Abstract
Last year, Gerdes and colleagues published a paper (1) describing experiments that failed to support earlier work from their group (2, 3) which had implicated 10 type II toxin-antitoxin (TA) systems in the formation of antibiotic-tolerant Escherichia coli K-12 persister cells. The problem apparently arose as a result of contamination by and activation of the cryptic bacteriophage Φ80 in mutant strains lacking TA genes. A more recent paper by Goormaghtigh et al. (4) confirms and extends this reappraisal by providing evidence that an independently constructed E. coli K-12 mutant strain lacking the 10 type II TAs and free of phage contamination produced levels of persisters similar to those of wild-type bacteria after exposure to antibiotics (4). In addition, this work questions the validity of TA::green fluorescent protein (GFP) transcriptional reporter fusions (3). Since the possible link between TA systems and the persister phenotype is being studied in many laboratories, these corrections are both important and salutary.
Highlights
Last year, Gerdes and colleagues published a paper [1] describing experiments that failed to support earlier work from their group [2, 3] which had implicated 10 type II toxin-antitoxin (TA) systems in the formation of antibiotic-tolerant Escherichia coli K-12 persister cells
The authors state that “The model linking TA systems and persistence to antibiotics had a major impact in the microbiology community as a whole
Evidence for the involvement of TA systems in persister formation has been obtained for several other bacteria, including uropathogenic E. coli [6], Burkholderia [7], and Salmonella [8,9,10]
Summary
Gerdes and colleagues published a paper [1] describing experiments that failed to support earlier work from their group [2, 3] which had implicated 10 type II toxin-antitoxin (TA) systems in the formation of antibiotic-tolerant Escherichia coli K-12 persister cells. The authors state that “The model linking TA systems and persistence to antibiotics had a major impact in the microbiology community as a whole. .” The purported invalidation relates only to nonstressed E. coli K-12.
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