ASC1 and RPS3: New actors in 18S non-functional rRNA decay
- ↵* Corresponding author; email: melissa.moore{at}umassmed.edu
Abstract
In budding yeast, inactivating mutations within the 40S ribosomal subunit decoding center lead to 18S rRNA clearance by a quality control mechanism known as nonfunctional 18S rRNA decay (18S NRD). We previously showed that 18S NRD is functionally related to No-Go mRNA Decay (NGD), a pathway for clearing translation complexes stalled on aberrant mRNAs. Whereas the NGD factors DOM34 and HBS1 contribute to 18S NRD, their genetic deletion (either singly or in combination) only partially stabilizes mutant 18S rRNA. Here we identify ASC1 (aka RACK1) and RPS3, both stable 40S subunit components, as additional 18S NRD factors. Complete stabilization of mutant 18S rRNA in dom34Δ;asc1Δ and hbs1Δ;asc1Δ strains indicates the existence of two genetically separable 18S NRD pathways. A small region of the RPS3 C-terminal tail known to be subject to post-translational modification is also crucial for 18S NRD. We combine these findings with the effects of mutations in the 5′ → 3′ and 3′ → 5′ decay machinery to propose a model wherein multiple targeting and decay pathways kinetically contribute to 18S NRD.
Keywords
- Received April 14, 2017.
- Accepted September 23, 2017.
- Published by Cold Spring Harbor Laboratory Press for the RNA Society
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