| First Author | Lin Y | Year | 2020 |
| Journal | Mol Cell | Volume | 79 |
| Issue | 4 | Pages | 575-587.e7 |
| PubMed ID | 32589965 | Mgi Jnum | J:297177 |
| Mgi Id | MGI:6468946 | Doi | 10.1016/j.molcel.2020.06.003 |
| Citation | Lin Y, et al. (2020) eIF3 Associates with 80S Ribosomes to Promote Translation Elongation, Mitochondrial Homeostasis, and Muscle Health. Mol Cell 79(4):575-587.e7 |
| abstractText | eIF3, a multi-subunit complex with numerous functions in canonical translation initiation, is known to interact with 40S and 60S ribosomal proteins and translation elongation factors, but a direct involvement in translation elongation has never been demonstrated. We found that eIF3 deficiency reduced early ribosomal elongation speed between codons 25 and 75 on a set of approximately 2,700 mRNAs encoding proteins associated with mitochondrial and membrane functions, resulting in defective synthesis of their encoded proteins. To promote elongation, eIF3 interacts with 80S ribosomes translating the first approximately 60 codons and serves to recruit protein quality-control factors, functions required for normal mitochondrial physiology. Accordingly, eIF3e(+/-) mice accumulate defective mitochondria in skeletal muscle and show a progressive decline in muscle strength. Hence, eIF3 interacts with 80S ribosomes to enhance, at the level of early elongation, the synthesis of proteins with membrane-associated functions, an activity that is critical for mitochondrial physiology and muscle health. |
