Norspermidine Is Not a Self-Produced Trigger for Biofilm Disassembly

Formation of Bacillus subtilis biofilms, consisting of cells encapsulated within an extracellular matrix of exopolysaccharide and protein, requires the polyamine spermidine. A recent study reported that (1) related polyamine norspermidine is synthesized by B. subtilis using the equivalent of the Vib...

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Published inCell Vol. 156; no. 4; pp. 844 - 854
Main Authors Hobley, Laura, Kim, Sok Ho, Maezato, Yukari, Wyllie, Susan, Fairlamb, Alan H., Stanley-Wall, Nicola R., Michael, Anthony J.
Format Journal Article
LanguageEnglish
Published United States Elsevier Inc 13.02.2014
Cell Press
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Abstract Formation of Bacillus subtilis biofilms, consisting of cells encapsulated within an extracellular matrix of exopolysaccharide and protein, requires the polyamine spermidine. A recent study reported that (1) related polyamine norspermidine is synthesized by B. subtilis using the equivalent of the Vibrio cholerae biosynthetic pathway, (2) exogenous norspermidine at 25 μM prevents B. subtilis biofilm formation, (3) endogenous norspermidine is present in biofilms at 50–80 μM, and (4) norspermidine prevents biofilm formation by condensing biofilm exopolysaccharide. In contrast, we find that, at concentrations up to 200 μM, exogenous norspermidine promotes biofilm formation. We find that norspermidine is absent in wild-type B. subtilis biofilms at all stages, and higher concentrations of exogenous norspermidine eventually inhibit planktonic growth and biofilm formation in an exopolysaccharide-independent manner. Moreover, orthologs of the V. cholerae norspermidine biosynthetic pathway are absent from B. subtilis, confirming that norspermidine is not physiologically relevant to biofilm function in this species. [Display omitted] •Norspermidine is not found or synthesized in Bacillus subtilis biofilms•Exogenous norspermidine inhibits growth of wild-type cells•Exogenous norspermidine inhibits growth of exopolysaccharide-deficient cells•Lower levels of exogenous norspermidine promote biofilm formation It has been reported that norspermidine is synthesized by the bacterium Bacillus subtilis and inhibits biofilm formation by condensing exopolysaccharide. Now it is shown that norspermidine is not synthesized by B. subtilis, and high levels of exogenous norspermidine inhibit cell growth in an exopolysaccharide-independent manner.
AbstractList Summary Formation of Bacillus subtilis biofilms, consisting of cells encapsulated within an extracellular matrix of exopolysaccharide and protein, requires the polyamine spermidine. A recent study reported that (1) related polyamine norspermidine is synthesized by B. subtilis using the equivalent of the Vibrio cholerae biosynthetic pathway, (2) exogenous norspermidine at 25 mu M prevents B. subtilis biofilm formation, (3) endogenous norspermidine is present in biofilms at 50-80 mu M, and (4) norspermidine prevents biofilm formation by condensing biofilm exopolysaccharide. In contrast, we find that, at concentrations up to 200 mu M, exogenous norspermidine promotes biofilm formation. We find that norspermidine is absent in wild-type B. subtilis biofilms at all stages, and higher concentrations of exogenous norspermidine eventually inhibit planktonic growth and biofilm formation in an exopolysaccharide-independent manner. Moreover, orthologs of the V. cholerae norspermidine biosynthetic pathway are absent from B. subtilis, confirming that norspermidine is not physiologically relevant to biofilm function in this species.
Formation of Bacillus subtilis biofilms, consisting of cells encapsulated within an extracellular matrix of exopolysaccharide and protein, requires the polyamine spermidine. A recent study reported that (1) related polyamine norspermidine is synthesized by B. subtilis using the equivalent of the Vibrio cholerae biosynthetic pathway, (2) exogenous norspermidine at 25 μM prevents B. subtilis biofilm formation, (3) endogenous norspermidine is present in biofilms at 50-80 μM, and (4) norspermidine prevents biofilm formation by condensing biofilm exopolysaccharide. In contrast, we find that, at concentrations up to 200 μM, exogenous norspermidine promotes biofilm formation. We find that norspermidine is absent in wild-type B. subtilis biofilms at all stages, and higher concentrations of exogenous norspermidine eventually inhibit planktonic growth and biofilm formation in an exopolysaccharide-independent manner. Moreover, orthologs of the V. cholerae norspermidine biosynthetic pathway are absent from B. subtilis, confirming that norspermidine is not physiologically relevant to biofilm function in this species.
Formation of Bacillus subtilis biofilms, consisting of cells encapsulated within an extracellular matrix of exopolysaccharide and protein, requires the polyamine spermidine. A recent study reported that (1) related polyamine norspermidine is synthesized by B. subtilis using the equivalent of the Vibrio cholerae biosynthetic pathway, (2) exogenous norspermidine at 25 μM prevents B. subtilis biofilm formation, (3) endogenous norspermidine is present in biofilms at 50–80 μM, and (4) norspermidine prevents biofilm formation by condensing biofilm exopolysaccharide. In contrast, we find that, at concentrations up to 200 μM, exogenous norspermidine promotes biofilm formation. We find that norspermidine is absent in wild-type B. subtilis biofilms at all stages, and higher concentrations of exogenous norspermidine eventually inhibit planktonic growth and biofilm formation in an exopolysaccharide-independent manner. Moreover, orthologs of the V. cholerae norspermidine biosynthetic pathway are absent from B. subtilis, confirming that norspermidine is not physiologically relevant to biofilm function in this species. [Display omitted] •Norspermidine is not found or synthesized in Bacillus subtilis biofilms•Exogenous norspermidine inhibits growth of wild-type cells•Exogenous norspermidine inhibits growth of exopolysaccharide-deficient cells•Lower levels of exogenous norspermidine promote biofilm formation It has been reported that norspermidine is synthesized by the bacterium Bacillus subtilis and inhibits biofilm formation by condensing exopolysaccharide. Now it is shown that norspermidine is not synthesized by B. subtilis, and high levels of exogenous norspermidine inhibit cell growth in an exopolysaccharide-independent manner.
Formation of Bacillus subtilis biofilms, consisting of cells encapsulated within an extracellular matrix of exopolysaccharide and protein, requires the polyamine spermidine. A recent study reported that (1) related polyamine norspermidine is synthesized by B. subtilis using the equivalent of the Vibrio cholerae biosynthetic pathway, (2) exogenous norspermidine at 25 μM prevents B. subtilis biofilm formation, (3) endogenous norspermidine is present in biofilms at 50–80 μM, and (4) norspermidine prevents biofilm formation by condensing biofilm exopolysaccharide. In contrast, we find that, at concentrations up to 200 μM, exogenous norspermidine promotes biofilm formation. We find that norspermidine is absent in wild-type B. subtilis biofilms at all stages, and higher concentrations of exogenous norspermidine eventually inhibit planktonic growth and biofilm formation in an exopolysaccharide-independent manner. Moreover, orthologs of the V. cholerae norspermidine biosynthetic pathway are absent from B. subtilis , confirming that norspermidine is not physiologically relevant to biofilm function in this species. • Norspermidine is not found or synthesized in Bacillus subtilis biofilms • Exogenous norspermidine inhibits growth of wild-type cells • Exogenous norspermidine inhibits growth of exopolysaccharide-deficient cells • Lower levels of exogenous norspermidine promote biofilm formation It has been reported that norspermidine is synthesized by the bacterium Bacillus subtilis and inhibits biofilm formation by condensing exopolysaccharide. Now it is shown that norspermidine is not synthesized by B . subtilis , and high levels of exogenous norspermidine inhibit cell growth in an exopolysaccharide-independent manner.
Formation of Bacillus subtilis biofilms, consisting of cells encapsulated within an extracellular matrix of exopolysaccharide and protein, requires the polyamine spermidine. A recent study reported that (1) related polyamine norspermidine is synthesized by B. subtilis using the equivalent of the Vibrio cholerae biosynthetic pathway, (2) exogenous norspermidine at 25 μM prevents B. subtilis biofilm formation, (3) endogenous norspermidine is present in biofilms at 50-80 μM, and (4) norspermidine prevents biofilm formation by condensing biofilm exopolysaccharide. In contrast, we find that, at concentrations up to 200 μM, exogenous norspermidine promotes biofilm formation. We find that norspermidine is absent in wild-type B. subtilis biofilms at all stages, and higher concentrations of exogenous norspermidine eventually inhibit planktonic growth and biofilm formation in an exopolysaccharide-independent manner. Moreover, orthologs of the V. cholerae norspermidine biosynthetic pathway are absent from B. subtilis, confirming that norspermidine is not physiologically relevant to biofilm function in this species.Formation of Bacillus subtilis biofilms, consisting of cells encapsulated within an extracellular matrix of exopolysaccharide and protein, requires the polyamine spermidine. A recent study reported that (1) related polyamine norspermidine is synthesized by B. subtilis using the equivalent of the Vibrio cholerae biosynthetic pathway, (2) exogenous norspermidine at 25 μM prevents B. subtilis biofilm formation, (3) endogenous norspermidine is present in biofilms at 50-80 μM, and (4) norspermidine prevents biofilm formation by condensing biofilm exopolysaccharide. In contrast, we find that, at concentrations up to 200 μM, exogenous norspermidine promotes biofilm formation. We find that norspermidine is absent in wild-type B. subtilis biofilms at all stages, and higher concentrations of exogenous norspermidine eventually inhibit planktonic growth and biofilm formation in an exopolysaccharide-independent manner. Moreover, orthologs of the V. cholerae norspermidine biosynthetic pathway are absent from B. subtilis, confirming that norspermidine is not physiologically relevant to biofilm function in this species.
Author Kim, Sok Ho
Stanley-Wall, Nicola R.
Hobley, Laura
Michael, Anthony J.
Maezato, Yukari
Fairlamb, Alan H.
Wyllie, Susan
AuthorAffiliation 3 Division of Biological Chemistry and Drug Discovery, College of Life Sciences, University of Dundee, Dundee DD15EH, UK
2 Department of Pharmacology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA
1 Division of Molecular Microbiology, College of Life Sciences, University of Dundee, Dundee DD15EH, UK
AuthorAffiliation_xml – name: 1 Division of Molecular Microbiology, College of Life Sciences, University of Dundee, Dundee DD15EH, UK
– name: 2 Department of Pharmacology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA
– name: 3 Division of Biological Chemistry and Drug Discovery, College of Life Sciences, University of Dundee, Dundee DD15EH, UK
Author_xml – sequence: 1
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  surname: Hobley
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Snippet Formation of Bacillus subtilis biofilms, consisting of cells encapsulated within an extracellular matrix of exopolysaccharide and protein, requires the...
Summary Formation of Bacillus subtilis biofilms, consisting of cells encapsulated within an extracellular matrix of exopolysaccharide and protein, requires the...
Formation of Bacillus subtilis biofilms, consisting of cells encapsulated within an extracellular matrix of exopolysaccharide and protein, requires the...
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SubjectTerms Amino Acid Sequence
Bacillus subtilis
Bacillus subtilis - growth & development
Bacillus subtilis - physiology
Biofilms - growth & development
gamma-Aminobutyric Acid - metabolism
Matters Arising
Molecular Sequence Data
Plankton - growth & development
Sequence Alignment
Spermidine - analogs & derivatives
Spermidine - biosynthesis
Spermidine - metabolism
Spermidine - physiology
Vibrio cholerae
Vibrio cholerae - physiology
Title Norspermidine Is Not a Self-Produced Trigger for Biofilm Disassembly
URI https://dx.doi.org/10.1016/j.cell.2014.01.012
https://www.ncbi.nlm.nih.gov/pubmed/24529384
https://www.proquest.com/docview/1499157735
https://search.proquest.com/docview/1773822837
https://pubmed.ncbi.nlm.nih.gov/PMC3969229
Volume 156
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