Some suicidal Type III toxin-antitoxin (TA) systems have the capacity to abort phage infection. The plasmid-encoded Type III TA system from Pectobacterium atrosepticum (ToxIN) is composed of a proteinaceous endoribonuclease toxin (ToxN) that is suppressed by a short RNA pseudoknot antitoxin (ToxI). The ToxIN complex is a triangular heterohexamer that is present in the bacterial cell prior to phage infection. The ToxIN system can be functionally reconstituted in other hosts such as E. coli and Serratia and in all of these hosts, environmental phages can be isolated that are aborted by the Pectobacterium system. Some of these phages can produce spontaneous mutants that escape the abortive infection (Abi) system, but at varying frequencies, depending on the phage.

The nature of some escape mutants has been investigated in environmental phages that infect Pectobacterium or Serratia. One Pectobacterium phage (φTE) escaped at very low frequency (10-8) and the escape mutants circumvented the Abi system through a viral RNA-based molecular mimicry of ToxI, which acts to suppress ToxN-induced lethality and thereby prevents bacterial suicide. Another pectobacterial phage (φM1) escaped at around 10-5. Multiple independent mutants were isolated and sequenced. All mutations mapped to the same viral gene.

The ToxIN system was transferred to a Serratia strain where it showed TA functionality. Several environmental Serratia phages isolated over a 2-3 year period were characterized and three independent, but very similar, phages that were aborted, yet could escape (at around 10-6) frequency, were characterized. Escape mutants arose by different mechanisms in these phages, but a large deletion locus was common among the escapes. In summary, different phages have the capacity to escape Abi in Pectobacterium and Serratia by different mechanisms and some phages may have the ability to escape via more than one route.