Please use this identifier to cite or link to this item: http://hdl.handle.net/2381/43242
Title: Function of BriC peptide in the pneumococcal competence and virulence portfolio.
Authors: Aggarwal, SD
Eutsey, R
West-Roberts, J
Domenech, A
Xu, W
Abdullah, IT
Mitchell, AP
Veening, J-W
Yesilkaya, H
Hiller, NL
First Published: 11-Oct-2018
Publisher: Public Library of Science
Citation: PLoS Pathogens, 2018, 14 (10), pp. e1007328-?
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.
DOI Link: 10.1371/journal.ppat.1007328
eISSN: 1553-7374
Links: https://journals.plos.org/plospathogens/article?id=10.1371/journal.ppat.1007328
http://hdl.handle.net/2381/43242
Version: Publisher Version
Status: Peer-reviewed
Type: Journal Article
Rights: Copyright © the authors, 2018. This is an open-access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Appears in Collections:Published Articles, Dept. of Infection, Immunity and Inflammation

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BriCFigures.pdfPost-review (final submitted author manuscript)9.34 MBAdobe PDFView/Open
BriCSupplementaryTables.xlsxPost-review (final submitted author manuscript)61.5 kBUnknownView/Open
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journal.ppat.1007328.pdfPublished (publisher PDF)7.32 MBAdobe PDFView/Open


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