The nascent polypeptide in the 60S subunit determines the Rqc2-dependency of ribosomal quality control

Masato Mizuno, Shuhei Ebine, Okuto Shounai, Shizuka Nakajima, Shota Tomomatsu, Ken Ikeuchi, Yoshitaka Matsuo, Toshifumi Inada

Research output: Contribution to journalArticlepeer-review

3 Citations (Scopus)


Ribosome stalling at tandem CGA codons or poly(A) sequences activates quality controls for nascent polypeptides including ribosome-associated quality control (RQC) and no-go mRNA decay (NGD). In RQC pathway, Hel2-dependent uS10 ubiquitination and the RQC-trigger (RQT) complex are essential for subunit dissociation, and Ltn1-dependent ubiquitination of peptidyl-tRNA in the 60S subunit requires Rqc2. Here, we report that polytryptophan sequences induce Rqc2-independent RQC. More than 11 consecutive tryptophan residues induced RQC in a manner dependent on Hel2-mediated ribosome ubiquitination and the RQT complex. Polytryptophan sequence-mediated RQC was not coupled with CAT-tailing, and Rqc2 was not required for Ltn1-dependent degradation of the arrest products. Eight consecutive tryptophan residues located at the region proximal to the peptidyl transferase center in the ribosome tunnel inhibited CAT-tailing by tandem CGA codons. Polytryptophan sequences also induced Hel2-mediated canonical RQC-coupled NGD and RQC-uncoupled NGD outside the stalled ribosomes. We propose that poly-tryptophan sequences induce Rqc2-independent RQC, suggesting that CAT-tailing in the 60S subunit could be modulated by the polypeptide in the ribosome exit tunnel.

Original languageEnglish
Pages (from-to)2102-2113
Number of pages12
JournalNucleic acids research
Issue number4
Publication statusPublished - 2021 Feb 26

ASJC Scopus subject areas

  • Genetics


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