An unmodified heptadecapeptide pheromone induces competence for genetic transformation in Streptococcus pneumoniae.

Håvarstein, Leiv Sigve; Coomaraswamy, Gowri.; Morrison, Donald A.

doi:10.1073/pnas.92.24.11140

Cited by 650 publications

(631 citation statements)

References 35 publications

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“…The regulation of bacteriocin production in L. sake LTH673 bears striking similarities to the regulation of competence for genetic transformation in Streptococcus pneumoniae (Hå varstein et al, 1995b;1996;Pestova et al, 1996;Cheng et al, 1997). Both regulatory mechanisms involve an unmodified, basic peptide pheromone whose secretion is directed by a typical double-glycine leader peptide (Håvarstein et al, 1995b) and whose gene is co-transcribed with a two-component signal transduction system (Cheng et al, 1997).…”

Section: Discussionmentioning

confidence: 99%

Pheromone‐induced production of antimicrobial peptides in Lactobacillus

Brurberg

Nes

Eijsink

1997

Molecular Microbiology

158

176

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SummaryProduction of the bacteriocin sakacin P by Lactobacillus sake LTH673 is dependent on a secreted 19-residue peptide pheromone (IP-673). The gene encoding IP-673 (sppIP ) was identified and sequenced. SppIP was shown to be co-transcribed with genes encoding a histidine kinase (sppK ) and a response regulator (sppR ) typical for signal transduction in bacteria. Further sequencing and transcription studies have shown that IP-673 induces transcription of its own gene and of what are often considered to be all genes necessary for bacteriocin production and immunity. Studies with a reporter gene showed that the promoter in front of the sakacin P structural gene (sppA) is strictly regulated. The promoter in front of sppIP turned out to be less strictly regulated, and low basal promoter activity could be detected in uninduced cells. Bacteriocin production in Bac ¹ isolates of L. plantarum C11 could be induced by the non-cognate IP-673 only after the introduction of sppK, indicating that sppK encodes the pheromone receptor. These results show that bacteriocin production in lactobacilli is regulated using a short, strain-specific peptide pheromone. Growth conditions were shown to have considerable effects on the functionality of this regulatory mechanism.

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Section: Discussionmentioning

confidence: 99%

Pheromone‐induced production of antimicrobial peptides in Lactobacillus

Brurberg

Nes

Eijsink

1997

Molecular Microbiology

158

176

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“…2) (22). Alternatively, some linear-peptide-based QS systems actively transport the autoinducers back into the cell where the peptide signal can interact directly with a cognate regulator to alter target gene expression.…”

Section: Peptide-based Quorum Sensingmentioning

confidence: 99%

Exploiting Quorum Sensing To Confuse Bacterial Pathogens

LaSarre

Federle

2013

Microbiol Mol Biol Rev

665

556

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SUMMARY Cell-cell communication, or quorum sensing, is a widespread phenomenon in bacteria that is used to coordinate gene expression among local populations. Its use by bacterial pathogens to regulate genes that promote invasion, defense, and spread has been particularly well documented. With the ongoing emergence of antibiotic-resistant pathogens, there is a current need for development of alternative therapeutic strategies. An antivirulence approach by which quorum sensing is impeded has caught on as a viable means to manipulate bacterial processes, especially pathogenic traits that are harmful to human and animal health and agricultural productivity. The identification and development of chemical compounds and enzymes that facilitate quorum-sensing inhibition (QSI) by targeting signaling molecules, signal biogenesis, or signal detection are reviewed here. Overall, the evidence suggests that QSI therapy may be efficacious against some, but not necessarily all, bacterial pathogens, and several failures and ongoing concerns that may steer future studies in productive directions are discussed. Nevertheless, various QSI successes have rightfully perpetuated excitement surrounding new potential therapies, and this review highlights promising QSI leads in disrupting pathogenesis in both plants and animals.

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“…CSP controls the natural genetic transformation of S. pneumoniae [13], with two overlapping waves of transcription of CSP-responsive genes, “early” and “late” competence genes. Those early genes participate in competence regulation and link signals to late gene expression [23], while deletion of late genes, such as coiA, celA , and celB , abolishes transformation [15,24].…”

Section: Discussionmentioning

confidence: 99%

“…When CSP is sensed, a transient shift in the transcriptome and proteome pattern is induced, which affects competence as well as pneumococcal virulence [13,14]. This transcriptional shift arises from two overlapping transcription waves of CSP-responsive genes, i.e.…”

Section: Introductionmentioning

confidence: 99%

Competence-induced protein Ccs4 facilitates pneumococcal invasion into brain tissue and virulence in meningitis

et al. 2018

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Streptococcus pneumoniae is a major pathogen that causes pneumonia, sepsis, and meningitis. The candidate combox site 4 (ccs4) gene has been reported to be a pneumococcal competence-induced gene. Such genes are involved in development of S. pneumoniae competence and virulence, though the functions of ccs4 remain unknown. In the present study, the role of Ccs4 in the pathogenesis of pneumococcal meningitis was examined. We initially constructed a ccs4 deletion mutant and complement strains, then examined their association with and invasion into human brain microvascular endothelial cells. Wild-type and Ccs4-complemented strains exhibited significantly higher rates of association and invasion as compared to the ccs4 mutant strain. Deletion of ccs4 did not change bacterial growth activity or expression of NanA and CbpA, known brain endothelial pneumococcal adhesins. Next, mice were infected either intravenously or intranasally with pneumococcal strains. In the intranasal infection model, survival rates were comparable between wild-type strain-infected and ccs4 mutant strain-infected mice, while the ccs4 mutant strain exhibited a lower level of virulence in the intravenous infection model. In addition, at 24 hours after intravenous infection, the bacterial burden in blood was comparable between the wild-type and ccs4 mutant strain-infected mice, whereas the wild-type strain-infected mice showed a significantly higher bacterial burden in the brain. These results suggest that Ccs4 contributes to pneumococcal invasion of host brain tissues and functions as a virulence factor.

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An unmodified heptadecapeptide pheromone induces competence for genetic transformation in Streptococcus pneumoniae.

Cited by 650 publications

References 35 publications

Pheromone‐induced production of antimicrobial peptides in Lactobacillus

Pheromone‐induced production of antimicrobial peptides in Lactobacillus

Exploiting Quorum Sensing To Confuse Bacterial Pathogens

Competence-induced protein Ccs4 facilitates pneumococcal invasion into brain tissue and virulence in meningitis

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