Hijacking host ribosomes via tRNA mimicry

The bacterial pathogen Legionella pneumophila uses effectors — toxins — to facilitate pathogenesis within host cells. A recent study identifies dual mechanisms of the effector SidI as an inhibitor of translation elongation. The N-terminal domain mimics tRNA, whereas the C-terminal domain glycosylate...

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Bibliographic Details
Published inNature cell biology Vol. 25; no. 11; pp. 1562 - 1563
Main Authors Uematsu, Saori, Qian, Shu-Bing
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group UK 01.11.2023
Nature Publishing Group
Subjects
38/90
631/337/574
631/45/500
Biology
Biomedical and Life Sciences
Cancer Research
Cell Biology
Cytoplasm
Developmental Biology
Elongation
Infections
Kinases
Legionnaires' disease bacterium
Life Sciences
Mass spectrometry
Microorganisms
Microscopy
Mimicry
News & Views
news-and-views
Pathogenesis
Pathogens
Phosphorylation
Protein synthesis
Proteins
Ribonucleic acid
Ribosomes
RNA
Scientific imaging
Stem Cells
Toxins
Transcription factors
Transfer RNA
Translation elongation
tRNA
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Summary:The bacterial pathogen Legionella pneumophila uses effectors — toxins — to facilitate pathogenesis within host cells. A recent study identifies dual mechanisms of the effector SidI as an inhibitor of translation elongation. The N-terminal domain mimics tRNA, whereas the C-terminal domain glycosylates the ribosome.
Bibliography:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
ISSN:1465-7392
1476-4679
DOI:10.1038/s41556-023-01249-y