The thermodynamic patterns of eukaryotic genes suggest a mechanism for intron–exon recognition

Marina N. Nedelcheva-Veleva, Mihail Sarov, Ivan Yanakiev, Eva Mihailovska, Miroslav P. Ivanov, Greta C. Panova and Stoyno S. Stoynov ()
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Marina N. Nedelcheva-Veleva: Institute of Molecular Biology ‘Roumen Tsanev’, Bulgarian Academy of Sciences
Mihail Sarov: Max Planck Institute of Molecular Cell Biology and Genetics, Pfotenhauerstrasse 108, Dresden 01307, Germany
Ivan Yanakiev: Institute of Molecular Biology ‘Roumen Tsanev’, Bulgarian Academy of Sciences
Eva Mihailovska: Institute of Molecular Biology ‘Roumen Tsanev’, Bulgarian Academy of Sciences
Miroslav P. Ivanov: Institute of Molecular Biology ‘Roumen Tsanev’, Bulgarian Academy of Sciences
Greta C. Panova: University of California Los Angeles, 520 Portola Plaza Math Sciences Building, Los Angeles, California 90095, USA
Stoyno S. Stoynov: Institute of Molecular Biology ‘Roumen Tsanev’, Bulgarian Academy of Sciences

Nature Communications, 2013, vol. 4, issue 1, 1-12

Abstract: Abstract The essential cis- and trans-acting elements required for RNA splicing have been defined, however, the detailed molecular mechanisms underlying intron–exon recognition are still unclear. Here we demonstrate that the ratio between stability of mRNA/DNA and DNA/DNA duplexes near 3′-spice sites is a characteristic feature that can contribute to intron–exon differentiation. Remarkably, throughout all transcripts, the most unstable mRNA/DNA duplexes, compared with the corresponding DNA/DNA duplexes, are situated upstream of the 3′-splice sites and include the polypyrimidine tracts. This characteristic instability is less pronounced in weak alternative splice sites and disease-associated cryptic 3′-splice sites. Our results suggest that this thermodynamic pattern can prevent the re-annealing of mRNA to the DNA template behind the RNA polymerase to ensure access of the splicing machinery to the polypyrimidine tract and the branch point. In support of this mechanism, we demonstrate that RNA/DNA duplex formation at this region prevents pre-spliceosome A complex assembly.

Date: 2013
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DOI: 10.1038/ncomms3101

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