ldhA-induced persister in Escherichia coli is formed through accidental SOS response via intracellular metabolic perturbation

Naoki Yamamoto, Yurino Ohno, Satoshi Tsuneda*

*この研究の対応する著者

研究成果: Article査読

抄録

Persisters are a subpopulation that exhibit growth suppression, antibiotic tolerance, and regrowth after antibiotic removal, without any genetic mutations, which causes the recalcitrance and recurrence of infectious diseases. Persisters are majorly induced through the repression of energy metabolism, but some exceptions have been reported. We have previously shown that ldhA, which encodes lactate dehydrogenase, induces Escherichia coli persisters, resulting in a state of high-energy metabolism. However, the detailed mechanism of persister formation upon ldhA expression remains elusive. In the present study, we focused on the SOS response pathway via the DNA repair pathway that consumes adenosine triphosphate and revealed that the SOS response pathway is activated upon ldhA expression even before antimicrobial treatment. Metabolome analysis of ldhA-overexpressing cells revealed that nucleotide metabolic pathways, such as de novo purine biosynthesis, were activated to prepare a nucleotide pool, as substrate for repairing ofloxacin-induced DNA damage. We provide a novel persister model that contributes to survival as a species by “accidentally” activating the SOS response even before receiving antimicrobial stress.

本文言語English
ページ(範囲)225-233
ページ数9
ジャーナルMicrobiology and Immunology
66
5
DOI
出版ステータスPublished - 2022 5月

ASJC Scopus subject areas

  • 微生物学
  • 免疫学
  • ウイルス学

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