Quorum sensing regulates virulence factors in the coral pathogen Vibrio coralliilyticus.
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA974004 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR24641400_1.fastq.gz | Fastqsanger.gz | |||
| SRR24641400_2.fastq.gz | Fastqsanger.gz | |||
| SRR24641401_1.fastq.gz | Fastqsanger.gz | |||
| SRR24641401_2.fastq.gz | Fastqsanger.gz | |||
| SRR24641402_1.fastq.gz | Fastqsanger.gz |
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Project description:The bacterial pathogen Vibrio coralliilyticus infects a variety of marine organisms globally and causes early onset of disease in multiple coral species. The etiology of coral disease and relative pathogenicity of V. coralliilyticus strains is well-documented, but the mechanisms of V. coralliilyticus coral colonization, virulence factor production, and interactions with coral microbiome are understudied. Many virulence factors responsible for pathogenic behaviors are controlled through a density-dependent, bacterial communication system called quorum sensing (QS). In other Vibrio species, behaviors like bioluminescence, biofilm formation, toxin secretion, and protease production are controlled via the master quorum sensing transcriptional regulator called LuxR/HapR. Comparative genomics indicated that V. coralliilyticus genomes share high sequence identity for most of the QS signaling and regulatory components identified in other Vibrio species. Here, we characterize active components of the V. coralliilyticus QS system and identify the VcpR (LuxR/HapR homolog) regulons in two strains with distinct infection etiologies. We show that VcpR transcription is dependent on signaling by autoinducer AI-2, whereas we were unable to detect production of acyl-homoserine lactone autoinducers. The VcpR regulator controls expression of >200 genes in both the type strain BAA-450 and isolate OCN008, including two genes encoding proteases (VcpA and VcpB) known to impact coral infection. In both isolates, VcpR activates the expression of Type VI Secretion System genes from both systems 1 and 2, which results in interbacterial competition and killing of prey bacteria. We conclude that the QS system in V. coralliilyticus is active and controls expression of genes involved in relevant bacterial behaviors that may influence coral infection.
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Project description:Bacterial quorum sensing (QS) systems are characterized by the regulated biogenesis and sensing of specialized signaling molecules. Here, we describe a peptide, Qsp1, secreted by the fungal pathogen Cryptococcus neoformans. Mutants lacking Qsp1 are attenuated for infection, pulmonary accumulation, and growth within macrophages. Qsp1 promotes density-dependent cell wall integrity and resistance to extreme environments. Qsp1 is also required for a secreted aspartyl protease activity required for virulence. Further biochemical and large-scale genetic investigations reveal that cleavage of Qsp1 from the C-terminal of a pro-peptide requires a cell-associated serine protease and Qsp1 sensing requires a predicted oligopeptide importer. Strikingly, these features closely mirror the hallmarks of a peptide-based QS system found in gram-positive bacteria, despite no ancestral relationship between individual components. Our studies thus reveal a convergently evolved, peptide-based QS system required for the virulence of a fungal pathogen.
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Project description:Atypical EPEC (aEPEC) strains are part of group of pathogens capable of forming the Attaching and Effacing (A/E) lesion. This lesion is characterized by intimate adherence of bacteria to enterocytes, and microvilli destruction. The genes responsible to cause that lesion are located in a pathogenicity island called Locus of Enterocyte Effacement (LEE). Transcription of LEE genes is subjected to various levels of regulation, including quorum sensing through autoinducer 3 (AI-3) system. AI-3 is an aromatic compound with similar characteristics to the epinephrine and norepinephrine hormones. This similarity allows bacteria to use these hormones and AI-3 to perform cell – to – cell signaling processes and bacteria - host communication processes in order to modulate its virulence. AI-3, epinephrine and norepinephrine are detected by a sensor kinase named quorum sensing E.coli regulator (QseC). In order to investigate the role of QseC and epinephrine in atypical EPEC O55:H7 virulence, we constructed a QseC mutant of this strain and performed transcription and phenotypic analyses in the presence or absence of epinephrine. We have reported here, for the first time, the quorum sensing QseC regulation of virulence genes in atypical EPEC. Our results shown that QseC is a global regulator of gene expression in aEPEC and positively regulates flagellar genes, LEE and non-LEE encoded factors. We also have shown that the presence of epinephrine could be sensed by other receptor that acts as negative regulator of LEE4 and LEE5 genes.
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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.
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Project description:Atypical EPEC (aEPEC) strains are part of group of pathogens capable of forming the Attaching and Effacing (A/E) lesion. This lesion is characterized by intimate adherence of bacteria to enterocytes, and microvilli destruction. The genes responsible to cause that lesion are located in a pathogenicity island called Locus of Enterocyte Effacement (LEE). Transcription of LEE genes is subjected to various levels of regulation, including quorum sensing through autoinducer 3 (AI-3) system. AI-3 is an aromatic compound with similar characteristics to the epinephrine and norepinephrine hormones. This similarity allows bacteria to use these hormones and AI-3 to perform cell M-bM-^@M-^S to M-bM-^@M-^S cell signaling processes and bacteria - host communication processes in order to modulate its virulence. AI-3, epinephrine and norepinephrine are detected by a sensor kinase named quorum sensing E.coli regulator (QseC). In order to investigate the role of QseC and epinephrine in atypical EPEC O55:H7 virulence, we constructed a QseC mutant of this strain and performed transcription and phenotypic analyses in the presence or absence of epinephrine. We have reported here, for the first time, the quorum sensing QseC regulation of virulence genes in atypical EPEC. Our results shown that QseC is a global regulator of gene expression in aEPEC and positively regulates flagellar genes, LEE and non-LEE encoded factors. We also have shown that the presence of epinephrine could be sensed by other receptor that acts as negative regulator of LEE4 and LEE5 genes. Comparison of transcriptional regulation of enteropathogenic E. coli serotype O55:H7 wild type and the qseC mutant in the absence or presence of epinephrine signal to identify the regulated targets
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Project description:Paenibacillus polymyxa is an agriculturally important plant growth promoting rhizobacterium (PGPR). Many Paenibacillus species are known to be engaged in complex bacteria-bacteria and bacteria-host interactions, which in other bacteria were shown to necessitate quorum sensing communication, but to date no quorum sensing systems have been described in Paenibacillus. Here we show that the type strain P. polymyxa ATCC 842 encodes at least 16 peptide-based communication systems. Each of these systems comprises a pro-peptide that is secreted to the growth medium and further processed to generate a mature short peptide. Each peptide has a cognate intracellular receptor of the RRNPP family, and we show that external addition of P. polymyxa communication peptides to the medium leads to reprogramming of the transcriptional response. We found that these quorum sensing systems are conserved across hundreds of species belonging to the Paenibacillaceae family, with some species encoding more than 25 different peptide-receptor pairs, representing a record number of quorum sensing systems encoded in a single genome.
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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.
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