Evasion of antiviral bacterial immunity by phage tRNAs.

Autor: Azam AH; Research Center for Drug and Vaccine Development, National Institute of Infectious Diseases, Shinjuku, Tokyo, Japan., Kondo K; Antimicrobial Resistance Research Center, National Institute of Infectious Diseases, Higashi Murayama, Tokyo, Japan., Chihara K; Research Center for Drug and Vaccine Development, National Institute of Infectious Diseases, Shinjuku, Tokyo, Japan., Nakamura T; Research Center for Drug and Vaccine Development, National Institute of Infectious Diseases, Shinjuku, Tokyo, Japan., Ojima S; Research Center for Drug and Vaccine Development, National Institute of Infectious Diseases, Shinjuku, Tokyo, Japan., Nie W; Research Center for Drug and Vaccine Development, National Institute of Infectious Diseases, Shinjuku, Tokyo, Japan., Tamura A; Research Center for Drug and Vaccine Development, National Institute of Infectious Diseases, Shinjuku, Tokyo, Japan., Yamashita W; Research Center for Drug and Vaccine Development, National Institute of Infectious Diseases, Shinjuku, Tokyo, Japan., Sugawara Y; Antimicrobial Resistance Research Center, National Institute of Infectious Diseases, Higashi Murayama, Tokyo, Japan., Sugai M; Antimicrobial Resistance Research Center, National Institute of Infectious Diseases, Higashi Murayama, Tokyo, Japan., Cui L; Division of Bacteriology, Department of Infection and Immunity, School of Medicine, Jichi Medical University, Shimotsuke-shi, Tochigi, Japan., Takahashi Y; Research Center for Drug and Vaccine Development, National Institute of Infectious Diseases, Shinjuku, Tokyo, Japan., Watashi K; Research Center for Drug and Vaccine Development, National Institute of Infectious Diseases, Shinjuku, Tokyo, Japan., Kiga K; Research Center for Drug and Vaccine Development, National Institute of Infectious Diseases, Shinjuku, Tokyo, Japan. k-kiga@niid.go.jp.; Division of Bacteriology, Department of Infection and Immunity, School of Medicine, Jichi Medical University, Shimotsuke-shi, Tochigi, Japan. k-kiga@niid.go.jp.
Jazyk: angličtina
Zdroj: Nature communications [Nat Commun] 2024 Nov 11; Vol. 15 (1), pp. 9586. Date of Electronic Publication: 2024 Nov 11.
DOI: 10.1038/s41467-024-53789-y
Abstrakt: Retrons are bacterial genetic elements that encode a reverse transcriptase and, in combination with toxic effector proteins, can serve as antiphage defense systems. However, the mechanisms of action of most retron effectors, and how phages evade retrons, are not well understood. Here, we show that some phages can evade retrons and other defense systems by producing specific tRNAs. We find that expression of retron-Eco7 effector proteins (PtuA and PtuB) leads to degradation of tRNA Tyr and abortive infection. The genomes of T5 phages that evade retron-Eco7 include a tRNA-rich region, including a highly expressed tRNA Tyr gene, which confers protection against retron-Eco7. Furthermore, we show that other phages (T1, T7) can use a similar strategy, expressing a tRNA Lys , to counteract a tRNA anticodon defense system (PrrC170).
Competing Interests: Competing interests A.H.A., Y.T., K.W., and K.Kiga are co-inventors on a pending patent submitted by the National Institute of Infectious Diseases, which is based on the results reported in this paper. The remaining authors declare no competing interests.
(© 2024. The Author(s).)
Databáze: MEDLINE
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