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RNA-sequencing of L. monocytogenes under PrfA-inducing conditions refines the PrfA regulon and reveals a putative novel PrfA-dependent gene and its associated PrfA box

ABSTRACT: RNA-sequencing of L. monocytogenes under PrfA-inducing conditions refines the PrfA regulon and reveals a putative novel PrfA-dependent gene and its associated PrfA box

PROVIDER: PRJNA610791 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11250100.fastq.gz	Fastqsanger.gz
	SRR11250101.fastq.gz	Fastqsanger.gz
	SRR11250102.fastq.gz	Fastqsanger.gz
	SRR11250103.fastq.gz	Fastqsanger.gz
	SRR11250104.fastq.gz	Fastqsanger.gz

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RNA-sequencing of L. monocytogenes under PrfA-inducing conditions refines the PrfA regulon and reveals a putative novel PrfA-dependent gene and its associated PrfA box

Project description:Purpose: The objective of the present study was to refine the PrfA regulatory network using RNA-seq to characterize the L. monocytogenes transcriptome in a wt, ∆prfA, and prfA* under PrfA-inducing conditions. Methods: Sequence reads were aligned to the L. monocytogenes 10403S genome using the BWA-MEM algorithm, version 0.7.3a. The data for coverage per base on the sense and antisense strands were analyzed separately using SAMtools. Differential expression of genes in each strain comparison (wt/∆prfA, wt/prfA*, and prfA*/∆prfA) were analyzed using the baySeq package for R version 2.2.0. Transcripts were considered differentially expressed if the FDR (False Discovery Rate) was ≤ 0.05, the FC (Fold Change) was ≥ 2.0 for up-regulated transcripts and ≤ 0.5 for down-regulated transcripts. Results: Our data indicate that we (i) confirmed transcription of known PrfA-dependent genes and (ii) identified a novel PrfA box and its putative ��A-dependent promoter region. Conclusions: Combined with many studies that have investigated the PrfA regulon and virulence in L. monocytogenes, we have shown tha PrfA directly regulates a small subset of genes; however, using RNA-seq and bioinformatics we were able to identify a novel PrfA-dependent gene and its putative PrfA box. This finding highlights the importance of using advanced approaches to analyze RNA-seq data, which can potentially reveal previously unidentified genes regulated under specific conditions.

2020-10-06 | GSE146507 | GEO

Characterization of the SigB-PrfA regulatory network in Listeria monocytogenes

Project description:Listeria monocytogenes SigB and PrfA are pleiotropic regulators of stress response and virulence gene expression, which have been shown to co-regulate genes in L. monocytogenes. We performed whole genome transcriptional profiling in the presence of PrfA* and active SigB, to identify the overlaps between the PrfA virulence regulon and the SigB stress response regulon. In L. monocytogenes, the PrfA* allele contributes to the activation of virulence genes to a level comparable to that of intracellular growing L. monocytogenes. Our results showed that the core PrfA regulon consists of 12 genes previously described as PrfA regulated. Furthermore, we found that the role of SigB during virulence gene regulation changes, dependent on the presence or absence of PrfA*. In the absence of PrfA*, SigB activated the transcription of virulence genes such as inlA and inlB. In the presence of PrfA*, SigB negatively influenced the transcription of genes in the PrfA core regulon. The observed effect of SigB on the transcript level of PrfA regulated genes was shown to reduce the cytotoxic effect of the PrfA* allele in HepG-2 cells. Our results indicate that the SigB-PrfA regulatory network is important for the adjustment of virulence gene transcription to ensure L. monocytogenes success as an intracellular pathogen. Keywords: comparison of gene expression of regulatory mutants

2008-10-01 | GSE11347 | GEO

Fibroblast starvation activates ECM remodeling gene transcription and putative enhancers despite inducing quiescence

Project description:Fibroblast starvation activates ECM remodeling gene transcription and putative enhancers despite inducing quiescence

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Characterization of the SigB-PrfA regulatory network in Listeria monocytogenes

2010-05-19 | E-GEOD-11347 | biostudies-arrayexpress

Regulation of Listeria monocytogenes PrfA regulon by environmental stimuli in gastrointestinal Tract

Project description:Regulation of Listeria monocytogenes PrfA regulon by environmental stimuli in gastrointestinal Tract

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Fibroblast starvation activates ECM remodeling gene transcription and putative enhancers despite inducing quiescence [chipseq]

Project description:Fibroblast starvation activates ECM remodeling gene transcription and putative enhancers despite inducing quiescence [chipseq]

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Fibroblast starvation activates ECM remodeling gene transcription and putative enhancers despite inducing quiescence [bruseq]

Project description:Fibroblast starvation activates ECM remodeling gene transcription and putative enhancers despite inducing quiescence [bruseq]

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σF regulon

Project description:The Alphaproteobacterium Caulobacter crescentus inhabits low-nutrient environments and can tolerate certain levels of heavy metal in these sites. It has been reported that C. crescentus responds to chromium exposure by altering expression of a large number of genes. In this work, we showed that the ECF sigma factor SigF is one of the regulatory proteins involved in the control of this transcriptional response. Microarray experiments from cells under dichromate stress showed that SigF controls a small regulon consisting of seven genes. Promoter analyses revealed that a conserved SigF-dependent sequence is located upstream of all but one gene of this regulon. Surprisingly, sigF itself was not found to be strongly auto-regulated under dichromate exposure. Furthermore, we showed that the second gene (CC3252) in the sigF operon acts as a negative regulator of SigF function, as overexpression of this putative membrane protein abolishes the transcriptional activation of sigF and its regulon under dichromate stress. Additionally, we found that substitution of one or both the conserved cysteines in the protein encoded by CC3252 (C131 and C181) affects the ability of this protein in maintaining expression of SigF-dependent genes at basal levels. Interestingly, we showed that the activation of SigF is not caused by reactive oxygen species generated as a consequence of dichromate exposure. Therefore, dichromate most probably may lead to conformational changes in the putative anti-sigma factor CC3252, releasing SigF to bind RNA polymerase core and drive transcription of its regulon.

2012-10-02 | GSE32406 | GEO

Fibroblast starvation activates ECM remodeling gene transcription and putative enhancers despite inducing quiescence [chipseq]

Project description:Depletion of growth factors and nutrients induces cellular quiescence, which often accompanies transcriptional silencing and chromatin compaction. Paradoxically, such depletion occurs in pathological microenvironments in which fibroblasts are activated to orchestrate tissue remodeling. The relationship between fibroblast activation and growth factor and nutrient depletion remains unclear. Here, we report that serum depletion in cell culture, a model for growth factor and nutrient depletions, extensively activates transcription in fibroblasts, despite inducing quiescence. Activated genes were enriched for extracellular matrix (ECM) structural components and proteases. The ECM-related transcription accompanied activation of putative distal enhancers, but not promoters. The activated putative enhancers were enriched for non-coding variants associated with inflammatory bowel disease (IBD) risk, suggesting an alteration in the ECM remodeling gene regulatory network in IBD. This study implicates nutrient and growth factor depletion in activating the ECM remodeling gene program in fibroblasts, challenging the prevailing view linking such depletion to transcriptional dormancy.

2025-06-01 | GSE272507 | GEO