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A random six-phase switch regulates pneumococcal virulence via global epigenetic changes.

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Streptococcus pneumoniae uses genetic rearrangements in its SpnD39III system to switch between forms that cause disease or asymptomatic carriage. This phase variation impacts gene expression and virulence, revealing a key epigenetic mechanism in this major bacterial pathogen.

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Area of Science:

  • Microbiology
  • Bacterial Pathogenesis
  • Epigenetics

Background:

  • Streptococcus pneumoniae is a leading cause of bacterial morbidity and mortality worldwide.
  • Phenotypic switching ('phase variation') in pneumococci, influencing carriage and disease, was observed in 1933.
  • The molecular basis for this critical phase variation remained largely unknown.

Purpose of the Study:

  • To elucidate the genetic mechanism underlying Streptococcus pneumoniae phase variation.
  • To investigate the role of Type I restriction-modification systems in pneumococcal adaptation.
  • To characterize the functional consequences of identified genetic rearrangements.

Main Methods:

  • Single-molecule, real-time (SMRT) methylomics to define methylation patterns.
  • Analysis of genetic rearrangements within the SpnD39III Type I restriction-modification system.
  • Assessment of gene expression profiles for different SpnD39III variants.
  • Experimental infection models and in vivo selection to evaluate virulence and switching.

Main Results:

  • Genetic rearrangements in the SpnD39III system were identified as the mechanism for phase variation.
  • Six distinct SpnD39III specificities with unique methylation patterns were generated.
  • SpnD39III variants exhibited differential gene expression and distinct virulence phenotypes.
  • In vivo selection demonstrated switching between SpnD39III variants during infection.

Conclusions:

  • SpnD39III phase variation is a crucial epigenetic regulatory mechanism in Streptococcus pneumoniae.
  • This switching influences pneumococcal virulence and adaptation, impacting disease dynamics.
  • The ubiquitous nature of SpnD39III suggests a fundamental role in pneumococcal biology.
  • Similar systems in other bacteria highlight potential for broad epigenetic regulation strategies.