ArticleJournal of bacteriology2015
The RapP-PhrP quorum-sensing system of Bacillus subtilis strain NCIB3610 affects biofilm formation through multiple targets, due to an atypical signal-insensitive allele of RapP.
Article in Journal of bacteriology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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44 citing papers in PubMed, 95 citations in OpenAlex.
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- Plasmid-encoded phosphatase RapP enhances cell growth in non-domesticated Bacillus subtilis strains.Nature communications · 2024Article
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- Extracellular lipopeptide bacillomycin L regulates serial expression of genes for modulating multicellular behavior in Bacillus velezensis Bs916.Applied microbiology and biotechnology · 2021Article
- Deletion of Rap-Phr systems in Bacillus subtilis influences in vitro biofilm formation and plant root colonization.MicrobiologyOpen · 2021Article
- A native conjugative plasmid confers potential selective advantages to plant growth-promoting Bacillus velezensis strain GH1-13.Communications biology · 2021Article
- Pervasive prophage recombination occurs during evolution of spore-forming Bacilli.The ISME journal · 2021Article
- Impact of Rap-Phr system abundance on adaptation of Bacillus subtilis.Communications biology · 2021Article
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4 authors at 1 institution in 1 country.
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Abstract
The genome of Bacillus subtilis 168 encodes eight rap-phr quorum-sensing pairs. Rap proteins of all characterized Rap-Phr pairs inhibit the function of one or several important response regulators: ComA, Spo0F, or DegU. This inhibition is relieved upon binding of the peptide encoded by the cognate phr gene. Bacillus subtilis strain NCIB3610, the biofilm-proficient ancestor of strain 168, encodes, in addition, the rapP-phrP pair on the plasmid pBS32. RapP was shown to dephosphorylate Spo0F and to regulate biofilm formation, but unlike other Rap-Phr pairs, RapP does not interact with PhrP. In this work we extend the analysis of the RapP pathway by reexamining its transcriptional regulation, its effect on downstream targets, and its interaction with PhrP. At the transcriptional level, we show that rapP and phrP regulation is similar to that of other rap-phr pairs. We further find that RapP has an Spo0F-independent negative effect on biofilm-related genes, which is mediated by the response regulator ComA. Finally, we find that the insensitivity of RapP to PhrP is due to a substitution of a highly conserved residue in the peptide binding domain of the rapP allele of strain NCIB3610. Reversing this substitution to the consensus amino acid restores the PhrP dependence of RapP activity and eliminates the effects of the rapP-phrP locus on ComA activity and biofilm formation. Taken together, our results suggest that RapP strongly represses biofilm formation through multiple targets and that PhrP does not counteract RapP due to a rare mutation in rapP.
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