Send to

Choose Destination
PLoS Pathog. 2017 Jul 24;13(7):e1006526. doi: 10.1371/journal.ppat.1006526. eCollection 2017 Jul.

Bacterial size matters: Multiple mechanisms controlling septum cleavage and diplococcus formation are critical for the virulence of the opportunistic pathogen Enterococcus faecalis.

Author information

Krebs Institute, University of Sheffield, Sheffield, United Kingdom.
Department of Molecular Biology and Biotechnology, University of Sheffield, Sheffield, United Kingdom.
Department of Infection and Immunity and Cardiovascular Disease, University of Sheffield, Sheffield, United Kingdom.
The Bateson Centre, University of Sheffield, Sheffield, United Kingdom.
Institute of Biology, Leiden University, Leiden, The Netherlands.
INSERM, UMR 1137, Infection, Antimicrobiens Modelisation, Evolution (IAME), Université Paris Diderot, Sorbonne Paris cité, Paris, France.


Enterococcus faecalis is an opportunistic pathogen frequently isolated in clinical settings. This organism is intrinsically resistant to several clinically relevant antibiotics and can transfer resistance to other pathogens. Although E. faecalis has emerged as a major nosocomial pathogen, the mechanisms underlying the virulence of this organism remain elusive. We studied the regulation of daughter cell separation during growth and explored the impact of this process on pathogenesis. We demonstrate that the activity of the AtlA peptidoglycan hydrolase, an enzyme dedicated to septum cleavage, is controlled by several mechanisms, including glycosylation and recognition of the peptidoglycan substrate. We show that the long cell chains of E. faecalis mutants are more susceptible to phagocytosis and are no longer able to cause lethality in the zebrafish model of infection. Altogether, this work indicates that control of cell separation during division underpins the pathogenesis of E. faecalis infections and represents a novel enterococcal virulence factor. We propose that inhibition of septum cleavage during division represents an attractive therapeutic strategy to control infections.

[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Public Library of Science Icon for PubMed Central
Loading ...
Support Center