An evolutionarily conserved metabolite inhibits biofilm formation in Escherichia coli K-12

Methylerythritol cyclodiphosphate (MEcPP) is an intermediate in the biosynthesis of isoprenoids in plant plastids and in bacteria, and acts as a stress signal in plants. Here, we show that MEcPP regulates biofilm formation in Escherichia coli K-12 MG1655. Increased MEcPP levels, triggered by genetic...

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Veröffentlicht in:Nature communications 2024-11, Vol.15 (1), p.10079-12, Article 10079
Hauptverfasser: Guo, Jingzhe, Van De Ven, Wilhelmina T, Skirycz, Aleksandra, Thirumalaikumar, Venkatesh P., Zeng, Liping, Zhang, Quanqing, Balcke, Gerd Ulrich, Tissier, Alain, Dehesh, Katayoon
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Sprache:eng
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Zusammenfassung:Methylerythritol cyclodiphosphate (MEcPP) is an intermediate in the biosynthesis of isoprenoids in plant plastids and in bacteria, and acts as a stress signal in plants. Here, we show that MEcPP regulates biofilm formation in Escherichia coli K-12 MG1655. Increased MEcPP levels, triggered by genetic manipulation or oxidative stress, inhibit biofilm development and production of fimbriae. Deletion of fimE , encoding a protein known to downregulate production of adhesive fimbriae, restores biofilm formation in cells with elevated MEcPP levels. Limited proteolysis-coupled mass spectrometry (LiP-MS) reveals that MEcPP interacts with the global regulatory protein H-NS, which is known to repress transcription of fimE . MEcPP prevents the binding of H-NS to the fimE promoter. Therefore, our results indicate that MEcPP can regulate biofilm formation by modulating H-NS activity and thus reducing fimbriae production. Further research is needed to test whether MEcPP plays similar regulatory roles in other bacteria. Methylerythritol cyclodiphosphate is an intermediate in the biosynthesis of isoprenoids in plants and bacteria, and acts as a stress signal in plants. Here, Guo et al. show that, in addition, the metabolite can inhibit biofilm formation in Escherichia coli by modulating the activity of the DNA-binding protein H-NS, thus downregulating the production of adhesive fimbriae.
ISSN:2041-1723
2041-1723
DOI:10.1038/s41467-024-54501-w