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Perturbation of manganese metabolism disrupts cell division in Streptococcus pneumoniae

Julia E Martin1, John P Lisher1,2, Malcolm E Winkler3,4

  • 1Department of Chemistry, Indiana University, Bloomington, IN, 47405-7102, USA.

Molecular Microbiology
|January 28, 2017
PubMed

Insights

Maintaining proper manganese (Mn) levels is crucial for Streptococcus pneumoniae growth. Excess Mn disrupts cell division by hyperactivating the PhpP phosphatase, highlighting the need for strict cellular control of manganese.

Area of Science:

  • Microbiology
  • Bacterial Physiology
  • Cell Biology

Background:

  • Manganese (Mn) is an essential micronutrient for bacterial function.
  • However, the mechanisms by which excess Mn impairs bacterial growth are not well understood.
  • Streptococcus pneumoniae, a major human respiratory pathogen, requires precise Mn homeostasis for survival.

Purpose of the Study:

  • To investigate the role of manganese homeostasis in Streptococcus pneumoniae growth.
  • To elucidate the mechanisms underlying manganese toxicity in this pathogen.
  • To explore the impact of manganese levels on bacterial cell division.

Main Methods:

  • Genetic manipulation of Mn homeostasis genes (psaBCA, mntE).
  • Analysis of Mn-stressed cells under aerobic and anaerobic conditions.
  • Assessment of metal accumulation (Mn, Fe, Cu) and cell morphology.
  • Investigation of protein dephosphorylation via the Mn-dependent phosphatase PhpP.

Main Results:

  • Disruption of Mn importer (psaBCA) or exporter (mntE) genes leads to Mn sensitivity.
  • Mn-stressed S. pneumoniae cells accumulate Mn, Fe, and Cu, exhibiting impaired growth.
  • Cellular elongation under Mn stress and shortening under Mn limitation (Zn addition) were observed.
  • Mn accumulation hyperactivates PhpP, causing aberrant dephosphorylation of cell division proteins.

Conclusions:

  • Proper manganese homeostasis is critical for Streptococcus pneumoniae growth and cell division.
  • Manganese toxicity, not iron-mediated Fenton chemistry, causes growth impairment.
  • Cellular Mn:Zn ratios regulate PhpP activity, controlling pneumococcal cell division.
  • Mn-metalloenzymes are susceptible to mismetallation, necessitating tight cellular Mn control.

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