, Canada.

No MeSH data available.


Related in: MedlinePlus