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The bacterial toxin colibactin triggers prophage induction
Justin E Silpe1, Joel W H Wong1, Siân V Owen2
1Department of Chemistry and Chemical Biology, Harvard University, Cambridge, MA, USA.
Nature
|February 24, 2022
Summary
Colibactin, a genotoxin from gut bacteria, triggers phage outbreaks in other microbes by activating the SOS response. Exogenous DNA or a resistance protein (ClbS) can prevent this effect.
Area of Science:
- Microbiology
- Molecular Biology
- Genomics
Background:
- Colibactin is a genotoxin produced by gut bacteria, with known effects on mammalian systems.
- Its impact on other microorganisms, particularly within the microbiome, remains largely uncharacterized.
Purpose of the Study:
- To investigate the effects of colibactin on microbial communities.
- To elucidate the mechanism by which colibactin influences bacterial populations and prophage activity.
Main Methods:
- Exposure of bacterial systems to colibactin.
- Investigating the role of the bacterial SOS response in colibactin's effects.
- Assessing the protective effects of exogenous DNA and the ClbS protein.
- Analyzing colibactin resistance and biosynthetic genes in various bacterial species.
Main Results:
- Colibactin targets bacteria containing prophages, inducing lytic development via the SOS response.
- Exogenous DNA and the colibactin resistance protein (ClbS) confer protection against colibactin.
- These prophage-inducing effects are observed across diverse phage-bacteria systems and complex communities.
- Bacteria with resistance genes but lacking biosynthetic genes are protected by ClbS homologs from colibactin-induced prophage expression.
Conclusions:
- Colibactin production influences microbiome dynamics by triggering prophage outbreaks.
- Microbial natural products like colibactin can mediate population-level events, including phage dissemination.
- The ClbS protein provides a mechanism for bacteria to resist colibactin's prophage-inducing effects.
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