Chimeric RNAs have been reported in varieties of organisms and are conventionally thought to be produced by trans-splicing of two or more distinct transcripts. Here, we conducted a large-scale search for chimeric RNAs in the budding yeast, fruit fly, mouse, and human. Thousands of chimeric transcripts were identified in these organisms except in yeast, in which five chimeric RNAs were observed. RT-PCR experiments for a sample of yeast and fly chimeric transcripts using specific primers show that about one-third of these chimeric RNAs can be reproduced. The results suggest that at least a considerable amount of chimeric RNAs is unlikely from aberrant transcription or splicing, and thus formation of chimeric RNAs is probably a widespread process and can greatly contribute to the complexity of the transcriptome and proteome of organisms. However, only a small fraction (<20%) of these chimeric RNAs has GU-AG at the junction sequences which fits the classical trans-splicing model. In contrast, we observed that about half of the chimeric RNAs have short homologous sequences (SHSs) at the junction sites of the source sequences. Our sequence mutation experiments in yeast showed that disruption of SHSs resulted in the disappearance of the corresponding chimeric RNAs, suggesting that SHSs are essential for generating this kind of chimeric RNA. In addition to the classical trans-splicing model, we propose a new model, the transcriptional slippage model, to explain the generation of those chimeric RNAs synthesized from templates with SHSs.
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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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Evidence ID | Analyze ID | File | Description |
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