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Streptococcus pneumoniae

ABSTRACT: Transcriptome and/or marker frequency analysis of S. pneumoniae (control vs. HPUra/Kanamycin/Ciprofloxacin/Hydroxyurea/Rifampicin)

PROVIDER: PRJNA286283 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR2058100_1.fastq.gz	Fastqsanger.gz
	SRR2058100_2.fastq.gz	Fastqsanger.gz
	SRR2058091_1.fastq.gz	Fastqsanger.gz
	SRR2058091_2.fastq.gz	Fastqsanger.gz
	SRR2058101_1.fastq.gz	Fastqsanger.gz

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Transcriptome and marker frequency analysis of E. coli (control vs. Trimethoprim) and S. pneumoniae (control vs. HPUra/Kanamycin)

Project description:Transcriptome and marker frequency analysis of E. coli (control vs. Trimethoprim) and S. pneumoniae (control vs. HPUra/Kanamycin)

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Transcriptome and marker frequency analysis of E. coli (control vs. Trimethoprim) and S. pneumoniae (control vs. HPUra/Kanamycin)

2014-04-10 | GSE54199 | GEO

Transcriptome and marker frequency analysis of E. coli (control vs. Trimethoprim) and S. pneumoniae (control vs. HPUra/Kanamycin)

Project description:We show that treatment with HPUra (for S. pneumoniae) and trimethoprim (for E. coli) leads to a skewed gene dosage profile (increase around the origin of replication), which is also propagated to the transcriptome level. Kanamycin, however, does not have this effect. In case of S. pneumoniae this shift in gene dosage distribution leads to the population-wide activation of competence. Pairwise comparison of untreated to antibiotic-treated cells (either DNA-seq or RNA-seq). It was performed with deep sequencing, using an Illumina HiSeq 2000 machine with 100 bp read length. S. pneumoniae samples treated with kanamycin was analysed from a single sample, while all other conditions were from duplicate samples.

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Project description:Comparison of the Streptococcus pneumoniae D39 spxB- mutant vs D39. For DNA microarray analysis, D39 wild-type and two independently obtained D39spxB- mutants were grown as four, two and two biological replicates, respectively, in Glc-M17 under semi-aerobic conditions and harvested at an OD595 of approximately 0.25 (mid-exponential). The RNA of both D39spxB- strains was compared to D39 and the combined data was analyzed. All other procedures regarding microarray analyses were done as described before. A gene was considered differentially expressed when the fold change was ≥ 2, ≤ 0.5, with a Bayes p ≤ 0.00001 and when at least 7 measurements were available.

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Deep phosphoproteomics of Klebsiella pneumoniae reveals HipA-mediated tolerance to ciprofloxacin

Project description:Klebsiella pneumoniae belongs to the group of bacterial pathogens causing the majority of antibiotic-resistant nosocomial infections worldwide; however, the molecular mechanisms underlying post-translational regulation of its physiology are poorly understood. Here we perform a comprehensive analysis of Klebsiella phosphoproteome, focusing on HipA, a Ser/Thr kinase involved in antibiotic tolerance in Escherichia coli. We show that overproduced K. pneumoniae HipA (HipAkp) is toxic to both E. coli and K. pneumoniae and its toxicity can be rescued by overproduction of the antitoxin HipBkp. Importantly, HipAkp overproduction leads to increased tolerance against ciprofloxacin, a commonly used antibiotic in the treatment of K. pneumoniae infections. Proteome and phosphoproteome analyses in the absence and presence of ciprofloxacin confirm that HipAkp has Ser/Thr kinase activity, auto-phosphorylates at S150, and shares multiple substrates with HipAec, thereby providing a valuable resource to clarify the molecular basis of tolerance and the role of Ser/Thr phosphorylation in this human pathogen.

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Methionine starvation caused reprogrammed metabolism in Streptococcus pneumoniae

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Project description:Zn and Mn are essential micronutrients for many bacteria including Streptococcus pneumoniae. While Zn performs vital structural or catalytic roles in certain proteins, in excess, Zn can inhibit Mn uptake by S. pneumoniae and displace, but not functionally replace Mn from key enzymes including superoxide dismutase A (SodA). Here, we show that the Ccn small regulatory RNAs promote S. pneumoniae Mn uptake and resistance to the oxidative stress. Furthermore, we demonstrate that these small regulatory RNAs modulate the ability of S. pneumoniae to cause invasive pneumonia. Altogether, these findings reveal a new layer of regulation of S. pneumoniae Zn and Mn homeostasis and suggest that there are factors in addition to known transporters that modulate intracellular Mn levels.

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