Polyubiquitin architecture editing on collided ribosomes maintains persistent RQC activity

In ribosome-associated quality control (RQC), K63-linked polyubiquitination of ribosomal protein uS10 on the stalled ribosome is crucial for recruiting the RQC-trigger (RQT) complex. However, the mechanisms governing the maintenance and recycling of polyubiquitin architecture on colliding ribosomes remain unclear. Here we demonstrate that two deubiquitinating enzymes (DUBs), Ubp2 and Ubp3, play key roles in editing and recycling polyubiquitin chains on yeast uS10, thereby contributing to the promotion of RQC activity. Specifically, Ubp2 eliminates K63-linked polyubiquitin chains from uS10 on the free 40S subunit for recycling, while Ubp3 predominantly cleaves K48-linked di-ubiquitin and K48/K63-mixed-linkage polyubiquitin chains from uS10 on the translating ribosomes. We further demonstrate that K48-linkage-containing ubiquitin chains on uS10 of the colliding ribosome act as a negative signal for the RQT-mediated ribosome dissociation process. Collectively, our findings provide insight into the ubiquitin code in RQC, and define positive functions of two DUBs in maintaining persistent RQC activity.

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Publication Details

Journal
The EMBO Journal
Published
2025-09-16
DOI
https://doi.org/10.1038/s44318-025-00568-0
Citations
3
Primary Topic
Ubiquitin and proteasome pathways
Type
article
Field-Weighted Citation Impact
2.42
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article

Polyubiquitin architecture editing on collided ribosomes maintains persistent RQC activity

Fumiaki Ohtake, Takuya Tomita, Yasushi Saeki, Shota Tomomatsu et al.
3 citations
The EMBO Journal
Ubiquitin and proteasome pathways
2.42
article

Polyubiquitin architecture editing on collided ribosomes maintains persistent RQC activity

Fumiaki Ohtake, Takuya Tomita, Yasushi Saeki, Shota Tomomatsu, Toshifumi Inada, Yoshitaka Matsuo
article en
3 citations

Abstract

In ribosome-associated quality control (RQC), K63-linked polyubiquitination of ribosomal protein uS10 on the stalled ribosome is crucial for recruiting the RQC-trigger (RQT) complex. However, the mechanisms governing the maintenance and recycling of polyubiquitin architecture on colliding ribosomes remain unclear. Here we demonstrate that two deubiquitinating enzymes (DUBs), Ubp2 and Ubp3, play key roles in editing and recycling polyubiquitin chains on yeast uS10, thereby contributing to the promotion of RQC activity. Specifically, Ubp2 eliminates K63-linked polyubiquitin chains from uS10 on the free 40S subunit for recycling, while Ubp3 predominantly cleaves K48-linked di-ubiquitin and K48/K63-mixed-linkage polyubiquitin chains from uS10 on the translating ribosomes. We further demonstrate that K48-linkage-containing ubiquitin chains on uS10 of the colliding ribosome act as a negative signal for the RQT-mediated ribosome dissociation process. Collectively, our findings provide insight into the ubiquitin code in RQC, and define positive functions of two DUBs in maintaining persistent RQC activity.

The EMBO JournalVol. 44(21)
Hoshi University (JP), Tokyo Metropolitan Institute of Medical Science (JP), Protein Research Foundation (JP), Advanced Institute of Industrial Technology (JP), The University of Tokyo (JP)
Openalex Percentile: Top 10%
Ubiquitin and proteasome pathways
2.42
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