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Genome-wide association study of signature genetic alterations among pseudomonas aeruginosa cystic fibrosis isolates

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dc.contributor.author윤상선-
dc.contributor.author이강무-
dc.contributor.author이강무-
dc.date.accessioned2021-09-29T01:05:17Z-
dc.date.available2021-09-29T01:05:17Z-
dc.date.issued2021-06-
dc.identifier.issn1553-7366-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/184187-
dc.description.abstractPseudomonas aeruginosa (PA) is an opportunistic pathogen that causes diverse human infections including chronic airway infection in patients with cystic fibrosis (CF). Comparing the genomes of CF and non-CF PA isolates has great potential to identify the genetic basis of pathogenicity. To gain a deeper understanding of PA adaptation in CF airways, we performed a genome-wide association study (GWAS) on 1,001 PA genomes. Genetic variations identified among CF isolates were categorized into (i) alterations in protein-coding regions, either large- or small-scale, and (ii) polymorphic variation in intergenic regions. We introduced each CF-associated genetic alteration into the genome of PAO1, a prototype PA strain, and validated the outcomes experimentally. Loci readily mutated among CF isolates included genes encoding a probable sulfatase, a probable TonB-dependent receptor (PA2332~PA2336), L-cystine transporter (YecS, PA0313), and a probable transcriptional regulator (PA5438). A promoter region of a heme/hemoglobin uptake outer membrane receptor (PhuR, PA4710) was also different between the CF and non-CF isolate groups. Our analysis highlights ways in which the PA genome evolves to survive and persist within the context of chronic CF infection.-
dc.description.statementOfResponsibilityopen-
dc.languageEnglish-
dc.publisherPublic Library of Science-
dc.relation.isPartOfPLOS PATHOGENS-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.titleGenome-wide association study of signature genetic alterations among pseudomonas aeruginosa cystic fibrosis isolates-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentDept. of Microbiology (미생물학교실)-
dc.contributor.googleauthorWontae Hwang-
dc.contributor.googleauthorJi Hyun Yong-
dc.contributor.googleauthorKyung Bae Min-
dc.contributor.googleauthorKang-Mu Lee-
dc.contributor.googleauthorBen Pascoe-
dc.contributor.googleauthorSamuel K Sheppard-
dc.contributor.googleauthorSang Sun Yoon-
dc.identifier.doi10.1371/journal.ppat.1009681-
dc.contributor.localIdA02558-
dc.contributor.localIdA02638-
dc.contributor.localIdA02638-
dc.relation.journalcodeJ02541-
dc.identifier.eissn1553-7374-
dc.identifier.pmid34161396-
dc.contributor.alternativeNameYoon, Sang Sun-
dc.contributor.affiliatedAuthor윤상선-
dc.contributor.affiliatedAuthor이강무-
dc.contributor.affiliatedAuthor이강무-
dc.citation.volume17-
dc.citation.number6-
dc.citation.startPagee1009681-
dc.identifier.bibliographicCitationPLOS PATHOGENS, Vol.17(6) : e1009681, 2021-06-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Microbiology (미생물학교실) > 1. Journal Papers

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