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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-Kyoung; Lee, Kyung-Ah; Hyeon, Do Young; Kyung, Minsoo; Jun, Kyu-Yeon; Seo, Seung Hee; Hwang, Daehee; Kwon, Youngjoo; Lee, Won-Jae
- Ewha Authors
- 권영주; 전규연
- SCOPUS Author ID
- 권영주; 전규연
- Issue Date
- 2020
- Journal Title
- CELL HOST & MICROBE
- ISSN
- 1931-3128
1934-6069
- Citation
- CELL HOST & MICROBE vol. 27, no. 3, pp. 345 - +
- Publisher
- CELL PRESS
- Indexed
- SCIE; 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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