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Transcriptional regulation by the stringent response-associated alarmone (p)ppGpp in Pseudomonas putida

ABSTRACT: The stringent response is an adaptive physiological response triggered by different conditions of nutritional or environmental stress and aimed at increasing survival under harsh conditions. This response is mediated the signalling nucleotides guanosine tetraphosphate (ppGpp) and pentaphospate (pppGpp), collectively known as (p)ppGpp. In this study we aim to identify genome-wide targets of regulation by the stringent-response associated alarmone (p)ppGpp in Pseudomonas putida by performing RNA-seq experiments using the wild-type KT2440tel strain and a KT2440tel-derivative bearing deletions of the (p)ppGpp synthetase-encoding genes relA and spoT (ppGpp0 mutant).

ORGANISM(S): Pseudomonas putida

PROVIDER: GSE281821 | GEO | 2024/11/18

REPOSITORIES: GEO

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Transcriptional regulation by the stringent response-associated alarmone (p)ppGpp in Pseudomonas putida

Project description:Transcriptional regulation by the stringent response-associated alarmone (p)ppGpp in Pseudomonas putida

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RelA/(p)ppGpp regulates the glucose-starvation induced stringent response in the zoonostic Streptococcus suis

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(p)ppGpp controls stringent factors by exploiting antagonistic allosteric coupling between catalytic domains

Project description:Escherichia coli RelA is a ribosomal factor with strong (p)ppGpp synthesis activity that is dramatically activated in the presence of deacylated tRNA in the ribosomal A-site. RelA is a unique enzyme in that it is directly positively regulated by its product, alarmone nucleotide (p)ppGpp. Using HDX-MS, mulecular docking, biochemsitry, and microbiology approaches, we localise the (p)ppGpp binding site of E. coli RelA and uncover the molecular mechanism of RelA regulation by the alarmone.

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(p)ppGpp promotes Enterococcus faecalis virulence in a murine model of catheter-associated urinary tract infection

Project description:In Firmicutes, the nutrient-sensing regulators (p)ppGpp, the effector molecule of the stringent response, and CodY work in tandem to maintain bacterial fitness during infection. Here, we tested (p)ppGpp and codY mutant strains of Enterococcus faecalis in a catheter-associated urinary tract infections (CAUTI) mouse model and used global transcriptional analysis to investigate the (p)ppGpp and CodY relationship. Absence of (p)ppGpp or single inactivation of codY led to lower bacterial loads in catheterized bladders, and diminished biofilm formation on fibrinogen-coated surfaces under in vitro and in vivo conditions. Single inactivation of the bifunctional (p)ppGpp synthetase/hydrolase rel did not affect virulence supporting previous evidence that association of (p)ppGpp with enterococcal virulence is not dependent on activation of the stringent response. Inactivation of codY in the (p)ppGpp0 strain restored E. faecalis virulence in the CAUTI model as well as the ability to form biofilms in vitro. Transcriptome analysis revealed that inactivation of codY restores, for the most part, the dysregulated metabolism of (p)ppGpp0 cells. While a clear linkage between (p)ppGpp and CodY with expression of virulence factors could not be established, targeted transcriptional analysis indicate that a possible association between (p)ppGpp and c-di-AMP signaling pathways in response to the conditions found in the bladder may plays a role in enterococcal CAUTI. Collectively, this study identifies the (p)ppGpp-CodY network as an important contributor to enterococcal virulence in catheterized mouse bladder and supports that basal (p)ppGpp pools promote virulence through maintenance of a balanced metabolism during adverse conditions.

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The alarmone (p)ppGpp is part of the heat shock response of Bacillus subtilis

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2020-03-09 | PXD015416 | Pride

The role of (p)ppGpp in the heat shock response in B. subtilis

Project description:Bacterial and eukaryotic cells survive an otherwise lethal heat shock once they are primed by a mild pre-heat shock. Using B. subtilis as a model organism, we investigated transcriptional changes during thermotolerance development at 37 °C, 48 °C, 53 °C and 48/53 °C and observed a comprehensive upregulation of genes of the general and heat shock response and the downregulation of many translation-related genes. In addition, strains lacking (p)ppGpp (ppGpp0) or with elevated (p)ppGpp levels (ΔrelA) were analyzed at 37 °C and 48 °C, revealing broad and pleiotropic transcripional changes mediated by (p)ppGpp in the ΔrelA mutant. In addition, our data suggests a contribution of the (p)ppGpp-mediated stringent response in the heat-mediated transcripional down-regulation of ribosomal genes and additional processes.

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The stringent response regulator (p)ppGpp mediates virulence gene expression and survival in Erwinia amylovora

Project description:This RNA-seq analysis mainly examined the global effect of stringent resonse in E. amylovora under the T3SS-inducing condition. The (p)ppGpp mutant showed differential expression of more than 30% genes in the genome, which include significant down-regulation of T3SS genes and gene related to motiliey. On the other hand, genes involved in amino acid biosynthesis, translation, SOS response, DNA replication, chromosome segregation, as well as nucleotide metabolism, fatty acid and lipid biosynthesis were significantly up-regulated in (p)ppGpp mutant. These findings sugested that (p)ppGpp mediate the balance between virulence and survival.

2020-03-23 | GSE143324 | GEO

The stringent response inhibits DNA replication initiation in E. coli by modulating supercoiling of oriC

Project description:The stringent response enables bacteria to respond to a variety of environmental stresses, especially various forms of nutrient limitation. During the stringent response the cell produces large quantities of the nucleotide alarmone ppGpp, which modulates many aspects of cell physiology, including reprogramming transcription, blocking protein translation, and inhibiting new rounds of DNA replication. The mechanism by which ppGpp inhibits DNA replication initiation in Escherichia coli remains unclear. Prior work suggested that ppGpp blocks new rounds of DNA replication by inhibiting transcription of the essential initiation factor dnaA, but we found that replication is still inhibited by ppGpp in cells ectopically producing DnaA. Instead, we provide evidence that a global reduction of transcription by ppGpp prevents replication initiation by modulating the supercoiling state of the origin of replication, oriC. Active transcription normally introduces negative supercoils into oriC to help promote replication initiation, so the accumulation of ppGpp reduces initiation potential at oriC. We find that maintaining transcription near oriC, either by expressing a ppGpp-blind RNA polymerase mutant or by inducing transcription from a ppGpp-insensitive promoter, can strongly bypass the inhibition of replication by ppGpp. Additionally, we show that increasing global negative supercoiling by inhibiting topoisomerase I or by deleting the nucleoid-associated protein seqA, also relieves inhibition. We propose a model, potentially conserved across proteobacteria, in which ppGpp indirectly creates an unfavorable energy landscape for initiation by preventing the introduction of negative supercoils into oriC.

2019-06-11 | GSE128606 | GEO

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