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A Mn-sensing riboswitch activates expression of a Mn2+/Ca2+ ATPase transporter in Streptococcus

Julia E Martin1, My T Le2, Nabin Bhattarai1

  • 1Department of Biological Sciences, Idaho State University, Pocatello, ID 83209, USA.

Nucleic Acids Research
|June 6, 2019
PubMed

Insights

This study reveals a manganese riboswitch in Streptococcus pneumoniae that prevents toxicity by increasing MgtA expression during manganese stress. This manganese homeostasis mechanism acts as a failsafe to protect bacteria from excess manganese.

Area of Science:

  • Microbiology
  • Molecular Biology
  • Bacterial Pathogenesis

Background:

  • Manganese (Mn) homeostasis is crucial for bacterial virulence.
  • Streptococcus pneumoniae utilizes PsaBCA, MntE, and PsaR for Mn homeostasis.
  • Manganese homeostasis is often regulated by yybP-ykoY riboswitches in bacteria.

Purpose of the Study:

  • To characterize a yybP-ykoY riboswitch controlling the mgtA gene in Streptococcus pneumoniae.
  • To investigate the role of this riboswitch in response to manganese and calcium ions.
  • To understand the mechanism of manganese toxicity prevention in S. pneumoniae.

Main Methods:

  • Structural analysis of the mgtA riboswitch aptamer domain.
  • In vitro transcription assays to assess riboswitch activation by Ca2+ and Mn2+.
  • Measurement of mgtA mRNA and protein levels under cellular manganese stress in wild-type and mutant strains.

Main Results:

  • The mgtA riboswitch adopts a canonical yybP-ykoY structure, compacted by Ca2+ or Mn2+.
  • Mn2+ activates mgtA transcription read-through more effectively than Ca2+, despite lower binding affinity.
  • mgtA expression increases significantly under Mn stress in Mn2+-sensitive strains, indicating a protective role.

Conclusions:

  • The characterized riboswitch functions as a failsafe to prevent Mn2+ toxicity by upregulating MgtA.
  • This mechanism is essential in S. pneumoniae and Bacillus subtilis strains sensitive to Mn2+.
  • The S. pneumoniae riboswitch may also play a role in regulating Ca2+ efflux.

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