A point mutation in cpsE renders Streptococcus pneumoniae nonencapsulated and enhances its growth, adherence and competence

Schaffner, Thierry Oliver; Hinds, Jason; Gould, Katherine A; Wüthrich, Daniel; Bruggmann, Rémy; Küffer, Marianne; Mühlemann, Kathrin; Hilty, Markus; Hathaway, Lucy Jane (2014). A point mutation in cpsE renders Streptococcus pneumoniae nonencapsulated and enhances its growth, adherence and competence. BMC microbiology, 14(210), p. 210. BioMed Central 10.1186/s12866-014-0210-x

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BackgroundThe polysaccharide capsule is a major virulence factor of the important human pathogen Streptococcus pneumoniae. However, S. pneumoniae strains lacking capsule do occur.ResultsHere, we report a nasopharyngeal isolate of Streptococcus pneumoniae composed of a mixture of two phenotypes; one encapsulated (serotype 18C) and the other nonencapsulated, determined by serotyping, electron microscopy and fluorescence isothiocyanate dextran exclusion assay.By whole genome sequencing, we demonstrated that the phenotypes differ by a single nucleotide base pair in capsular gene cpsE (C to G change at gene position 1135) predicted to result in amino acid change from arginine to glycine at position 379, located in the cytoplasmic, enzymatically active, region of this transmembrane protein. This SNP is responsible for loss of capsule production as the phenotype is transferred with the capsule operon. The nonencapsulated variant is superior in growth in vitro and is also 117-fold more adherent to and more invasive into Detroit 562 human epithelial cells than the encapsulated variant.Expression of six competence pathway genes and one competence-associated gene was 11 to 34-fold higher in the nonencapsulated variant than the encapsulated and transformation frequency was 3.7-fold greater.ConclusionsWe identified a new single point mutation in capsule gene cpsE of a clinical S. pneumoniae serotype 18C isolate sufficient to cause loss of capsule expression resulting in the co-existence of the encapsulated and nonencapsulated phenotype. The mutation caused phenotypic changes in growth, adherence to epithelial cells and transformability. Mutation in capsule gene cpsE may be a way for S. pneumoniae to lose its capsule and increase its colonization potential.

Item Type:

Journal Article (Original Article)

Division/Institute:

04 Faculty of Medicine > Service Sector > Institute for Infectious Diseases
04 Faculty of Medicine > Pre-clinic Human Medicine > BioMedical Research (DBMR) > DCR Services > Genomics
04 Faculty of Medicine > Service Sector > Institute for Infectious Diseases > Mycobacteriology
04 Faculty of Medicine > Service Sector > Institute for Infectious Diseases > Research
04 Faculty of Medicine > Department of Haematology, Oncology, Infectious Diseases, Laboratory Medicine and Hospital Pharmacy (DOLS) > Clinic of Infectiology

Graduate School:

Graduate School for Cellular and Biomedical Sciences (GCB)

UniBE Contributor:

Schaffner, Thierry Oliver; Wüthrich, Daniel; Bruggmann, Rémy; Küffer, Marianne; Mühlemann, Kathrin; Hilty, Markus and Hathaway, Lucy Jane

Subjects:

500 Science > 570 Life sciences; biology
600 Technology > 610 Medicine & health

ISSN:

1471-2180

Publisher:

BioMed Central

Language:

English

Submitter:

Annelies Luginbühl

Date Deposited:

28 Nov 2014 16:38

Last Modified:

12 Jan 2017 16:55

Publisher DOI:

10.1186/s12866-014-0210-x

PubMed ID:

25163487

Additional Information:

Hilty and Hathaway contributed equally to this work. Co-senior authorship.

BORIS DOI:

10.7892/boris.58378

URI:

https://boris.unibe.ch/id/eprint/58378

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