In the yeast Saccharomyces cerevisiae, premature translation termination promotes rapid degradation of mRNAs. Accelerated decay requires the presence of specific cis-acting sequences which have been defined as downstream elements. It has been proposed that the role of the downstream element may be to promote translational reinitiation or ribosomal pausing. The GCN4 gene produces an mRNA that contains four short upstream open reading frames (uORFs) preceding the GCN4 protein-coding region in which translational initiation and reinitiation events occur. It was anticipated that these uORFs would function in a manner analogous to nonsense codons, promoting rapid degradation of the mRNA. However, the GCN4 transcript was not degraded by the nonsense-mediated mRNA decay pathway. We have investigated the role of the leader region of the GCN4 transcript in an effort to identify possible sequence elements that inactivate this decay pathway. We show that the GCN4 leader region does not harbor a downstream element needed to promote mRNA decay. In addition, using hybrid GCN4-PGK1 transcripts, we demonstrate that if a translational reinitiation signal precedes a downstream element, the mRNA will no longer be sensitive to nonsense-mediated decay. Furthermore, we demonstrate that the downstream element is functional only after a translational initiation and termination cycle has been completed but is unable to promote nonsense-mediated mRNA decay if it is situated 5' of a translational initiation site. Based on these results, the role of the downstream element will be discussed.
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Evidence ID | Analyze ID | Gene/Complex | Systematic Name/Complex Accession | Qualifier | Gene Ontology Term ID | Gene Ontology Term | Aspect | Annotation Extension | Evidence | Method | Source | Assigned On | Reference |
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Evidence ID | Analyze ID | Gene | Gene Systematic Name | Phenotype | Experiment Type | Experiment Type Category | Mutant Information | Strain Background | Chemical | Details | Reference |
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Evidence ID | Analyze ID | Gene | Gene Systematic Name | Disease Ontology Term | Disease Ontology Term ID | Qualifier | Evidence | Method | Source | Assigned On | Reference |
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Evidence ID | Analyze ID | Regulator | Regulator Systematic Name | Target | Target Systematic Name | Direction | Regulation of | Happens During | Regulator Type | Direction | Regulation Of | Happens During | Method | Evidence | Strain Background | Reference |
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Site | Modification | Modifier | Source | Reference |
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Evidence ID | Analyze ID | Interactor | Interactor Systematic Name | Interactor | Interactor Systematic Name | Allele | Assay | Annotation | Action | Phenotype | SGA score | P-value | Source | Reference | Note |
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Evidence ID | Analyze ID | Interactor | Interactor Systematic Name | Interactor | Interactor Systematic Name | Assay | Annotation | Action | Modification | Source | Reference | Note |
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Complement ID | Locus ID | Gene | Species | Gene ID | Strain background | Direction | Details | Source | Reference |
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Evidence ID | Analyze ID | Dataset | Description | Keywords | Number of Conditions | Reference |
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