Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

RNA-seq of Pseudomonas aeruginosa PAO1 wild-type and ersA (sRNA) knock-out mutant

ABSTRACT: We investigate the differences in total gene expression between P.aeruginosa PAO1 (wild-type) and ΔersA isogenic mutant. ErsA is a small RNA involved in several P. aeruginosa phenotypes, including biofilm formation and antibiotic resistance. Cells were grown in a rich medium (BHI, Brain Heart Infusion) without any selective pressure (shaking at 37°C) and cells were harvested during stationary phase at OD600 2.7.

INSTRUMENT(S): NextSeq 500

ORGANISM(S): Pseudomonas aeruginosa PAO1

SUBMITTER: Elio Rossi

PROVIDER: E-MTAB-6247 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

The Small RNA ErsA of Pseudomonas aeruginosa Contributes to Biofilm Development and Motility through Post-transcriptional Modulation of AmrZ.

Falcone Marilena M Ferrara Silvia S Rossi Elio E Johansen Helle K HK Molin Søren S Bertoni Giovanni G

Frontiers in microbiology 20180215

The small RNA ErsA of Pseudomonas aeruginosa was previously suggested to be involved in biofilm formation via negative post-transcriptional regulation of the algC gene that encodes the virulence-associated enzyme AlgC, which provides sugar precursors for the synthesis of several polysaccharides. In this study, we show that a knock-out ersA mutant strain forms a flat and uniform biofilm, not characterized by mushroom-multicellular structures typical of a mature biofilm. Conve ...[more]

PMID: 29497413

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Project description:PrfA activity was studied in L. monocytogenes strain EGD and in an isogenic prfA deletion mutant (EGDΔprfA) carrying multiple copies of the wild-type prfA or the mutant prfA* gene (strains EGDΔprfApPrfA and EGDΔprfApPrfA*) after growth in brain heart infusion (BHI), Luria-Bertani broth (LB) or a defined minimal medium (MM) supplemented either with one of the three PTS-carbohydrates, glucose, mannose and cellobiose, or the non-PTS carbon source glycerol. Low PrfA activity was observed in the wild-type EGD strain in BHI and LB with either of these carbon sources, while PrfA activity was high in minimal medium in presence of glycerol but significantly reduced in presence of cellobiose. The strains expressing the prfA and prfA* gene under the prfA promoters, P1 and P2, produced equally large amounts of PrfA protein and high PrfA activity was observed in strain EGDΔprfApPrfA* under all growth conditions. In contrast, high PrfA activity in strain EGDΔprfApPrfA was only observed when this strain was cultured in BHI but not in LB or MM (in presence of either carbon source). A ptsH mutant (lacking a functional HPr) was able to grow in BHI suggesting that growth of L. monocytogenes in this culture medium is supported by carbon sources whose uptake and metabolism are independent of the PTS pathway. However, this mutant was unable to grow in LB and MM regardless which of the four carbon sources was added, suggesting that uptake of the used carbohydrates and the catabolism of glycerol depend fully on the functional common PTS pathway. Furthermore, the growth rates of L. monocytogenes are strongly reduced in presence of large amounts of PrfA protein when growing MM but less in LB and only slightly in BHI. The expression profiles of the genes encoding PTS permeases were determined in the three strains under various growth conditions. The data suggest that PrfA activity correlates with the expression level and the phosphorylation state of specific PTS permeases. This SuperSeries is composed of the following subset Series: GSE12143: Listeria monocytogenes EGD after growth BHI vs. LB vs. MM GSE12145: Listeria monocytogenes EGDΔprfApPrfA and EGDΔprfApPrfA* compared to the wild type strain EGD GSE12146: Listeria monocytogenes EGD and EGD-e

Dataset Information

RNA-seq of Pseudomonas aeruginosa PAO1 wild-type and ersA (sRNA) knock-out mutant

Publications

The Small RNA ErsA of <i>Pseudomonas aeruginosa</i> Contributes to Biofilm Development and Motility through Post-transcriptional Modulation of AmrZ.

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