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Rørvik GH, Naemi AO, Edvardsen PKT, et al. The c-di-AMP signaling system influences stress tolerance and biofilm formation of Streptococcus mitis. Microbiologyopen. 2021;10(4):e1203doi: 10.1002/mbo3.1203.
Rørvik, G. H., Naemi, A. O., Edvardsen, P. K. T., & Simm, R. (2021). The c-di-AMP signaling system influences stress tolerance and biofilm formation of Streptococcus mitis. MicrobiologyOpen, 10(4), e1203. https://doi.org/10.1002/mbo3.1203
Rørvik, Gro Herredsvela, et al. "The c-di-AMP signaling system influences stress tolerance and biofilm formation of Streptococcus mitis." MicrobiologyOpen vol. 10,4 (2021): e1203. doi: https://doi.org/10.1002/mbo3.1203
Rørvik GH, Naemi AO, Edvardsen PKT, Simm R. The c-di-AMP signaling system influences stress tolerance and biofilm formation of Streptococcus mitis. Microbiologyopen. 2021 Aug;10(4):e1203. doi: 10.1002/mbo3.1203. PMID: 34459556; PMCID: PMC8289670.
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Microbiologyopen. 2021 Aug;10(4):e1203. doi: 10.1002/mbo3.1203.

The c-di-AMP signaling system influences stress tolerance and biofilm formation of Streptococcus mitis.

MicrobiologyOpen

Gro Herredsvela Rørvik, Ali-Oddin Naemi, Per Kristian Thorén Edvardsen, Roger Simm

Affiliations

  1. Institute of Oral Biology, University of Oslo, Oslo, Norway.

PMID: 34459556 PMCID: PMC8289670 DOI: 10.1002/mbo3.1203

Abstract

Streptococcus mitis is a commensal bacterial species of the oral cavity, with the potential for opportunistic pathogenesis. For successful colonization, S. mitis must be able to adhere to surfaces of the oral cavity and survive and adapt to frequently changing environmental conditions. Cyclic-di-AMP (c-di-AMP) is a nucleotide second messenger, involved in the regulation of stress responses and biofilm formation in several bacterial species. Cyclic-di-AMP is produced by diadenylate cyclases and degraded by phosphodiesterases. We have previously shown that in S. mitis, one diadenylate cyclase (CdaA) and at least two phosphodiesterases (Pde1 and Pde2) regulate the intracellular concentration of c-di-AMP. In this study, we utilized S. mitis deletion mutants of cdaA, pde1, and pde2 to analyze the role of c-di-AMP signaling in various stress responses, biofilm formation, and adhesion to eukaryotic cells. Here, we demonstrate that the Δpde1 mutant displayed a tendency toward increased susceptibility to acetic acid at pH 4.0. Deletion of cdaA increases auto-aggregation of S. mitis but reduces biofilm formation on an abiotic surface. These phenotypes are more pronounced under acidic extracellular conditions. Inactivation of pde1 or pde2 reduced the tolerance to ciprofloxacin, and UV radiation and the Δpde1 mutant was more susceptible to Triton X-100, indicating a role for c-di-AMP signaling in responses to DNA damage and cell membrane perturbation. Finally, the Δpde2 mutant displayed a tendency toward a reduced ability to adhere to oral keratinocytes. Taken together, our results indicate an important role for c-di-AMP signaling in cellular processes important for colonization of the mouth.

© 2021 The Authors. MicrobiologyOpen published by John Wiley & Sons Ltd.

Keywords: Streptococcus mitis ; DNA damage; acid stress; biofilm; c-di-AMP; β-lactam antibiotics

References

  1. Trends Microbiol. 2018 Mar;26(3):175-185 - PubMed
  2. Infect Immun. 2019 May 21;87(6): - PubMed
  3. Immunity. 2017 Mar 21;46(3):433-445 - PubMed
  4. FEMS Microbiol Rev. 2020 May 1;44(3):351-368 - PubMed
  5. J Bacteriol. 2018 May 24;200(12): - PubMed
  6. Front Microbiol. 2018 May 29;9:1121 - PubMed
  7. Curr Opin Microbiol. 2018 Feb;41:21-28 - PubMed
  8. PLoS Pathog. 2011 Sep;7(9):e1002217 - PubMed
  9. Mol Microbiol. 2016 Jul;101(1):12-26 - PubMed
  10. J Bacteriol. 2020 Apr 9;202(9): - PubMed
  11. J Hosp Infect. 1993 Dec;25(4):229-38 - PubMed
  12. Caries Res. 1989;23(5):315-9 - PubMed
  13. Cell Host Microbe. 2015 Jun 10;17(6):788-98 - PubMed
  14. Front Microbiol. 2018 Sep 27;9:2347 - PubMed
  15. mBio. 2018 Mar 27;9(2): - PubMed
  16. Infect Immun. 2014 May;82(5):1840-9 - PubMed
  17. EMBO Rep. 2011 Jun;12(6):594-601 - PubMed
  18. mBio. 2013 Apr 30;4(3):e00018-13 - PubMed
  19. Microbiol Res. 2014 Sep-Oct;169(9-10):749-58 - PubMed
  20. J Bacteriol. 2013 Nov;195(22):5123-32 - PubMed
  21. Environ Microbiol. 2016 Mar;18(3):904-22 - PubMed
  22. Sci Rep. 2019 Jul 22;9(1):10550 - PubMed
  23. PLoS One. 2015 Apr 17;10(4):e0124358 - PubMed
  24. Mol Microbiol. 2012 Feb;83(3):623-39 - PubMed
  25. Emerg Infect Dis. 2014 May;20(5):762-71 - PubMed
  26. J Clin Microbiol. 2005 Nov;43(11):5721-32 - PubMed
  27. PLoS Genet. 2018 Apr 16;14(4):e1007342 - PubMed
  28. Science. 2010 Jun 25;328(5986):1703-5 - PubMed
  29. FEMS Microbiol Rev. 2003 Jan;26(5):493-510 - PubMed
  30. Mol Microbiol. 2018 Sep;109(5):600-614 - PubMed
  31. Nagoya J Med Sci. 2011 Feb;73(1-2):49-57 - PubMed
  32. Environ Microbiol. 2016 Nov;18(11):3612-3619 - PubMed
  33. J Biol Chem. 2012 Feb 24;287(9):6250-65 - PubMed
  34. Antimicrob Agents Chemother. 2012 Jan;56(1):579-81 - PubMed
  35. Microorganisms. 2020 Aug 20;8(9): - PubMed
  36. mBio. 2013 May 28;4(3):e00282-13 - PubMed
  37. Clin Infect Dis. 2000 Nov;31(5):1126-30 - PubMed
  38. J Biol Chem. 2010 Jan 1;285(1):473-82 - PubMed
  39. J Bacteriol. 2020 Nov 19;202(24): - PubMed
  40. Annu Rev Microbiol. 2019 Sep 8;73:313-334 - PubMed
  41. Mol Microbiol. 2016 Mar;99(5):945-59 - PubMed
  42. Cell Host Microbe. 2016 Jul 13;20(1):49-59 - PubMed
  43. J Bacteriol. 2020 Dec 7;203(1): - PubMed
  44. J Clin Microbiol. 2003 Jul;41(7):3051-5 - PubMed
  45. J Bacteriol. 2019 Feb 25;201(6): - PubMed
  46. Case Rep Infect Dis. 2018 May 30;2018:5156085 - PubMed
  47. Antimicrob Agents Chemother. 1995 Aug;39(8):1820-3 - PubMed
  48. Proc Natl Acad Sci U S A. 2017 Jul 18;114(29):E5969-E5978 - PubMed
  49. Appl Environ Microbiol. 2012 Nov;78(21):7753-9 - PubMed
  50. DNA Repair (Amst). 2008 Mar 1;7(3):353-79 - PubMed
  51. J Biol Chem. 2016 Dec 30;291(53):26970-26986 - PubMed
  52. Appl Microbiol Biotechnol. 2020 Jan;104(1):51-65 - PubMed
  53. Case Rep Infect Dis. 2018 Oct 9;2018:2616787 - PubMed
  54. Front Microbiol. 2016 May 25;7:804 - PubMed
  55. Case Rep Infect Dis. 2017;2017:7289032 - PubMed
  56. Mol Biol Rep. 2020 Nov;47(11):9149-9157 - PubMed
  57. Nucleic Acids Res. 2019 Jun 4;47(10):5141-5154 - PubMed
  58. Jpn J Infect Dis. 2019 Jan 23;72(1):1-6 - PubMed
  59. Nat Immunol. 2012 Dec;13(12):1155-61 - PubMed
  60. PLoS One. 2013 Aug 27;8(8):e73512 - PubMed
  61. Nat Immunol. 2018 Feb;19(2):141-150 - PubMed
  62. PLoS One. 2013 Jul 15;8(7):e69425 - PubMed
  63. Mol Oral Microbiol. 2016 Aug;31(4):302-13 - PubMed
  64. Mol Cell. 2008 Apr 25;30(2):167-78 - PubMed

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