Bacterial Nucleoside Catabolism Controls Quorum Sensing and Commensal-to-Pathogen Transition in the Drosophila Gut
- 주제(기타) Microbiology
- 주제(기타) Parasitology
- 주제(기타) Virology
- 설명문(일반) [Kim, Eun-Kyoung; Lee, Kyung-Ah; Hyeon, Do Young; Kyung, Minsoo; Hwang, Daehee; Lee, Won-Jae] Seoul Natl Univ, Sch Biol Sci, Seoul 08826, South Korea; [Kim, Eun-Kyoung; Lee, Kyung-Ah; Lee, Won-Jae] Seoul Natl Univ, Natl Creat Res Initiat Ctr Hologen, Seoul 08826, South Korea; [Lee, Kyung-Ah; Lee, Won-Jae] Seoul Natl Univ, Inst Mol Biol & Genet, Seoul 151742, South Korea; [Jun, Kyu-Yeon; Seo, Seung Hee; Kwon, Youngjoo] Ewha Womans Univ, Grad Sch Pharmaceut Sci, Coll Pharm, Seoul 120750, South Korea
- 등재 SCIE, SCOPUS
- OA유형 Bronze
- 발행기관 CELL PRESS
- 발행년도 2020
- 총서유형 Journal
- URI http://www.dcollection.net/handler/ewha/000000168906
- 본문언어 영어
- Published As https://dx.doi.org/10.1016/j.chom.2020.01.025
- PubMed https://pubmed.ncbi.nlm.nih.gov/32078802
초록/요약
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.
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