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The pneumococcal cell envelope stress-sensing system LiaFSR is activated by murein hydrolases and lipid

Vegard Eldholm1, Beatrice Gutt, Ola Johnsborg

  • 1Department of Chemistry, Biotechnology, and Food Science, Norwegian University of Life Sciences, As, Norway.

Journal of Bacteriology
|February 2, 2010
PubMed

Insights

The Streptococcus pneumoniae LiaFSR system protects competent cells from self-lysis caused by fratricide. This system senses cell wall damage from murein hydrolases, adding a crucial self-protection layer during genetic transformation.

Area of Science:

  • Microbiology
  • Bacterial genetics
  • Cell envelope biology

Background:

  • Two-component regulatory systems like LiaSR in Firmicutes respond to cell envelope perturbations.
  • Streptococcus pneumoniae utilizes fratricide during competence for genetic transformation, involving murein hydrolases like CbpD, LytA, and LytC for target cell lysis.
  • Competent pneumococci require self-protection mechanisms against autolytic enzymes, with ComM being a known component.

Purpose of the Study:

  • To investigate the role of the LiaFSR system in Streptococcus pneumoniae's response to cell envelope stress.
  • To determine if the LiaFSR system contributes to the self-protection of competent pneumococci against fratricide-induced lysis.
  • To identify specific genes within the LiaFSR regulon involved in this protective mechanism.

Main Methods:

  • Comparative analysis of LiaFSR system activity in response to various cell envelope stressors.
  • Genetic manipulation of Streptococcus pneumoniae strains to assess the impact of LiaFSR components and regulon members on survival during fratricide.
  • Assays to measure cell lysis and survival rates in competent versus non-competent pneumococcal populations.

Main Results:

  • The Streptococcus pneumoniae LiaFSR system, in addition to responding to lipid II cycle inhibitors, is activated by cell envelope stress induced by murein hydrolases.
  • The LiaFSR system provides a secondary layer of self-protection for competent pneumococci against lysis mediated by CbpD, LytA, and LytC during fratricide.
  • Specific LiaFSR regulon members, spr0810 and PcpC (spr0351), were identified as contributing to this fratricide-induced self-lysis resistance.

Conclusions:

  • The LiaFSR system is a critical component of the self-protection strategy employed by competent Streptococcus pneumoniae.
  • This system complements the known ComM-mediated immunity, providing robust defense against autolytic enzymes during fratricide.
  • Understanding the LiaFSR system's role enhances our knowledge of bacterial competence, horizontal gene transfer, and bacterial survival mechanisms.

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