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  Exonization of active mouse L1s: a driver of transcriptome evolution?

Zemojtel, T., Penzkofer, T., Schultz, J., Dandekar, T., Badge, R., & Vingron, M. (2007). Exonization of active mouse L1s: a driver of transcriptome evolution? BMC Genomics, 8, e392-e392. doi:10.1186/1471-2164-8-392.

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Item Permalink: http://hdl.handle.net/11858/00-001M-0000-0010-813C-0 Version Permalink: http://hdl.handle.net/11858/00-001M-0000-0010-813D-E
Genre: Journal Article
Alternative Title : BMC Genomics

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Zemojtel, Tomasz1, Author              
Penzkofer, Tobias, Author
Schultz, Jörg, Author
Dandekar, Thomas, Author
Badge, Richard, Author
Vingron, Martin2, Author              
Affiliations:
1Dept. of Computational Molecular Biology (Head: Martin Vingron), Max Planck Institute for Molecular Genetics, Max Planck Society, ou_1433547              
2Gene regulation (Martin Vingron), Dept. of Computational Molecular Biology (Head: Martin Vingron), Max Planck Institute for Molecular Genetics, Max Planck Society, ou_1479639              

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 Abstract: Background: Long interspersed nuclear elements (LINE-1s, L1s) have been recently implicated in the regulation of mammalian transcriptomes. Results: Here, we show that members of the three active mouse L1 subfamilies (A, GF and TF) contain, in addition to those on their sense strands, conserved functional splice sites on their antisense strands, which trigger multiple exonization events. The latter is particularly intriguing in the light of the strong antisense orientation bias of intronic L1s, implying that the toleration of antisense insertions results in an increased potential for exonization. Conclusion: In a genome-wide analysis, we have uncovered evidence suggesting that the mobility of the large number of retrotransposition-competent mouse L1s (~2400 potentially active L1s in NCBIm35) has significant potential to shape the mouse transcriptome by continuously generating insertions into transcriptional units.

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Language(s): eng - English
 Dates: 2007-10-26
 Publication Status: Published in print
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Title: BMC Genomics
  Alternative Title : BMC Genomics
Source Genre: Journal
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Pages: - Volume / Issue: 8 Sequence Number: - Start / End Page: e392 - e392 Identifier: ISSN: 1471-2164