An interbacterial DNA deaminase toxin directly mutagenizes surviving target populations

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.

Automated summary

When bacterial cells come in contact, antagonism mediated by the delivery of toxins frequently ensues, leading to potential long-term beneficial consequences in recipient cells. Investigation has shown that despite the killing potential of toxins like DddA, some bacterial species can resist and accumulate mutations, potentially acquiring antibiotic resistance. Furthermore, it has been discovered that toxins from the deaminase superfamily have mutagenic activity, suggesting that antagonistic interactions between bacteria could promote adaptation via the action of directly mutagenic toxins.