Unknown,Transcriptomics,Genomics,Proteomics

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Gene expression in P. aeruginosa cystic fibrosis isolates grown on Nematode Growth Medium

ABSTRACT: Pseudomonas aeruginosa (P. aeruginosa) lung infection is a significant cause of mortality in patients with cystic fibrosis (CF). Existing experimental data in our lab showed significantly different levels of virulence of "early" and "late" P. aeruginosa infection isolates in a C. elegans slow killing model. We wished to examine the expression profile of these isolates in order to explore genes that may be responsible for the observed differences. The expression profiles of two pairs of isolates (four isolates in total) were compared to each other using the Affymetrix P. aeruginosa PAO1 genome array, to gain insight into properties mediating virulence in these isolates. Data analysis was carried out using BIOCONDUCTOR software. Keywords: Comparative strain hybridization Two pairs of isolates (four isolates in total) were compared to each other when grown on Nematode Growth Medium (NGM).

ORGANISM(S): Pseudomonas aeruginosa

SUBMITTER: Jim Manos

PROVIDER: E-GEOD-33275 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Project description:Background. The Beijing family of Mycobacterium tuberculosis is dominant in countries in East Asia. Genomic polymorphisms are a source of diversity within the M.tuberculosis genome and may account for the variation of virulence among M.tuberculosis isolates. To date there are no studies that have examined the genomic composition of M.tuberculosis isolates from the high TB-burden country, Myanmar. Methodology/Principle findings. Twenty-two M.tuberculosis isolates from Myanmar were screened on whole-genome arrays containing genes from M.tuberculosis H37Rv, M.tuberculosis CDC1551 and M.bovis AF22197. Screening identified 198 deletions or extra regions in the clinical isolates compared to H37Rv. Twenty-two regions differentiated between Beijing and non-Beijing isolates and were verified by PCR on an additional 40 isolates. Six regions (Rv0071-0074 [RD105], Rv1572-1576c [RD149], Rv1585c-1587c[RD149], MT1798-Rv1755c [RD152], Rv1761c [RD152] and Rv0279c) were deleted in Beijing isolates, of which 4 (Rv1572-1576c, Rv1585c-1587c, MT1798-Rv1755c and Rv1761c) were variably deleted among ST42 isolates, indicating a closer relationship between the Beijing and ST42 lineages. The TbD1 region, Mb1582-Mb1583 was deleted in Beijing and ST42 isolates. One M.bovis gene of unknown function, Mb3184c was present in all isolates, except 11 of 13 ST42 isolates. The CDC1551 gene, MT1360 coding for a putative adenylate cyclase, was present in all Beijing and ST42 isolates (except 1). The pks15/1 gene, coding for a putative virulence factor, was intact in all Beijing and non-Beijing isolates, except in ST42 and ST53 isolates. Conclusion. This study describes previously unreported deletions/extra regions in Beijing and non-Beijing M.tuberculosis isolates. The modern and highly frequent ST42 lineage showed a closer relationship to the hypervirulent Beijing lineage than to the ancient non-Beijing lineages. The pks15/1 gene was disrupted only in modern non-Beijing isolates. This is the first report of an in-depth analysis on the genomic diversity of M.tuberculosis isolates from Myanmar. Data is also available from http://bugs.sgul.ac.uk/E-BUGS-66