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Genetic heterogeneity of the Spy1336/R28-Spy1337 virulence axis in Streptococcus pyogenes and effect on gene

Jesus M Eraso1, Priyanka Kachroo1, Randall J Olsen1,2

  • 1Center for Molecular and Translational Human Infectious Diseases Research, Department of Pathology and Genomic Medicine, Houston Methodist Research Institute and Houston Methodist Hospital, Houston, Texas, United States of America.

Plos One
|March 28, 2020
PubMed

Insights

Genetic variations in Streptococcus pyogenes M28 strains, specifically in the Spy1336/R28 gene and its regulatory elements, significantly impact bacterial virulence and host interactions.

Area of Science:

  • Microbiology
  • Genetics
  • Infectious Diseases

Background:

  • Streptococcus pyogenes (S. pyogenes) is a major human pathogen causing millions of infections globally.
  • M28 serotype strains are frequently linked to invasive diseases, including puerperal sepsis and neonatal infections.
  • Previous research identified a one-nucleotide indel affecting S. pyogenes virulence.

Purpose of the Study:

  • To investigate the genetic variability within the homopolymeric tract and Spy1336/R28 gene in M28 S. pyogenes strains.
  • To determine how these variations influence gene expression, protein structure, and bacterial virulence in relevant models.

Main Methods:

  • Analysis of size variation in homopolymeric tracts and tandem repeats within Spy1336/R28.
  • In vitro studies on transcript levels of Spy1336/R28 and Spy1337.
  • Virulence assessment in mouse models of necrotizing myositis and nonhuman primate models.
  • RNAseq analysis of isogenic mutant strains to study global transcriptome changes.

Main Results:

  • Both homopolymeric tract and Spy1336/R28 repeat sequences are highly polymorphic in natural M28 strains.
  • Variations in the homopolymeric tract alter Spy1336/R28 and Spy1337 transcript levels and bacterial virulence.
  • Mutant strains lacking R28 or Spy1337 show significantly reduced virulence in a nonhuman primate model.

Conclusions:

  • Genetic polymorphisms in the homopolymeric tract and Spy1336/R28 gene contribute to M28 S. pyogenes virulence.
  • The R28 protein and Spy1337 regulator play crucial roles in pathogen-host interactions.
  • Further research is warranted to explore the implications of R28 and Spy1337 variation in disease pathogenesis.

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