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Transcriptome analysis of gene expression of strains JNB5-1 and SK8-37

ABSTRACT: RNAseq analysis was performed to evaluate gene expression differences between strains JNB5-1 and SK8-37. S. marcescens JNB5-1 and SK8-37 cells were grown in LB medium for 10 h before harvesting. The collected cells were then treated with RNAprep pure Kit (TIANGEN) to extract total bacterial RNA and delivered to GENEWIZ in dry ice for transcriptome resequencing analysis. For annotation, the genome of S. marcescens WW4 (NC_020211.1) was used as reference. A total of 31206068 reads matched to the referenced genome in the sample of JNB5-1, and 29862970 reads in the sample of SK8-37. The significantly differentially expressed genes (DEGs) were determined between strains JNB5-1 and SK8-37 with the standards of p-value≤ 0.05, fold change |log2Ratio|≥1. Transcriptome data showed that expression of 60 genes were significantly up-regulated while 558 genes were significantly down-regulated by at least 2-fold when comparing the psrA mutant strain SK8-37 to its parent strain JNB5-1. Based on the annotation of KEGG_B_class, the up-regulated and down-regulated genes were classified into 10 and 19 major cellular processes, respectively. The transcriptome data indicated that PsrA may controls a variety of cellular processes in S. marcescens, including prodigiosin synthesis, serrawttin W1 biosynthesis, extracellular polysaccharide production, biofilm formation, cell motility and T6SS-mediated antibacterial activity.

ORGANISM(S): Serratia marcescens

PROVIDER: GSE158829 | GEO | 2020/10/01

REPOSITORIES: GEO

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Transcriptome analysis of gene expression of strains JNB5-1 and SK68

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2020-04-28 | GSE149400 | GEO

Transcriptome analysis of gene expression of strains JNB5-1 and ZK66

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2019-09-15 | GSE137185 | GEO

Ambigols from the Cyanobacterium Fischerella ambigua increase Prodigiosin Production in Serratia sp.

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| PRJNA91953 | ENA

Transcription profiling of Pseudomonas aeruginosa PAO1-psrA::Tn vs. PAO1 in LB

Project description:b-Oxidative enzymes for fatty acid degradation (Fad) of long-chain fatty acid (LCFA), a component of lung surfactant phosphatidylcholine, are induced in vivo during lung infection in cystic fibrosis patients, which could contribute to nutrient acquisition and pathogenesis of Pseudomonas aeruginosa. In addition, fatty acid biosynthesis (Fab) is essential for the syntheses of two virulence controlling acylated-homoserine-lactone molecules in this organism. We mapped the promoter regions of the fadBA5-operon (PA3014 and PA3013) and a fadE homologue (PA2815) involved in Fad and the fabAB-operon involved in Fab. Focusing on the transposon mutagenesis of strain PAO1 carrying the PfadBA5-lacZ fusion, we identified a regulator for the fadBA5-operon to be PsrA (PA3006). Transcriptome analysis of the DpsrA mutant indicates its importance in regulating b-oxidative enzymes, which confirms a previous proteomic study. We further showed that induction of the fadBA-operon responds to LCFA signals, and this induction requires the presence of PsrA, suggesting that PsrA binds to LCFA to derepress fadBA5. Electrophoresis mobility shift assay indicate specific binding of PsrA to the fadBA5-promoter region. This binding is disrupted by specific LCFA (C18:1D9, C16:0, and to a lesser extent C14:0), but not by the first intermediate of b-oxidation, acyl-CoA. We proposed that PsrA is a Fad-regulator that binds and responds to LCFA signals in Pseudomonas aeruginosa. Experiment Overall Design: PAO1 and PAO1-psrA::Tn cultures grown in LB and cells were harvested at mid-log phase. Total RNA was isolated from both samples, and used for cDNA synthesis. And then, the cDNA for both samples were fragmented and labeled. The cDNA of PAO1 was used for 2 GeneChips, and PAO1-psrA::Tn cDNA was used for three GeneChips.

2008-04-07 | E-GEOD-8083 | biostudies-arrayexpress

PAO1-psrA::Tn expression compared to PAO1 in LB

Project description:b-Oxidative enzymes for fatty acid degradation (Fad) of long-chain fatty acid (LCFA), a component of lung surfactant phosphatidylcholine, are induced in vivo during lung infection in cystic fibrosis patients, which could contribute to nutrient acquisition and pathogenesis of Pseudomonas aeruginosa. In addition, fatty acid biosynthesis (Fab) is essential for the syntheses of two virulence controlling acylated-homoserine-lactone molecules in this organism. We mapped the promoter regions of the fadBA5-operon (PA3014 and PA3013) and a fadE homologue (PA2815) involved in Fad and the fabAB-operon involved in Fab. Focusing on the transposon mutagenesis of strain PAO1 carrying the PfadBA5-lacZ fusion, we identified a regulator for the fadBA5-operon to be PsrA (PA3006). Transcriptome analysis of the DpsrA mutant indicates its importance in regulating b-oxidative enzymes, which confirms a previous proteomic study. We further showed that induction of the fadBA-operon responds to LCFA signals, and this induction requires the presence of PsrA, suggesting that PsrA binds to LCFA to derepress fadBA5. Electrophoresis mobility shift assay indicate specific binding of PsrA to the fadBA5-promoter region. This binding is disrupted by specific LCFA (C18:1D9, C16:0, and to a lesser extent C14:0), but not by the first intermediate of b-oxidation, acyl-CoA. We proposed that PsrA is a Fad-regulator that binds and responds to LCFA signals in Pseudomonas aeruginosa. Keywords: Pseudomonas aeruginosa, wild-type PAO1 compared to PAO1-psrA::Tn

2008-02-14 | GSE8083 | GEO

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2023-10-24 | PXD043247 | Pride

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