期刊
MOLECULAR AND CELLULAR BIOLOGY
卷 33, 期 5, 页码 1016-1026出版社
AMER SOC MICROBIOLOGY
DOI: 10.1128/MCB.00879-12
关键词
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资金
- National Institutes of Health [R01GM084547, 3R01GM084547-01A1S1]
- UAB Cancer Center HIV-Associated Malignancy pilot research grant (UAB Comprehensive Cancer Center core support grant) [P30 CA13148]
- Medical Research Council [MC_UP_A600_1023] Funding Source: researchfish
- MRC [MC_UP_A600_1023] Funding Source: UKRI
During viral infection or cellular stress, cap-dependent translation is shut down. Proteins that are synthesized under these conditions use alternative mechanisms to initiate translation. This study demonstrates that at least two alternative translation initiation routes, internal ribosome entry site (IRES) initiation and ribosome shunting, rely on ribosomal protein S25 (RPS25). This suggests that they share a mechanism for initiation that is not employed by cap-dependent translation, since cap-dependent translation is not affected by the loss of RPS25. Furthermore, we demonstrate that viruses that utilize an IRES or a ribosome shunt, such as hepatitis C virus, poliovirus, or adenovirus, have impaired amplification in cells depleted of RPS25. In contrast, viral amplification of a virus that relies solely on cap-dependent translation, herpes simplex virus, is not hindered. We present a model that explains how RPS25 can be a nexus for multiple alternative translation initiation pathways.
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