RETRACTED ARTICLE: A switch in the poly(dC)/RmlB complex regulates bacterial persister formation

Xu Chen, Gen Li, Xuewei Liao, Jie Fang, Bo Li, Shanshan Yu, Mingming Sun, Jun Wu (), Lihao Zhang, Yi Hu, Jiaguo Jiao, Ting Liu, Li Xu, Xiaoyun Chen, Manqiang Liu, Huixin Li, Feng Hu and Kouhong Sun
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Xu Chen: Nanjing Agricultural University
Gen Li: Nanjing Agricultural University
Xuewei Liao: Nanjing Normal University
Jie Fang: Nanjing Agricultural University
Bo Li: Nanjing Agricultural University
Shanshan Yu: Nanjing Agricultural University
Mingming Sun: Nanjing Agricultural University
Jun Wu: Nanjing Agricultural University
Lihao Zhang: Nanjing Agricultural University
Yi Hu: Nanjing Agricultural University
Jiaguo Jiao: Nanjing Agricultural University
Ting Liu: Nanjing Agricultural University
Li Xu: Nanjing Agricultural University
Xiaoyun Chen: Nanjing Agricultural University
Manqiang Liu: Nanjing Agricultural University
Huixin Li: Nanjing Agricultural University
Feng Hu: Nanjing Agricultural University
Kouhong Sun: Zoonbio Biotechnology Co., Ltd

Nature Communications, 2019, vol. 10, issue 1, 1-14

Abstract: Abstract Bacterial persisters are phenotypic variants that tolerate exposure to lethal antibiotics. These dormant cells are responsible for chronic and recurrent infections. Multiple mechanisms have been linked to persister formation. Here, we report that a complex, consisting of an extracellular poly(dC) and its membrane-associated binding protein RmlB, appears to be associated with persistence of the opportunistic pathogen Pseudomonas aeruginosa. Environmental stimuli triggers a switch in the complex physiological state (from poly(dC)/RmlB to P-poly(dC)/RmlB or RmlB). In response to the switch, bacteria decrease proton motive force and intracellular ATP levels, forming dormant cells. This alteration in complex status is linked to a (p)ppGpp-controlled signaling pathway that includes inorganic polyphosphate, Lon protease, exonuclease VII (XseA/XseB), and the type III secretion system. The persistence might be also an adaptive response to the lethal action of the dTDP-l-rhamnose pathway shutdown, which occurs due to switching of poly(dC)/RmlB.

Date: 2019
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DOI: 10.1038/s41467-018-07861-z

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