ArticleJournal of bacteriology2007
sigmaB regulates IS256-mediated Staphylococcus aureus biofilm phenotypic variation.
Article in Journal of bacteriology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 71 citations in OpenAlex.
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- The staphylococcal exopolysaccharide PIA - Biosynthesis and role in biofilm formation, colonization, and infection.Computational and structural biotechnology journal · 2020Review
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- High abundance and expression of transposases in bacteria from the Baltic Sea.The ISME journal · 2017Article
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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 Deltasigma(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 Deltasigma(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.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.