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Briefings in Functional Genomics (1)
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Gebauer, Fátima (3)
Cuesta, Rafael (1)
Martínez-Sánchez, Aida (1)
Szostak, Emilia (1)
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Versatility of the translational machinery during stress: changing partners to keep dancing
Cap-dependent translation is initiated by the binding of eIF4E to the cap structure at the 5′ end of mRNAs. During hypoxic stress, global translation decreases because eIF4E is inactivated. In a recent article in Nature, Lee and colleagues show that residual hypoxic translation is maintained by a specialized isoform of eIF4E, which binds to target mRNAs in complex with a hypoxia-induced RNP.
Translational control by 3′-UTR-binding proteins
Briefings in Functional Genomics
The regulation of mRNA translation is a major checkpoint in the flux of information from the transcriptome to the proteome. Critical for translational control are the trans-acting factors, RNA-binding proteins (RBPs) and small RNAs that bind to the mRNA and modify its translatability. This review summarizes the mechanisms by which RBPs regulate mRNA translation, with special focus on those binding to the 3′-untranslated region. It also discusses how recent high-throughput technologies are revealing exquisite layers of complexity and are helping to untangle translational regulation at a genome-wide scale.
RNA-binding protein; translation; UTR; RNP; CLIP; ribosome profiling
miR-181a Regulates Cap-Dependent Translation of p27kip1 mRNA in Myeloid Cells▿
Molecular and Cellular Biology
p27kip1 (p27) is a cell cycle inhibitor and tumor suppressor whose expression is tightly regulated in the cell. Translational control of p27 mRNA has emerged as a prominent mechanism to regulate p27 expression during differentiation, quiescence, and cancer progression. The microRNAs miR-221 and miR-222 repress p27 expression in various cancer cells, and this repression promotes tumor cell proliferation. In addition, the presence of an internal ribosome entry site in the 5′ untranslated region (UTR) of p27 mRNA has been reported. Here, we show that p27 mRNA is translated via a cap-dependent mechanism in HeLa and HL60 cells and that the previously reported IRES activity can be attributed to cryptic promoters in the sequence corresponding to the p27 5′ UTR. Furthermore, cap-dependent translation of p27 mRNA is repressed by miR-181a in undifferentiated HL60 cells. Repression by miR-181a is relieved during differentiation of HL60 into monocyte-like cells, allowing the accumulation of p27, which is necessary to fully block cell cycle progression and reach terminal differentiation. These results identify miR-181a as a regulator of p27 mRNA translation during myeloid cell differentiation.
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