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Rap phosphatase of virulence plasmid pXO1 inhibits Bacillus anthracis sporulation

Cristina Bongiorni1, Ricarda Stoessel, Dorinda Shoemaker

  • 1Division of Cellular Biology, Mail Code: MEM-116, Department of Molecular and Experimental Medicine, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037. mperego@scripps.edu.

Journal of Bacteriology
|December 31, 2005
PubMed

Insights

Bacillus anthracis sporulation is regulated by a plasmid-borne Rap-Phr system. This system controls the initiation of sporulation, impacting bacterial virulence and survival.

Area of Science:

  • Microbiology
  • Bacterial Pathogenesis
  • Molecular Biology

Background:

  • Bacillus anthracis is a Gram-positive bacterium responsible for anthrax.
  • Sporulation is a critical developmental pathway in B. anthracis, enabling survival in harsh environments.
  • The pXO1 plasmid is a key virulence factor in B. anthracis.

Purpose of the Study:

  • To investigate the role of the Rap-Phr system on the pXO1 plasmid in regulating B. anthracis sporulation.
  • To elucidate the mechanism by which the Rap-Phr system controls sporulation initiation.

Main Methods:

  • Biochemical assays to determine Rap protein activity.
  • Genetic manipulation (overexpression and deletion) of Rap-Phr system components.
  • Analysis of sporulation initiation in wild-type and mutant strains.

Main Results:

  • The pXO1 plasmid carries a Rap-Phr system (BXA0205) that regulates sporulation initiation.
  • The BXA0205Rap protein dephosphorylates the Spo0F response regulator, a key component of the phosphorelay.
  • Phr pentapeptide inhibits Rap activity; its absence or Rap overexpression severely inhibits sporulation.
  • Additional Rap-Phr systems on the chromosome also influence sporulation.

Conclusions:

  • The plasmid-borne Rap-Phr system is essential for proper sporulation initiation in B. anthracis.
  • This regulatory system likely contributes to the virulence and survival advantage of B. anthracis.
  • Rap-Phr systems represent a conserved regulatory mechanism in B. anthracis.

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