2025-12-16 東京大学
リボソーム競合に起因するリボソーム分解経路
<関連情報>
- https://www.ims.u-tokyo.ac.jp/imsut/jp/about/press/page_00365.html
- https://www.ims.u-tokyo.ac.jp/imsut/content/000012087.pdf
- https://www.nature.com/articles/s41467-025-66026-x
リボソームの競合と翻訳の摂動によって引き起こされる衝突誘発リボソーム分解 Collision-induced ribosome degradation driven by ribosome competition and translational perturbations
Sihan Li,Okuto Shounai,Misaki Kato,Ken Ikeuchi & Toshifumi Inada
Nature Communications Published:12 December 2025
DOI:https://doi.org/10.1038/s41467-025-66026-x
Abstract
Individual stalling of catalytically inactive ribosomes at the start codon triggers ubiquitination of ribosomal protein uS3 and subsequent 18S rRNA decay. While collisions between ribosomes during translation elongation represent a more widespread form of translation perturbation, their impact on ribosome stability remains unknown. Here, we clarify a bifurcation in ubiquitination-mediated ribosome turnover, identifying a collision-induced branch of uS3 ubiquitination and small subunit destabilization in yeast. This pathway eliminates not only non-functional ribosomes but also translationally active ones with a prokaryotic-like decoding center, driven by competition with wild-type ribosomes due to differing translation rates. We further show that endogenous ribosomal subunit stoichiometry shifts toward a small-subunit-shortage state via ubiquitination upon perturbed translation triggered by the anti-cancer drug cisplatin and the growth phase transition. These findings reveal a mechanism by which ribosome dynamics generally affects ribosome stability, implicating ribosome dysfunction, heterogeneity, and stress-related translational disturbances in small subunit degradation.
