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Proceedings of the National Academy of Sciences of the United States of America logoLink to Proceedings of the National Academy of Sciences of the United States of America
. 2019 May 20;116(22):11077. doi: 10.1073/pnas.1906160116

Retraction for Germain et al., Stochastic induction of persister cells by HipA through (p)ppGpp-mediated activation of mRNA endonucleases

PMCID: PMC6561198  PMID: 31110010

MICROBIOLOGY Retraction for “Stochastic induction of persister cells by HipA through (p)ppGpp-mediated activation of mRNA endonucleases,” by Elsa Germain, Mohammad Roghanian, Kenn Gerdes, and Etienne Maisonneuve, which was first published April 6, 2015; 10.1073/pnas.1423536112 (Proc Natl Acad Sci USA 112:5171–5176).

The authors wish to note the following: “In this article, we reported that HipA-induced persistence in Escherichia coli K-12 depends on (p)ppGpp-mediated activation of the ten mRNase-encoding toxin antitoxin (TA) modules through a signaling pathway involving the inorganic polyphosphate and the protease Lon. After the publication of the article, we became aware that the previously described contribution of polyphosphate and TA modules to bacterial persistence (1) were artifact results of inadvertent lysogenization with the bacteriophage ϕ80, a notorious laboratory contaminant (2, 3). Therefore, the role and the connection of polyphosphate and TA modules in a linear pathway in persister cells formation are no longer supported. In this article, the following data were likely affected by the lysogenic bacteriophage: Fig. 3, Fig. 4 C and D, Fig. 5 C and D, Fig. S2, Fig. S3, and Fig. S4 C and D. For these figures, we indeed confirmed ϕ80 lysogenization for the Δ10TA and the Δ(ppk ppx) strains. We believe that the most appropriate course of action is to retract the paper. We offer our sincerest apologies to the scientific community for these inadvertent errors and for any inconvenience they may have caused.”

1. Maisonneuve E, Castro-Camargo M, Gerdes K (2013) (p) ppGpp controls bacterial persistence by stochastic induction of toxin-antitoxin activity. Cell 154:1140–1150, retracted (2018) 172:1135.

2. Harms A, Fino C, Sørensen MA, Semsey S, Gerdes K (2017) Prophages and growth dynamics confound experimental results with antibiotic-tolerant persister cells. MBio 8:e01964-17.

3. Goormaghtigh F, et al. (2018) Reassessing the role of type II toxin-antitoxin systems in formation of escherichia coli type II persister cells. MBio 9:e00640-18.


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