Panel A: Multiple ribosomes translate a single mRNA strand. When a defective ribosome (orange) stalls, it causes a collision with a trailing canonical ribosome (grey). This interaction, mediated by the RACK1 protein (yellow oval), triggers the selective degradation of the defective subunit, represented by a disposal icon. Panel B: Ribosomes are distributed across separate mRNA strands (black and red lines). The spatial separation prevents physical contact, thereby avoiding collisions even if a ribosome is defective. Panel C: A state of low translation initiation or reduced ribosome density. A single ribosome occupies each mRNA strand; collisions are stochastically limited. Panel D: In the absence of RACK1 (RACK1-deficient subunits, indicated by dashed outlines), collisions between canonical and defective ribosomes still occur. The lack of the RACK1 signaling protein prevents the cell from recognizing the stall, shown by a red X blocking the degradation pathway.
Ribosome collisions purify the ribosome pool under some conditions. (A) Ribosome collisions identify defective ribosomes (in orange) via the collisions that they incur with canonical ribosomes, which then lead to the degradation of the defective ribosome (Li et al., 2025; Parker et al., 2024). The collided interface that is recognized by the degradation machinery includes the RP Asc1/RACK1 (in yellow). (B) Collisions between defective or heterogeneous ribosomes (in orange) and canonical ribosomes (in gray) cannot occur if the different ribosomes sort on different mRNAs (black or red), either because of strong mRNA specificity or due to subcellular localization. (C) Collisions between defective or heterogeneous ribosomes (in orange) and canonical ribosomes (in gray) cannot occur in cells with low ribosome levels or low translation (initiation), which both limit ribosomes to one or a few on each mRNA, thus precluding collisions. (D) Collisions between defective or heterogeneous ribosome species (in orange) and canonical ribosomes (in gray) can occur but are not recognized by the degradation machinery if the collision interface is destabilized by the absence of nonessential RPs like Asc1 (Ikeuchi and Inada, 2016; Limoncelli et al., 2017; Sitron et al., 2017; Wang et al., 2018) (shown in yellow in A) or mutation of other interface components (Matsuo et al., 2017; Narita et al., 2022).