Exonization of active mouse L1s: a driver of transcriptome evolution?
- Equal contributors
1 Department of Computational Molecular Biology, Max-Planck-Institute for Molecular Genetics, Ihnestrasse 73, D-14195 Berlin, Germany
2 Department of Bioinformatics, University of Würzburg, Am Hubland, D-97074 Würzburg, Germany
3 Department of Genetics, University of Leicester, University Road, Leicester LE1 7RH, UK
BMC Genomics 2007, 8:392 doi:10.1186/1471-2164-8-392Published: 26 October 2007
Long interspersed nuclear elements (LINE-1s, L1s) have been recently implicated in the regulation of mammalian transcriptomes.
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.
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.