Function of BriC peptide in the pneumococcal competence and virulence portfolio.

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State: Public
Version: author
Serval ID
serval:BIB_977A8BEECDD5
Type
Article: article from journal or magazin.
Collection
Publications
Institution
Title
Function of BriC peptide in the pneumococcal competence and virulence portfolio.
Journal
PLoS pathogens
Author(s)
Aggarwal S.D., Eutsey R., West-Roberts J., Domenech A., Xu W., Abdullah I.T., Mitchell A.P., Veening J.W., Yesilkaya H., Hiller N.L.
ISSN
1553-7374 (Electronic)
ISSN-L
1553-7366
Publication state
Published
Issued date
10/2018
Peer-reviewed
Oui
Volume
14
Number
10
Pages
e1007328
Language
english
Notes
Publication types: Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
Publication Status: epublish
Abstract
Streptococcus pneumoniae (pneumococcus) is an opportunistic pathogen that causes otitis media, sinusitis, pneumonia, meningitis and sepsis. The progression to this pathogenic lifestyle is preceded by asymptomatic colonization of the nasopharynx. This colonization is associated with biofilm formation; the competence pathway influences the structure and stability of biofilms. However, the molecules that link the competence pathway to biofilm formation are unknown. Here, we describe a new competence-induced gene, called briC, and demonstrate that its product promotes biofilm development and stimulates colonization in a murine model. We show that expression of briC is induced by the master regulator of competence, ComE. Whereas briC does not substantially influence early biofilm development on abiotic surfaces, it significantly impacts later stages of biofilm development. Specifically, briC expression leads to increases in biofilm biomass and thickness at 72h. Consistent with the role of biofilms in colonization, briC promotes nasopharyngeal colonization in the murine model. The function of BriC appears to be conserved across pneumococci, as comparative genomics reveal that briC is widespread across isolates. Surprisingly, many isolates, including strains from clinically important PMEN1 and PMEN14 lineages, which are widely associated with colonization, encode a long briC promoter. This long form captures an instance of genomic plasticity and functions as a competence-independent expression enhancer that may serve as a precocious point of entry into this otherwise competence-regulated pathway. Moreover, overexpression of briC by the long promoter fully rescues the comE-deletion induced biofilm defect in vitro, and partially in vivo. These findings indicate that BriC may bypass the influence of competence in biofilm development and that such a pathway may be active in a subset of pneumococcal lineages. In conclusion, BriC is a part of the complex molecular network that connects signaling of the competence pathway to biofilm development and colonization.
Keywords
Amino Acid Sequence, Animals, Bacterial Proteins/metabolism, Biofilms/growth & development, Chinchilla, Female, Mice, Peptide Fragments/metabolism, Pneumococcal Infections/genetics, Pneumococcal Infections/metabolism, Pneumococcal Infections/microbiology, Promoter Regions, Genetic, Sequence Homology, Streptococcus pneumoniae/genetics, Streptococcus pneumoniae/growth & development, Streptococcus pneumoniae/metabolism, Virulence
Pubmed
Web of science
Open Access
Yes
Create date
17/10/2018 10:38
Last modification date
20/08/2019 15:59
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