Journal
SCIENCE
Volume 368, Issue 6488, Pages 281-+Publisher
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.aay6912
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Funding
- Boehringer Ingelheim Fonds
- Deutsche Forschungsgemeinschaft [BE1814/15-1]
- Japan Society for the Promotion of Science [26116003, 18H03977, 19K06481]
- Takeda Foundation
- Kato Memorial Bioscience Foundation
- NIH [GM118018, GM115086]
- Grants-in-Aid for Scientific Research [19K06481, 18H03977] Funding Source: KAKEN
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Control of messenger RNA (mRNA) decay rate is intimately connected to translation elongation, but the spatial coordination of these events is poorly understood. The Ccr4-Not complex initiates mRNA decay through deadenylation and activation of decapping. We used a combination of cryo-electron microscopy, ribosome profiling, and mRNA stability assays to examine the recruitment of Ccr4-Not to the ribosome via specific interaction of the Not5 subunit with the ribosomal E-site in Saccharomyces cerevisiae. This interaction occurred when the ribosome lacked accommodated A-site transfer RNA, indicative of low codon optimality. Loss of the interaction resulted in the inability of the mRNA degradation machinery to sense codon optimality. Our findings elucidate a physical link between the Ccr4-Not complex and the ribosome and provide mechanistic insight into the coupling of decoding efficiency with mRNA stability.
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