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Yersinia pestis CO92

ABSTRACT: Functional and structural analysis of a highly-expressed Yersinia pestis small RNA upon host cell infection

PROVIDER: PRJNA294782 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR2341560_1.fastq.gz	Fastqsanger.gz
	SRR2341560_2.fastq.gz	Fastqsanger.gz
	SRR2341531_1.fastq.gz	Fastqsanger.gz
	SRR2341531_2.fastq.gz	Fastqsanger.gz
	SRR2341532_1.fastq.gz	Fastqsanger.gz

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Yersinia pestis CO92

Project description:Yersinia pestis CO92 Genome sequencing

| PRJNA235224 | ENA

Gene expression profiles of wild-type Yersinia pestis CO92 and its Braun lipoprotein mutant at flea and human temp

Project description:Braun/murein lipoprotein (Lpp) is one of the major outer membrane components of gram-negative bacteria belonging to the enterobacteriaceae family that that is involved in inflammatory responses and septic shock. We previously characterized a delta-lpp isogenic mutant of Yersinia pestis CO92 and found that this mutant was defective in surviving in macrophages and was attenuated in a mouse inhalation model of plague when compared to the highly virulent wild-type (WT) bacterium. To better understand how deletion of the lpp gene might affect Yersinia virulence, we performed global transcriptional profiling of the genes in the WT Y. pestis CO92 and its delta-lpp mutant by using microarrays. The organisms were cultured at both 26 and 37 degrees Celsius to simulate the flea vector and mammalian host environments, respectively. Our data revealed vastly different effects of lpp mutation on the transcriptomes of Y. pestis grown at 37 versus 26°C. While the absence of Lpp resulted mainly in the down-regulation of metabolic genes at 26°C, the Y. pestis CO92 lpp mutant cultured at 37°C exhibited profound alterations in stress response and virulence genes, compared to the WT bacterium. We further investigated one of the stress-related genes (htrA) down-regulated in the lpp mutant relative to WT Y. pestis, as HtrA was previously shown to be important for intracellular survival of Y. enterocolitica in macrophages. Indeed, complementation of the delta-lpp mutant with the htrA gene in trans restored intracellular survival of the Y. pestis lpp mutant. Our results support a role for Lpp in Y. pestis CO92 adapatation to the host environment, possibly via transcriptional activation of htrA.

2010-06-04 | GSE19840 | GEO

Transcriptional analysis of quorum sensing deficient in Yersinia pestis CO92 at 37°C

Project description:Yersinia pestis, the etiological agent of plague, is able to sense cell density by quorum sensing. The function of quorum sensing in Y. pestis is not clear. Here, the process of quorum sensing was investigated by comparing transcript profiles when three quorum-sensing synthase genes are knocked out. Two strains, ∆pgm (pigmentation-negative) mutant R88 as treatment and quorum sensing null strain R115 with mutations (∆pgm, ∆ypeIR, ∆yspIR, and ∆luxS) as control, are used in this analysis.

2013-09-05 | GSE21911 | GEO

Transcriptional analysis of luxS-null strain in Yersinia pestis CO92 at 37°C

Project description:Yersinia pestis, the etiological agent of plague, is able to sense cell density by quorum sensing. The function of quorum sensing in Y. pestis is not clear. Here, the process of autoinducer 2 (AI-2) quorum sensing was investigated by comparing transcript profiles when luxS gene was knocked out. The luxS gene encodes S-ribosylhomocysteinase which can produce DPD, a precursor of AI-2. The strain ∆pgm (pigmentation-negative) mutant R88 was called wild type. The ∆pgm ∆luxS mutant was called control.

2013-09-05 | GSE22849 | GEO

Transcriptional analysis of temperature regulation in Yersinia pestis

Project description:Temperature is a key environmental factor for facultative pathogens during the host adaptation response. To assess the functional role of temperature in Yersinia pestis, a microarray study was conducted comparing the Δpgm (pigmentation-negative) R88 strain grown at 37°C or 30°C.

2016-01-01 | GSE30333 | GEO

Transcription analysis of AI-2 signal add in experiment in Yersinia pestis CO92 at 37°C

Project description:Yersinia pestis, the etiological agent of plague, is able to sense cell density by quorum sensing. The function of quorum sensing in Y. pestis is not clear. Here, the process of autoinducer-2 (AI-2) quorum sensing was investigated by comparing transcript profiles when AI-2 quorum-sensing signal is added in. The strain ∆pgm(pigmentation-negative) mutant R88 was used as wild type. The control consisted of cells grown and treated under the same conditions without added signals.

2013-09-05 | GSE22848 | GEO

Transcriptional analysis of quorum sensing null strain in Yersinia pestis CO92 at 30°C

Project description:Yersinia pestis is the etiology of plague that is able to sense cell density by quorum sensing. The function of quorum sensing in Y.pestis is not clear. Here, the process of quorum sensing was investigated by comparing transcript profiles when three quorum sensing synthase genes are knocked out. Two strains, ∆pgm (pigmentation-negative) mutant R88 as treatment and 3XQS mutant with mutation (∆pgm, ∆ypeIR, ∆yspIR, and ∆luxS) R115 as control are used in this analysis.

2016-01-01 | GSE20217 | GEO

Yersinia pestis CO92

Project description:Gene expression profiles of wild-type Yersinia pestis CO92 and its Braun lipoprotein mutant at flea and human temp

| PRJNA122061 | ENA

Yersinia pestis strain:CO92(pCD1-)

Project description:Yersinia pestis strain:CO92(pCD1-) Transcriptome or Gene expression

| PRJNA384395 | ENA

CRISPR-Cas9 mutagenesis of U937 cells for variants resistant to Yersinia pestis intoxication

Project description:The plague agent, Yersinia pestis, employs a type III secretion system (T3SS) to selectively destroy human immune cells, thereby enabling its replication in the bloodstream and transmission to new hosts via fleabite. The host factors responsible for the selective destruction of immune cells by plague bacteria were not known. Here we show that LcrV, the needle cap protein of the Y. pestis T3SS, binds N-formylpeptide receptor (FPR1) on human immune cells to promote the translocation of bacterial effectors.

2019-07-04 | GSE133826 | GEO

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