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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Effects of (E)-4-bromo-5-(bromomethylene)-3-methylfuran-2(5H)-one (BF8) on P. aeruginosa PAO1 persister cells (three biological replicates)

ABSTRACT: Twenty eight genes in PAO1 persister cells were consistently induced by treatment with 1 ug/mL BF8 for 1 h. Persister cells were isolated from PAO1 overnight cultures and treated with and without BF8 for microarray analysis.

ORGANISM(S): Pseudomonas aeruginosa PAO1

SUBMITTER: Jiachuan Pan

PROVIDER: E-GEOD-36753 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Effects of (E)-4-bromo-5-(bromomethylene)-3-methylfuran-2(5H)-one (BF8) on E. coli RP437 persister cells (two biological replicates)

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Effects of (E)-4-bromo-5-(bromomethylene)-3-methylfuran-2(5H)-one (BF8) on P. aeruginosa PAO1 persister cells (three biological replicates)

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BW25113 H202 and delta rpoS persister cells vs. stationary phase BW25113 wild-type

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Expression data from persister and normal cells of Pseudomonas aeruginosa PAO1

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E. coli BW25113 K-12 hfq vs. wild-type persister

Project description:Persisters are cells which evade stresses like antibiotics and which are characterized by reduced metabolism and a lack of genetic alterations required to achieve this state. We showed previously that MqsR and MqsA of Escherichia coli are a toxin-antitoxin pair that influence cell physiology (e.g., biofilm formation and motility) via RNase activity as well as through regulation of toxin CspD. Here, we show that deletion of the mqsRA locus decreases persister cell formation and, consistent with this result, overexpression of MqsR increases persister cell formation. Furthermore, toxins Hha, CspD, and HokA increase persister cell formation. In addition, by overproducing MqsR in a series of isogenic mutants, we show that Hha and CspD are necessary for persister cell formation via MqsR overexpression. Surprisingly, Hfq, a small RNA chaperone, decreases persistence. A whole-transcriptome study shows that Hfq induces transport-related genes (oppA, oppB, oppC, oppD, oppF, and dppA), outer membrane protein-related genes (ybfM and ybfN), toxins (hha), and proteases (clpX, clpP, and lon). Taken together, these results indicate that toxins CspD and Hha influence persister cell formation via MqsR and that Hfq plays an important role in the regulation of persister cell formation via regulation of transport or outer membrane proteins. Strains: E. coli BW25113 K-12 hfq deleted mutant vs. wild-type Medium: LB Culture: Planktonic cell grown OD=0.5, adjusted OD=1.0, and then exposed to 100 ug/mL ampicillin for 2 h.

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Transcription Profiling of the Persister Phenotype in Escherichia Coli

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Gene expression analysis of Mycobacterium tuberculosis high-persister (hip) mutants.

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Effects of (E)-4-bromo-5-(bromomethylene)-3-methylfuran-2(5H)-one (BF8) on E. coli RP437 persister cells (two biological replicates)

Project description:Eighteen genes in RP437 persister cells were consistently induced/decreased by treatment with 5 µg/mL BF8 for 1 h.

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Project description:Persisters represent a small bacterial population that is dormant and that survives under antibiotic treatment without experiencing genetic adaptation. Persisters are also considered one of the major reasons for recalcitrant chronic bacterial infections. Although several mechanisms of persister formation have been proposed, it is not clear how cells enter the dormant state in the presence of antibiotics or how persister cell formation can be effectively controlled. A fatty acid compound, cis-2-decenoic acid, was reported to decrease persister formation as well as revert the dormant cells to a metabolically active state. We reasoned that some fatty acid compounds may be effective in controlling bacterial persistence because they are known to benefit host immune systems. This study investigated persister cell formation by pathogens that were exposed to nine fatty acid compounds during antibiotic treatment. We found that three medium chain unsaturated fatty acid ethyl esters (ethyl trans-2-decenoate, ethyl trans-2-octenoate, and ethyl cis-4-decenoate) decreased the level of Escherichia coli persister formation up to 110-fold when cells were exposed to ciprofloxacin or ampicillin antibiotics. RNA sequencing analysis and gene deletion persister studies elucidated that these fatty acids inhibit bacterial persistence by regulating antitoxin HipB. A similar persister cell reduction was observed for pathogenic E. coli EDL933, Pseudomonas aeruginosa PAO1, and Serratia marcescens ICU2-4 strains. This study demonstrates that fatty acid ethyl esters can be used to disrupt bacterial dormancy to combat persistent infectious diseases.

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