Contribution of phosphoglucosamine mutase to determination of bacterial cell morphology in Streptococcus gordonii

Kisaki Shimazu1, Yukihiro Takahashi, Hiroyuki Karibe

  • 1Department of Pediatric Dentistry, The Nippon Dental University School of Life Dentistry at Tokyo, 1-9-20 Fujimi, Chiyoda-ku, Tokyo, 102-8159, Japan. kisaki-s@tky.ndu.ac.jp

Odontology
|May 14, 2011
PubMed

Insights

Mutations in the phosphoglucosamine mutase (GlmM) gene of Streptococcus gordonii significantly alter bacterial cell morphology, causing chain elongation and cell enlargement. These changes occur independently of the carbon source utilized by the bacteria.

Area of Science:

  • Microbiology
  • Molecular Biology
  • Biochemistry

Background:

  • Phosphoglucosamine mutase (GlmM) is crucial for peptidoglycan precursor synthesis.
  • Streptococcus gordonii is an oral bacterium linked to infective endocarditis.
  • Previous studies indicated glmM mutations affect S. gordonii growth, morphology, and penicillin sensitivity.

Purpose of the Study:

  • To investigate the impact of glmM mutations on Streptococcus gordonii morphology and cell growth.
  • To determine if carbon source influences the morphological effects of glmM mutations.

Main Methods:

  • Genetic manipulation to create a glmM mutant in S. gordonii.
  • Cultivation of wild-type and mutant strains with various sugars (glucose, fructose, lactose, sucrose).
  • Microscopic analysis of bacterial cell morphology and chain formation.

Main Results:

  • The glmM mutation caused significant morphological changes, including cell elongation and enlarged cells.
  • Defects in cell separation and distorted cell surfaces were observed in the mutant.
  • These morphological alterations were consistent across different tested carbon sources.

Conclusions:

  • The glmM gene plays a vital role in regulating Streptococcus gordonii cell shape and division.
  • The observed morphological defects are independent of the bacterial carbon source.
  • Understanding GlmM function is important for targeting S. gordonii pathogenesis.

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