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Nucleic Acids Research 2004 32(17):4969-4978; doi:10.1093/nar/gkh823
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Published online 23 September 2004

Nucleic Acids Research, Vol. 32 No. 17 © Oxford University Press 2004; all rights reserved

Transcription-coupled and splicing-coupled strand asymmetries in eukaryotic genomes

Marie Touchon, Alain Arneodo1, Yves d'Aubenton-Carafa and Claude Thermes*

Centre de Génétique Moléculaire (CNRS), Allée de la Terrasse, 91198 Gif-sur-Yvette, France and 1 Laboratoire de Physique, Ecole Normale Supérieure de Lyon, 46 Allée d'Italie, 69364 Lyon Cedex 07, France

* To whom correspondence should be addressed. Tel: +33 1 69 82 38 28; Fax: +33 1 69 82 38 77; Email: thermes{at}cgm.cnrs-gif.fr

Received May 7, 2004; Revised July 27, 2004; Accepted August 25, 2004

Under no-strand bias conditions, each genomic DNA strand should present equimolarities of A and T and of G and C. Deviations from these rules are attributed to asymmetric properties intrinsic to DNA mutation–repair processes. In bacteria, strand biases are associated with replication or transcription. In eukaryotes, recent studies demonstrate that human genes present transcription-coupled biases that might reflect transcription-coupled repair processes. Here, we study strand asymmetries in intron sequences of evolutionarily distant eukaryotes, and show that two superimposed intron biases can be distinguished. (i) Biases that are maximum at intron extremities and decrease over large distances to zero values in internal regions, possibly reflecting interactions between pre-mRNA and splicing machinery; these extend over ~0.5 kb in mammals and Arabidopsis thaliana, and over 1 kb in Caenorhabditis elegans and Drosophila melanogaster. (ii) Biases that are constant along introns, possibly associated with transcription. Strikingly, in C.elegans, these latter biases extend over intergenic regions that separate co-oriented genes. When appropriately examined, all genomes present transcription-coupled excess of T over A in the coding strand. On the opposite, GC skews are either positive (mammals, plants) or negative (invertebrates). These results suggest that transcription-coupled asymmetries result from mutation–repair mechanisms that differ between vertebrates and invertebrates.


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