RNAseq analysis of Vibrio cholerae A1552 ∆rpoS (∆VC0534) from Smooth and Rugose backgrounds
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PROVIDER: PRJNA1075132 | ENA |
REPOSITORIES: ENA
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Project description:RNA-sequencing of Vibrio cholerae A1552 ∆rpoS and parental strains from smooth and rugose backgrounds grown as spots on LB agar
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Project description:In this study, we determined the TfoY regulon of V. cholerae using RNA-seq to better uderstand the protein's function. mRNA profiles of a WT V. cholerae O1 El Tor strain (A1552) and of a TfoY-producing derivative of the WT strain (A1552-TntfoY). 3 independent biological replicates are provided for each bacterial strain. The bacteria were grown to high cell density and in the presence of arabinose (to induce TfoY in strain A1552-TntfoY).
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Project description:We identified the mutated gene locus in a pigment overproducing Vibrio cholerae mutant of strain A1552. The deduced gene product is suggested to be a oxidoreductase based on partial homology to putative homogentisate 1,2-dioxygenase in Pseudomonas aeruginosa and Mesorhizobium loti and we propose that the gene VC1345 in the V. cholerae genome be denoted hmgA in accordance with the nomenclature for other species. The hmgA::miniTn5 mutant showed a non-pigmented phenotype after complementation with a plasmid clone carrying the wild type hmgA+ locus. Microarray transcription analysis revealed that expression of hmgA, and the neighboring genes encoding a postulated two component sensor system, was growth phase dependent. Results from qRT-PCR analysis showed that hmgA operon expression was reduced in the rpoS mutant, but pigment production by the wild type V. cholerae or the hmgA mutant was not detectably influenced by the stationary phase regulator RpoS. The pigmented mutant showed increased UV resistance in comparison with the wild-type strain. Interestingly, the pigment producing mutant expressed more toxin co-regulated pili and cholera toxin in comparison with wild type V. cholerae. Moreover, the hmgA mutant showed a 5-fold increase in the ability to colonize the intestines of infant mice. A possible mechanism by which pigment production might cause induction of the ToxR regulon due to generation of hydrogen peroxide was supported by results from tests showing that externally supplied H2O2 led to higher TcpA levels. Taken together, our findings suggest that melanin pigment formation may play a role in V. cholerae virulence factor expression. Groups of assays that are related as part of a time series. Elapsed Time: Wild type V. cholerae strain A1552 bacteria were cultured statically for 4 h in AKI medium at 37C and then shifted to aerobic growth for 6 h using shaken culture flasks. Samples were taken at hourly during the this process. Keywords: time_series_design
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Project description:We identified the mutated gene locus in a pigment overproducing Vibrio cholerae mutant of strain A1552. The deduced gene product is suggested to be a oxidoreductase based on partial homology to putative homogentisate 1,2-dioxygenase in Pseudomonas aeruginosa and Mesorhizobium loti and we propose that the gene VC1345 in the V. cholerae genome be denoted hmgA in accordance with the nomenclature for other species. The hmgA::miniTn5 mutant showed a non-pigmented phenotype after complementation with a plasmid clone carrying the wild type hmgA+ locus. Microarray transcription analysis revealed that expression of hmgA, and the neighboring genes encoding a postulated two component sensor system, was growth phase dependent. Results from qRT-PCR analysis showed that hmgA operon expression was reduced in the rpoS mutant, but pigment production by the wild type V. cholerae or the hmgA mutant was not detectably influenced by the stationary phase regulator RpoS. The pigmented mutant showed increased UV resistance in comparison with the wild-type strain. Interestingly, the pigment producing mutant expressed more toxin co-regulated pili and cholera toxin in comparison with wild type V. cholerae. Moreover, the hmgA mutant showed a 5-fold increase in the ability to colonize the intestines of infant mice. A possible mechanism by which pigment production might cause induction of the ToxR regulon due to generation of hydrogen peroxide was supported by results from tests showing that externally supplied H2O2 led to higher TcpA levels. Taken together, our findings suggest that melanin pigment formation may play a role in V. cholerae virulence factor expression. Groups of assays that are related as part of a time series. Elapsed Time: Wild type V. cholerae strain A1552 bacteria were cultured statically for 4 h in AKI medium at 37C and then shifted to aerobic growth for 6 h using shaken culture flasks. Samples were taken at hourly during the this process. Keywords: time_series_design Using regression correlation
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Project description:In this study, we compared the QstR regulon to the TfoX regulon (and TfoY regulon) of V. cholerae in WT strain A1552 and its ΔhapRΔvpsA derivative using RNA-seq to better understand QstR's function.
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Project description:For expression analysis of wild-type V. cholerae, hapR, and rpoS deletion mutants in mid-exponential or stationary phase, the strains were grown to either OD600 of 0.3 or for 11 h in LB media at 37 0C, and bacteria from 2-ml culture were quickly pelleted, resuspended in Trizol reagent (GIBCO/BRL, San Diego, California, United States), and frozen on dry ice. RNA was isolated from the Trizol agent, treated with DNaseI (Ambion, Austin, Texas, United States), and cleaned by using the RNeasy kit (Qiagen, Valencia, California, United States). Labeling of cDNA and microarray hybridizations were performed as described [Yiliz et al. 2001, Mol. Micro. 53: 497-515]. Microarrays were scanned with a GenePix 400A instrument (Axon Instruments), using the GENEPIX 5.0 software. At least four microarray experiments were performed for each of two biological replicates for the tested strains. Gene expression of V. cholerae, rpoS, and hapR deletion mutants in stationary phase LB cultures was analyzed and compared to the wild-type parent under identical conditions. Gene expression of the wild-type parent during stationary phase after 11 h growth in LB was analyzed using RNA from an exponentially growing culture as a reference.
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