Practice question

No-go decay NGD resolves stalled elongation complexes blocked by strong structures, damaged bases, rare codons, or adducts. Colliding ribosomes upstream recognized by Pelota Dom34 and Hbs1 GTPase resembling termination factors, facilitating endonucleolytic cleavage near stall site via Cue2 nuclease activated by ubiquitination of uS3, uS10 by Hel2 ligase. Resulting fragments degraded by exosome and Xrn1, nascent peptide ubiquitinated and degraded proteasomally. NGD prevents ribosome sequestration maintaining translational capacity and avoids accumulation of incomplete aggregation-prone polypeptides. Distinct from NMD triggered by premature termination, NGD specificity for elongation arrest maintains proteostasis and ribosome recycling efficiency under stress.