4.8 Article

Human gut bacteria contain acquired interbacterial defence systems

Journal

NATURE
Volume 575, Issue 7781, Pages 224-+

Publisher

NATURE PUBLISHING GROUP
DOI: 10.1038/s41586-019-1708-z

Keywords

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Funding

  1. National Institutes of Health (NIH) [AI080609, P30DK089507, R01DK095869, K99GM129874, R01GM124312]
  2. National Institutes of Health (NIH) New Innovator Award [DP2AT00780201]
  3. Burroughs Wellcome Fund
  4. Natural Sciences and Engineering Research Council of Canada
  5. Simons Foundation-sponsored Life Sciences Research Foundation postdoctoral fellowship

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The human gastrointestinal tract consists of a dense and diverse microbial community, the composition of which is intimately linked to health. Extrinsic factors such as diet and host immunity are insufficient to explain the constituents of this community, and direct interactions between co-resident microorganisms have been implicated as important drivers of microbiome composition. The genomes of bacteria derived from the gut microbiome contain several pathways that mediate contact-dependent interbacterial antagonism(1-3). Many members of the Gram-negative order Bacteroidales encode the type VI secretion system (T6SS), which facilitates the delivery of toxic effector proteins into adjacent cells(4,5). Here we report the occurrence of acquired interbacterial defence (AID) gene clusters in Bacteroidales species that reside within the human gut microbiome. These clusters encode arrays of immunity genes that protect against T6SS-mediated intra- and inter-species bacterial antagonism. Moreover, the clusters reside on mobile elements, and we show that their transfer is sufficient to confer resistance to toxins in vitro and in gnotobiotic mice. Finally, we identify and validate the protective capability of a recombinase-associated AID subtype (rAID-1) that is present broadly in Bacteroidales genomes. These rAID-1 gene clusters have a structure suggestive of active gene acquisition and include predicted immunity factors of toxins derived from diverse organisms. Our data suggest that neutralization of contact-dependent interbacterial antagonism by AID systems helps to shape human gut microbiome ecology.

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