Proteomics

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The integrated stress response regulates 18S nonfunctional rRNA decay in mammals

ABSTRACT: Abstract - 18S nonfunctional rRNA decay (NRD) detects and eliminates translationally nonfunctional 18S rRNA. While this process is critical for ribosome quality control, the mechanisms underlying nonfunctional 18S rRNA turnover remain elusive, particularly in mammals. Here, we show that mammalian 18S NRD initiates through the integrated stress response (ISR) via GCN2. Nonfunctional 18S rRNA induces translational arrest at start sites. Biochemical analyses demonstrate that ISR activation limits translation initiation and attenuates collisions between scanning 43S preinitiation complexes and stalled nonfunctional ribosomes. The ISR promotes 18S NRD and 40S ribosomal protein turnover by RNF10-mediated ubiquitination. Ultimately, RIOK3 binds the resulting ubiquitinated 40S subunits and facilitates 18S rRNA decay. Overall, mammalian 18S NRD acts through GCN2, followed by ubiquitin-dependent 18S rRNA degradation involving the ubiquitin E3 ligase RNF10 and the atypical protein kinase RIOK3. These findings establish a dynamic feedback mechanism by which the GCN2-RNF10-RIOK3 axis surveils ribosome functionality at the translation initiation step.

INSTRUMENT(S): Orbitrap Eclipse

ORGANISM(S): Homo Sapiens (ncbitaxon:9606)

SUBMITTER: Colin Wu  

PROVIDER: MSV000096620 | MassIVE | Mon Dec 09 08:04:00 GMT 2024

REPOSITORIES: MassIVE

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The integrated stress response regulates 18S nonfunctional rRNA decay in mammals.

Coria Aaztli R AR   Shah Akruti A   Shafieinouri Mohammad M   Taylor Sarah J SJ   Guiblet Wilfried W   Miller Jennifer T JT   Mani Sharma Indra I   Wu Colin Chih-Chien CC  

bioRxiv : the preprint server for biology 20240730

18S nonfunctional rRNA decay (NRD) detects and eliminates translationally nonfunctional 18S rRNA. While this process is critical for ribosome quality control, the mechanisms underlying nonfunctional 18S rRNA turnover remain elusive. NRD was originally identified and has exclusively been studied in <i>Saccharomyces cerevisiae.</i> Here, we show that 18S NRD is conserved in mammals. Using genome-wide CRISPR genetic interaction screens, we find that mammalian NRD acts through the integrated stress  ...[more]

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