Transcriptional Regulation and Mechanism of SigN (ZpdN), a pBS32 encoded Sigma Factor
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ABSTRACT:
PROVIDER: PRJNA555096 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR9699330.fastq.gz | Fastqsanger.gz | |||
| SRR9699331.fastq.gz | Fastqsanger.gz | |||
| SRR9699332.fastq.gz | Fastqsanger.gz | |||
| SRR9699333.fastq.gz | Fastqsanger.gz |
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Similar Datasets
Project description:Laboratory strains of Bacillus subtilis encodes as many as 16 alternative sigma factors, each dedicated to expressing a unique regulon such as those involved in stress resistance, sporulation, and motility. The ancestral strain of B. subtilis also encodes an additional sigma factor homolog, ZpdN, not found in lab strains due to it being encoded on the large, low copy number plasmid pBS32 that was lost during domestication. DNA damage triggers pBS32 hyper-replication and cell death in a manner that depends on ZpdN but how ZpdN mediates these effects was unknown. Here we show that ZpdN is a bona fide sigma factor that can direct RNA polymerase to transcribe ZpdN-dependent genes and we rename ZpdN to SigN accordingly. Rend-seq analysis was used to determine the SigN regulon on pBS32, and the 5’ ends of transcripts were used to predict the SigN consensus sequence. Finally, we characterize the regulation of SigN itself, and show that it is transcribed by at least three promoters: PsigN1, a strong SigA-dependent LexA-repressed promoter, PsigN2, a weak SigA-dependent constitutive promoter, and PsigN3, a SigN-dependent promoter. Thus, in response to DNA damage LexA is derepressed, SigN is expressed and then experiences positive feedback. How cells die in a pBS32-dependent manner remains unknown, but we predict that death is the product of expressing one or more genes in the SigN regulon.
2019-08-22 | GSE134424 | GEO
Project description:Phage-encoded sigma factors alter bacterial dormancy
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Project description:By entering a reversible state of reduced metabolic activity, dormant microorganisms are able to contend with suboptimal conditions that would otherwise reduce their fitness. In addition, certain types of dormancy like sporulation, can serve as a refuge from parasitic infections. Phages are unable to attach to spores, but their genomes can be entrapped in the resting structures and are able to resume infection upon host germination. Thus, dormancy has the potential to affect both the reproductive and survival components of phage fitness. Here, we characterized the distribution and diversity of sigma factors in nearly 3,500 phage genomes. Homologs of bacterial sigma factors that are responsible for directing transcription during sporulation were preferentially recovered in phages that infect spore-forming hosts. While non-essential for lytic infection, when expressed in Bacillus subtilis, we demonstrate that phage-encoded sigma factors activated sporulation gene networks and reduced spore yield. Our findings suggest that the acquisition of host-like transcriptional regulators may allow phages to manipulate the expression of complex traits, like the transitions involved in bacterial dormancy.
2021-11-05 | GSE187004 | GEO
Project description:Predictive design of sigma factor-specific promoters
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Project description:Laboratory strains of Bacillus subtilis encode many alternative sigma factors, each dedicated to expressing a unique regulon such as those involved in stress resistance, sporulation, and motility. The ancestral strain of B. subtilis also encodes an additional sigma factor homolog, ZpdN, not found in lab strains due to being encoded on the large, low-copy-number plasmid pBS32, which was lost during domestication. DNA damage triggers pBS32 hyperreplication and cell death in a manner that depends on ZpdN, but how ZpdN mediates these effects is unknown. Here, we show that ZpdN is a bona fide sigma factor that can direct RNA polymerase to transcribe ZpdN-dependent genes, and we rename ZpdN SigN accordingly. Rend-seq (end-enriched transcriptome sequencing) analysis was used to determine the SigN regulon on pBS32, and the 5' ends of transcripts were used to predict the SigN consensus sequence. Finally, we characterize the regulation of SigN itself and show that it is transcribed by at least three promoters: PsigN1 , a strong SigA-dependent LexA-repressed promoter; PsigN2 , a weak SigA-dependent constitutive promoter; and PsigN3 , a SigN-dependent promoter. Thus, in response to DNA damage SigN is derepressed and then experiences positive feedback. How cells die in a pBS32-dependent manner remains unknown, but we predict that death is the product of expressing one or more genes in the SigN regulon.IMPORTANCE Sigma factors are utilized by bacteria to control and regulate gene expression. Some sigma factors are activated during times of stress to ensure the survival of the bacterium. Here, we report the presence of a sigma factor that is encoded on a plasmid that leads to cellular death after DNA damage.
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Project description:The sigma factor FliA (σ28) has been described to activate the expression of several chemoreceptor-encoding genes and the late flagellar genes in Pseudomonas putida, enabling synthesis of the filament, an stator complex and completion of the flagella-associated chemotaxis machinery. The activity of FliA is repressed in the cytoplasm by the anti-sigma factor FlgM upon completion of the flagellar hook. In this study we aim to identify genome-wide targets of regulation by FliA in P. putida KT2442 (a spontaneous rifampicin-resistant mutant of the reference strain KT2440) by performing RNA-seq experiments using a fliA deletion mutant and a constitutively active strain that combines the deletion of flgM with ectopic production of FliA.
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Project description:Sigma factors are master regulators of bacterial transcription which direct gene expression of specific subsets of genes. In particular, alternative sigma factors are well-known to be key players of bacterial adaptation to changing environments. To elucidate the regulatory network of sigma factors in P. aeruginosa, an integrative approach including sigma factor-dependent mRNA profiling was performed to define the primary regulon of each sigma factor.
2015-02-12 | GSE54998 | GEO
Project description:Mycobacterium tuberculosis (Mtb) is well adapted to survive in macrophages and usually subverts the bactericidal mechanisms of these professional phagocytes. The adaptation of Mtb to the intracellular life depends on its ability to regulate the expression of its genes. Among the most important bacterial transcription activators are the sigma factors that bind to the RNA polymerase and give it promotor specificity. Sigma factor E (SigE) controls the expression of genes that are essential for Mtb virulence. Analysis of the macrophage transcriptional response indicated that proteins encoded by the sigE regulon are involved in the modulation of the macrophage inflammatory response. Keywords: Comparison of responses to infections
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