Fig. 5: Model of a branched enzymatic pathway of uS3 ubiquitination linking translational perturbations to ribosomal small subunit degradation. | Nature Communications

Fig. 5: Model of a branched enzymatic pathway of uS3 ubiquitination linking translational perturbations to ribosomal small subunit degradation.

From: Collision-induced ribosome degradation driven by ribosome competition and translational perturbations

Fig. 5

During translation, stalled or slow ribosomes first receive a yellow card from Mag2, marked by mono-ubiquitination at uS3 as potential degradation substrates. These ribosomes remain stable unless further stalling or collisions occur. However, persistent translational disturbances trigger additional recognition steps and extension of the ubiquitin chain on uS3: Individual stalled ribosomes are poly-ubiquitinated by Fap1, while collided ribosomes are poly-ubiquitinated by Hel2. Poly-ubiquitination of uS3, along with ubiquitination of uS5 (and, depending on the context, uS10), acts as a red card committing ribosomes to small subunit degradation. We refer to the Mag2-Fap1-mediated pathway as stalling-induced ribosome destabilization (SRD) and the Mag2-Hel2-mediated pathway as collision-induced ribosome destabilization (CoRD). Ribosomes moving smoothly in translation but encounter abrupt stalling and collisions, e.g., at mRNA sequences with strong road-blocking effects, may bypass Mag2 binding, leading Hel2 to ubiquitinate uS10 in the absence of uS3 mono-ubiquitination and triggering RQC/NGD rather than CoRD. Ub: ubiquitination.

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