ArticleNature cell biology2025
An avoidance segment resolves a lethal nuclear-mitochondrial targeting conflict during ribosome assembly.
Article in Nature cell biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- The N-terminal extension of ribosomal protein Rps2 shapes its early fate through Chaperone-Importin competition and arginine methylation.The Journal of biological chemistry · 2026Article
- The IQ-compete assay for measuring mitochondrial protein import efficiencies in living yeast cells.FEBS letters · 2026Article
- Article
- Intracristal space proteome mapping using super-resolution proximity labeling with isotope-coded probes.Nature communications · 2025Article
- Dysfunctional mitochondria trap proteins in the intermembrane space.The EMBO journal · 2025Article
- Dodging mitochondrial mislocalization.Nature reviews. Molecular cell biology · 2025Article
- How a ribosomal protein avoids mixed signals.Nature cell biology · 2025Article
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Authors and funding
11 authors.
Funding
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Abstract
The correct sorting of nascent ribosomal proteins from the cytoplasm to the nucleus or to mitochondria for ribosome production poses a logistical challenge for cellular targeting pathways. Here we report the discovery of a conserved mitochondrial avoidance segment (MAS) within the cytosolic ribosomal protein uS5 that resolves an evolutionary lethal conflict between the nuclear and mitochondrial targeting machinery. MAS removal mistargets uS5 to the mitochondrial matrix and disrupts the assembly of the cytosolic ribosome. The resulting lethality can be rescued by impairing mitochondrial import. We show that MAS triages nuclear targeting by disabling a cryptic mitochondrial targeting activity within uS5 and thereby prevents fatal capture by mitochondria. Our findings identify MAS as an essential acquisition by the primordial eukaryote that reinforced organelle targeting fidelity while developing an endosymbiotic relationship with its mitochondrial progenitor.
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Registered trials
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