An interbacterial DNA deaminase toxin directly mutagenizes surviving target populations.
basic_science · Level V
Where this comes from
- Record sourced from PubMed, PMID 33448264.
- Also identified by DOI 10.7554/eLife.62967 and PMC identifier 7901873.
- Licence recorded as CC BY.
- The licence permits redistribution, so the abstract is shown in full and the full text is available from the publisher.
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 <i>Burkholderia cenocepacia</i>. 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.
Medical subject headings
- Bacterial Proteins
- Bacterial Toxins
- Burkholderia cenocepacia
- Cytosine Deaminase
- Escherichia coli
- Microbial Interactions