SigmaB (σB) Regulates IS256-Mediated Staphylococcus aureus Biofilm Phenotypic Variation
Biofilm formation in Staphylococcus aureus is subject to phase variation, and biofilm-negative derivatives emerge sporadically from a biofilm-positive bacterial population. To date, the only known mechanism for generating biofilm phenotypic variation in staphylococci is the reversible insertion/exci...
| Main Authors: | , , , , |
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| Format: | Artículo |
| Language: | Inglés |
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2017
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| Online Access: | http://hdl.handle.net/20.500.11939/4670 https://journals.asm.org/doi/10.1128/JB.01767-06 |
| _version_ | 1855491795390038016 |
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| author | Valle, Jaione Vergara-Irigaray, Marta Merino, Nekane Penadés, José R. Lasa, Inigo |
| author_browse | Lasa, Inigo Merino, Nekane Penadés, José R. Valle, Jaione Vergara-Irigaray, Marta |
| author_facet | Valle, Jaione Vergara-Irigaray, Marta Merino, Nekane Penadés, José R. Lasa, Inigo |
| author_sort | Valle, Jaione |
| collection | ReDivia |
| description | Biofilm formation in Staphylococcus aureus is subject to phase variation, and biofilm-negative derivatives emerge sporadically from a biofilm-positive bacterial population. To date, the only known mechanism for generating biofilm phenotypic variation in staphylococci is the reversible insertion/excision of IS256 in biofilm-essential genes. In this study, we present evidence suggesting that the absence of the sigma(B) transcription factor dramatically increases the rate of switching to the biofilm-negative phenotype in the clinical isolate S. aureus 15981, under both steady-state and flow conditions. The phenotypic switching correlates with a dramatic increase in the number of IS256 copies in the chromosomes of biofilm-negative variants, as well as with an augmented IS256 insertion frequency into the icaC and the sarA genes. IS256-mediated biofilm switching is reversible, and biofilm-positive variants could emerge from biofilm-negative sigma(B) mutants. Analysis of the chromosomal insertion frequency using a recombinant IS256 element tagged with an erythromycin marker showed an almost three-times-higher transposition frequency in a Delta sigma(B) strain. However, regulation of IS256 activity by sigma(B) appears to be indirect, since transposase transcription is not affected in the absence of sigma(B) and IS256 activity is inhibited to wild-type levels in a Delta sigma(B) strain under NaCl stress. Overall, our results identify a new role for sigma(B) as a negative regulator of insertion sequence transposition and support the idea that deregulation of IS256 activity abrogates biofilm formation capacity in S. aureus. |
| format | Artículo |
| id | ReDivia4670 |
| institution | Instituto Valenciano de Investigaciones Agrarias (IVIA) |
| language | Inglés |
| publishDate | 2017 |
| publishDateRange | 2017 |
| publishDateSort | 2017 |
| record_format | dspace |
| spelling | ReDivia46702025-04-25T14:44:08Z SigmaB (σB) Regulates IS256-Mediated Staphylococcus aureus Biofilm Phenotypic Variation Valle, Jaione Vergara-Irigaray, Marta Merino, Nekane Penadés, José R. Lasa, Inigo Biofilm formation in Staphylococcus aureus is subject to phase variation, and biofilm-negative derivatives emerge sporadically from a biofilm-positive bacterial population. To date, the only known mechanism for generating biofilm phenotypic variation in staphylococci is the reversible insertion/excision of IS256 in biofilm-essential genes. In this study, we present evidence suggesting that the absence of the sigma(B) transcription factor dramatically increases the rate of switching to the biofilm-negative phenotype in the clinical isolate S. aureus 15981, under both steady-state and flow conditions. The phenotypic switching correlates with a dramatic increase in the number of IS256 copies in the chromosomes of biofilm-negative variants, as well as with an augmented IS256 insertion frequency into the icaC and the sarA genes. IS256-mediated biofilm switching is reversible, and biofilm-positive variants could emerge from biofilm-negative sigma(B) mutants. Analysis of the chromosomal insertion frequency using a recombinant IS256 element tagged with an erythromycin marker showed an almost three-times-higher transposition frequency in a Delta sigma(B) strain. However, regulation of IS256 activity by sigma(B) appears to be indirect, since transposase transcription is not affected in the absence of sigma(B) and IS256 activity is inhibited to wild-type levels in a Delta sigma(B) strain under NaCl stress. Overall, our results identify a new role for sigma(B) as a negative regulator of insertion sequence transposition and support the idea that deregulation of IS256 activity abrogates biofilm formation capacity in S. aureus. 2017-06-01T10:10:42Z 2017-06-01T10:10:42Z 2007 APR 2007 article Valle, J., Vergara-Irigaray, M., Merino, N., Penades, J. R. & Lasa, I. (2007). σB regulates IS256-mediated Staphylococcus aureus biofilm phenotypic variation. Journal of Bacteriology, 189(7), 2886-2896. 0021-9193 http://hdl.handle.net/20.500.11939/4670 10.1128/JB.01767-06 https://journals.asm.org/doi/10.1128/JB.01767-06 en openAccess Impreso |
| spellingShingle | Valle, Jaione Vergara-Irigaray, Marta Merino, Nekane Penadés, José R. Lasa, Inigo SigmaB (σB) Regulates IS256-Mediated Staphylococcus aureus Biofilm Phenotypic Variation |
| title | SigmaB (σB) Regulates IS256-Mediated Staphylococcus aureus Biofilm Phenotypic Variation |
| title_full | SigmaB (σB) Regulates IS256-Mediated Staphylococcus aureus Biofilm Phenotypic Variation |
| title_fullStr | SigmaB (σB) Regulates IS256-Mediated Staphylococcus aureus Biofilm Phenotypic Variation |
| title_full_unstemmed | SigmaB (σB) Regulates IS256-Mediated Staphylococcus aureus Biofilm Phenotypic Variation |
| title_short | SigmaB (σB) Regulates IS256-Mediated Staphylococcus aureus Biofilm Phenotypic Variation |
| title_sort | sigmab σb regulates is256 mediated staphylococcus aureus biofilm phenotypic variation |
| url | http://hdl.handle.net/20.500.11939/4670 https://journals.asm.org/doi/10.1128/JB.01767-06 |
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