| 1. |
- Carninci, P, et al.
(författare)
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The transcriptional landscape of the mammalian genome
- 2005
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Ingår i: Science (New York, N.Y.). - : American Association for the Advancement of Science (AAAS). - 1095-9203 .- 0036-8075. ; 309:5740, s. 1559-1563
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Tidskriftsartikel (refereegranskat)abstract
- This study describes comprehensive polling of transcription start and termination sites and analysis of previously unidentified full-length complementary DNAs derived from the mouse genome. We identify the 5′ and 3′ boundaries of 181,047 transcripts with extensive variation in transcripts arising from alternative promoter usage, splicing, and polyadenylation. There are 16,247 new mouse protein-coding transcripts, including 5154 encoding previously unidentified proteins. Genomic mapping of the transcriptome reveals transcriptional forests, with overlapping transcription on both strands, separated by deserts in which few transcripts are observed. The data provide a comprehensive platform for the comparative analysis of mammalian transcriptional regulation in differentiation and development.
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| 2. |
- Forrest, ARR, et al.
(författare)
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A promoter-level mammalian expression atlas
- 2014
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Ingår i: Nature. - : Springer Science and Business Media LLC. - 1476-4687 .- 0028-0836. ; 507:7493, s. 462-
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Tidskriftsartikel (refereegranskat)
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| 3. |
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| 4. |
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| 5. |
- Frith, Martin C., et al.
(författare)
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Pseudo-messenger RNA : Phantoms of the transcriptome
- 2006
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Ingår i: PLoS Genetics. - : Public Library of Science (PLoS). - 1553-7390 .- 1553-7404. ; 2:4, s. 504-514
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Tidskriftsartikel (refereegranskat)abstract
- The mammalian transcriptome harbours shadowy entities that resist classification and analysis. In analogy with pseudogenes, we define pseudo-messenger RNA to be RNA molecules that resemble protein- coding mRNA, but cannot encode full-length proteins owing to disruptions of the reading frame. Using a rigorous computational pipeline, which rules out sequencing errors, we identify 10,679 pseudo - messenger RNAs ( approximately half of which are transposonassociated) among the 102,801 FANTOM3 mouse cDNAs: just over 10% of the FANTOM3 transcriptome. These comprise not only transcribed pseudogenes, but also disrupted splice variants of otherwise protein- coding genes. Some may encode truncated proteins, only a minority of which appear subject to nonsense- mediated decay. The presence of an excess of transcripts whose only disruptions are opal stop codons suggests that there are more selenoproteins than currently estimated. We also describe compensatory frameshifts, where a segment of the gene has changed frame but remains translatable. In summary, we survey a large class of non- standard but potentially functional transcripts that are likely to encode genetic information and effect biological processes in novel ways. Many of these transcripts do not correspond cleanly to any identifiable object in the genome, implying fundamental limits to the goal of annotating all functional elements at the genome sequence level.
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| 6. |
- Huminiecki, L, et al.
(författare)
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Divergence of spatial gene expression profiles following species-specific gene duplications in human and mouse
- 2004
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Ingår i: Genome research. - : Cold Spring Harbor Laboratory. - 1088-9051. ; 14:10A, s. 1870-1879
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Tidskriftsartikel (refereegranskat)abstract
- To examine the process by which duplicated genes diverge in function, we studied how the gene expression profiles of orthologous gene sets in human and mouse are affected by the presence of additional recent species-specific paralogs. Gene expression profiles were compared across 16 homologous tissues in human and mouse using microarray data from the Gene Expression Atlas for 1575 sets of orthologs including 250 with species-specific paralogs. We find that orthologs that have undergone recent duplication are less likely to have strongly correlated expression profiles than those that remain in a one-to-one relationship between human and mouse. There is a general trend for paralogous genes to become more specialized in their expression patterns, with decreased breadth and increased specificity of expression as gene family size increases. Despite this trend, detailed examination of some particular gene families where species-specific duplications have occurred indicated several examples of apparent neofunctionalization of duplicated genes, but only one case of subfunctionalization. Often, the expression of both copies of a duplicated gene appears to have changed relative to the ancestral state. Our results suggest that gene expression profiles are surprisingly labile and that expression in a particular tissue may be gained or lost repeatedly during the evolution of even small gene families. We conclude that gene duplication is a major driving force behind the emergence of divergent gene expression patterns.
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