An interbacterial DNA deaminase toxin directly mutagenizes surviving target populations
Abstract
When bacterial cells come in contact, antagonism mediated by the delivery of toxins frequently ensues. The potential for such encounters to have long-term beneficial consequences in recipient cells has not been investigated. Here we examined the effects of intoxication by DddA, a cytosine deaminase delivered via the type VI secretion system (T6SS) of Burkholderia cenocepacia. Despite its killing potential, we observed that several bacterial species resist DddA and instead accumulate mutations. These mutations can lead to the acquisition of antibiotic resistance, indicating that even in the absence of killing, interbacterial antagonism can have profound consequences on target populations. Investigation of additional toxins from the deaminase superfamily revealed that mutagenic activity is a common feature of these proteins, including a representative we show targets single-stranded DNA and displays a markedly divergent structure. Our findings suggest that a surprising consequence of antagonistic interactions between bacteria could be the promotion of adaptation via the action of directly mutagenic toxins.
Data availability
Diffraction data have been deposited in PDB under the accession code 7JTU.Sequencing data have been deposited at the NCBI Trace and Short-Read Archive (SRA) under BioProject accession ID PRJNA659516.
Article and author information
Author details
Funding
National Institutes of Health (GM128191)
- Paul A Wiggins
National Institutes of Health (AI080609)
- Joseph D Mougous
Howard Hughes Medical Institute
- Joseph D Mougous
Cystic Fibrosis Foundation (DEMORA18F0)
- Marcos H de Moraes
The funders had no role in study design, data collection and interpretation, or the decision to submit the work for publication.
Copyright
© 2021, de Moraes et al.
This article is distributed under the terms of the Creative Commons Attribution License permitting unrestricted use and redistribution provided that the original author and source are credited.
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