Colibactin produced by a honeybee gut symbiont mediates pathogen defence

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Abstract
Colibactin is a bacterial genotoxin that damages DNA and is linked to colorectal cancer. It is implicated in interbacterial competition but its role in natural microbiomes is unclear. Here we show that Frischella perrara, a colibactin-producing symbiont restricted to honeybee guts, lowers bee lifespan but increases survivorship following challenge with the opportunistic bee pathogen Serratia marcescens. F. perrara mutants lacking colibactin production fail to improve survivorship following challenge. The symbiont reduces pathogen loads by causing colibactin-dependent DNA damage and prophage induction. Colibactin is toxic to the pathogen under anoxic conditions, reflecting the bee gut. clbS, a gene conferring protection from colibactin, is ubiquitous among bacteria restricted to bee guts but absent from opportunistic colonizers, including pathogens. Indeed, F. perrara colonization representing colibactin pressure had limited impact on the bee gut microbiome where strains encode clbS. Our findings suggest that colibactin functions in interbacterial competition and protects against pathogens while permitting co-evolved symbionts to persist.
Funding Information
  • Howard Hughes Medical Institute
  • National Institutes of Health (R35GM131738)
  • National Institutes of Health (R35GM158145)
  • Army Research Office (W911NF-20-1-0195)

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