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Bacterial Nucleoside Catabolism Controls Quorum Sensing and Commensal-to-Pathogen Transition in the Drosophila Gut

Title
Bacterial Nucleoside Catabolism Controls Quorum Sensing and Commensal-to-Pathogen Transition in the Drosophila Gut
Authors
Kim, Eun-KyoungLee, Kyung-AhHyeon, Do YoungKyung, MinsooJun, Kyu-YeonSeo, Seung HeeHwang, DaeheeKwon, YoungjooLee, Won-Jae
Ewha Authors
권영주전규연
SCOPUS Author ID
권영주scopus
Issue Date
2020
Journal Title
CELL HOST & MICROBE
ISSN
1931-3128JCR Link

1934-6069JCR Link
Citation
CELL HOST & MICROBE vol. 27, no. 3, pp. 345 - +
Publisher
CELL PRESS
Indexed
SCI; SCIE; SCOPUS WOS scopus
Document Type
Article
Abstract
Although the gut microbiome is generally symbiotic or commensal, some microbiome members become pathogenic under certain circumstances. However, the factors driving this pathogenic switch are largely unknown. Pathogenic bacteria can generate uracil that triggers host dual oxidase (DUOX) to produce antimicrobial reactive oxygen species (ROS). We show that pathogens generate uracil and ribose upon nucleoside catabolism of gut luminal uridine, which triggers not only host defenses but also inter-bacterial communication and pathogenesis in Drosophila. Uridine-derived uracil triggers DUOX-dependent ROS generation, whereas ribose induces bacterial quorum sensing (QS) and virulence gene expression. Genes implicated in nucleotide metabolism are found in pathogens but not commensal bacteria, and their genetic ablation blocks QS and the commensal-to-pathogen transition in vivo. Furthermore, commensal bacteria lack functional nucleoside catabolism, which is required to achieve gut-microbe symbiosis, but can become pathogenic by enabling nucleotide catabolism. These findings reveal molecular mechanisms governing the commensal-to-pathogen transition in different contexts of host-microbe interactions.
DOI
10.1016/j.chom.2020.01.025
Appears in Collections:
약학대학 > 약학과 > Journal papers
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