Journal
CELL
Volume 176, Issue 3, Pages 625-+Publisher
CELL PRESS
DOI: 10.1016/j.cell.2018.12.030
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Funding
- Chinese Academy of Sciences of China [XDB29010203, KFZD-SW-209]
- National Health Commission of China [2017ZX10201101-001-005]
- Ministry of Science and Technology of China [2018YFA0507202]
- National Natural Science Foundation of China [81530066]
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Programmed -1 ribosomal frameshifting (-1PRF) is a widely used translation recoding mechanism. HIV-1 expresses Gag-Pol protein from the Gag-coding mRNA through -1PRF, and the ratio of Gag to Gag-Pol is strictly maintained for efficient viral replication. Here, we report that the interferon-stimulated gene product C19orf66 (herein named Shiftless) is a host factor that inhibits the -1PRF of HIV-1. Shiftless (SFL) also inhibited the -1PRF of a variety of mRNAs from both viruses and cellular genes. SFL interacted with the -1PRF signal of target mRNA and translating ribosomes and caused premature translation termination at the frameshifting site. Downregulation of translation release factor eRF3 or eRF1 reduced SFL-mediated premature translation termination. We propose that SFL binding to target mRNA and the translating ribosome interferes with the frameshifting process. These findings identify SFL as a broad-spectrum inhibitor of -1PRF and help to further elucidate the mechanisms of -1PRF.
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