Cristin-resultat-ID: 769574
Sist endret: 2. juni 2017 13:02
NVI-rapporteringsår: 2010
Resultat
Vitenskapelig artikkel
2010

The Pneumococcal Cell Envelope Stress-Sensing System LiaFSR Is Activated by Murein Hydrolases and Lipid II-Interacting Antibiotics

Bidragsytere:
  • Vegard Eldholm
  • Beatrice Gutt
  • Ola Johnsborg
  • Reinhold Brückner
  • Patrick Maurer
  • Regine Hakenbeck
  • mfl.

Tidsskrift

Journal of Bacteriology
ISSN 0021-9193
e-ISSN 1098-5530
NVI-nivå 1

Om resultatet

Vitenskapelig artikkel
Publiseringsår: 2010
Volum: 192
Hefte: 7
Sider: 1761 - 1773

Importkilder

Isi-ID: 000275529100002

Beskrivelse Beskrivelse

Tittel

The Pneumococcal Cell Envelope Stress-Sensing System LiaFSR Is Activated by Murein Hydrolases and Lipid II-Interacting Antibiotics

Sammendrag

In the Firmicutes, two-component regulatory systems of the LiaSR type sense and orchestrate the response to various agents that perturb cell envelope functions, in particular lipid II cycle inhibitors. In the current study, we found that the corresponding system in Streptococcus pneumoniae displays similar properties but, in addition, responds to cell envelope stress elicited by murein hydrolases. During competence for genetic transformation, pneumococci attack and lyse noncompetent siblings present in the same environment. This phenomenon, termed fratricide, increases the efficiency of horizontal gene transfer in vitro and is believed to stimulate gene exchange also under natural conditions. Lysis of noncompetent target cells is mediated by the putative murein hydrolase CbpD, the key effector of the fratricide mechanism, and the autolysins LytA and LytC. To avoid succumbing to their own lysins, competent attacker cells must possess a protective mechanism rendering them immune. The most important component of this mechanism is ComM, an integral membrane protein of unknown function that is expressed only in competent cells. Here, we show that a second layer of self-protection is provided by the pneumococcal LiaFSR system, which senses the damage inflicted to the cell wall by CbpD, LytA, and LytC. Two members of the LiaFSR regulon, spr0810 and PcpC (spr0351), were shown to contribute to the LiaFSR-coordinated protection against fratricide-induced self-lysis.

Bidragsytere

Vegard Eldholm

  • Tilknyttet:
    Forfatter
    ved Realfag og teknologi ved Norges miljø- og biovitenskapelige universitet

Beatrice Gutt

  • Tilknyttet:
    Forfatter
    ved Karlsruher Institut für Technologie

Ola Johnsborg

  • Tilknyttet:
    Forfatter
    ved Kjemi, bioteknologi og matvitenskap ved Norges miljø- og biovitenskapelige universitet

Reinhold Brückner

  • Tilknyttet:
    Forfatter
    ved Technische Universität Kaiserslautern

Patrick Maurer

  • Tilknyttet:
    Forfatter
    ved Technische Universität Kaiserslautern
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