The virulence regulator VirB from Shigella flexneri uses a CTP-dependent switch mechanism to activate gene expression
The transcriptional antisilencer VirB acts as a master regulator of virulence gene expression in the human pathogen Shigella flexneri. It binds DNA sequences (virS) upstream of VirB-dependent promoters and counteracts their silencing by the nucleoid-organizing protein H-NS. However, its precise mode...
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| Hauptverfasser: | , , , , , , , , , , , , |
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| Dokumenttyp: | Article (Journal) |
| Sprache: | Englisch |
| Veröffentlicht: |
05 January 2024
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| In: |
Nature Communications
Year: 2024, Jahrgang: 15, Pages: 1-18 |
| ISSN: | 2041-1723 |
| DOI: | 10.1038/s41467-023-44509-z |
| Online-Zugang: | Verlag, kostenfrei, Volltext: https://doi.org/10.1038/s41467-023-44509-z Verlag, kostenfrei, Volltext: https://www.nature.com/articles/s41467-023-44509-z 
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| Verfasserangaben: | Sara Jakob, Wieland Steinchen, Juri Hanßmann, Julia Rosum, Katja Langenfeld, Manuel Osorio-Valeriano, Niklas Steube, Pietro I. Giammarinaro, Georg K.A. Hochberg, Timo Glatter, Gert Bange, Andreas Diepold & Martin Thanbichler |
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| 245 | 1 | 4 | |a The virulence regulator VirB from Shigella flexneri uses a CTP-dependent switch mechanism to activate gene expression |c Sara Jakob, Wieland Steinchen, Juri Hanßmann, Julia Rosum, Katja Langenfeld, Manuel Osorio-Valeriano, Niklas Steube, Pietro I. Giammarinaro, Georg K.A. Hochberg, Timo Glatter, Gert Bange, Andreas Diepold & Martin Thanbichler |
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| 520 | |a The transcriptional antisilencer VirB acts as a master regulator of virulence gene expression in the human pathogen Shigella flexneri. It binds DNA sequences (virS) upstream of VirB-dependent promoters and counteracts their silencing by the nucleoid-organizing protein H-NS. However, its precise mode of action remains unclear. Notably, VirB is not a classical transcription factor but related to ParB-type DNA-partitioning proteins, which have recently been recognized as DNA-sliding clamps using CTP binding and hydrolysis to control their DNA entry gate. Here, we show that VirB binds CTP, embraces DNA in a clamp-like fashion upon its CTP-dependent loading at virS sites and slides laterally on DNA after clamp closure. Mutations that prevent CTP-binding block VirB loading in vitro and abolish the formation of VirB nucleoprotein complexes as well as virulence gene expression in vivo. Thus, VirB represents a CTP-dependent molecular switch that uses a loading-and-sliding mechanism to control transcription during bacterial pathogenesis. | ||
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