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Accumulation of GC donor splice signals in mammals

The GT dinucleotide in the first two intron positions is the most conserved element of the U2 donor splice signals. However, in a small fraction of donor sites, GT is replaced by GC. A substantial enrichment of GC in donor sites of alternatively spliced genes has been observed previously in human, n...

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Detalles Bibliográficos
Autores principales: Churbanov, Alexander, Winters-Hilt, Stephen, Koonin, Eugene V, Rogozin, Igor B
Formato: Texto
Lenguaje:English
Publicado: BioMed Central 2008
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2490688/
https://www.ncbi.nlm.nih.gov/pubmed/18613975
http://dx.doi.org/10.1186/1745-6150-3-30
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author Churbanov, Alexander
Winters-Hilt, Stephen
Koonin, Eugene V
Rogozin, Igor B
author_facet Churbanov, Alexander
Winters-Hilt, Stephen
Koonin, Eugene V
Rogozin, Igor B
author_sort Churbanov, Alexander
collection PubMed
description The GT dinucleotide in the first two intron positions is the most conserved element of the U2 donor splice signals. However, in a small fraction of donor sites, GT is replaced by GC. A substantial enrichment of GC in donor sites of alternatively spliced genes has been observed previously in human, nematode and Arabidopsis, suggesting that GC signals are important for regulation of alternative splicing. We used parsimony analysis to reconstruct evolution of donor splice sites and inferred 298 GT > GC conversion events compared to 40 GC > GT conversion events in primate and rodent genomes. Thus, there was substantive accumulation of GC donor splice sites during the evolution of mammals. Accumulation of GC sites might have been driven by selection for alternative splicing. This article was reviewed by Jerzy Jurka and Anton Nekrutenko. For the full reviews, please go to the Reviewers' Reports section.
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spelling pubmed-24906882008-07-30 Accumulation of GC donor splice signals in mammals Churbanov, Alexander Winters-Hilt, Stephen Koonin, Eugene V Rogozin, Igor B Biol Direct Discovery Notes The GT dinucleotide in the first two intron positions is the most conserved element of the U2 donor splice signals. However, in a small fraction of donor sites, GT is replaced by GC. A substantial enrichment of GC in donor sites of alternatively spliced genes has been observed previously in human, nematode and Arabidopsis, suggesting that GC signals are important for regulation of alternative splicing. We used parsimony analysis to reconstruct evolution of donor splice sites and inferred 298 GT > GC conversion events compared to 40 GC > GT conversion events in primate and rodent genomes. Thus, there was substantive accumulation of GC donor splice sites during the evolution of mammals. Accumulation of GC sites might have been driven by selection for alternative splicing. This article was reviewed by Jerzy Jurka and Anton Nekrutenko. For the full reviews, please go to the Reviewers' Reports section. BioMed Central 2008-07-09 /pmc/articles/PMC2490688/ /pubmed/18613975 http://dx.doi.org/10.1186/1745-6150-3-30 Text en Copyright © 2008 Churbanov et al; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( (http://creativecommons.org/licenses/by/2.0) ), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Discovery Notes
Churbanov, Alexander
Winters-Hilt, Stephen
Koonin, Eugene V
Rogozin, Igor B
Accumulation of GC donor splice signals in mammals
title Accumulation of GC donor splice signals in mammals
title_full Accumulation of GC donor splice signals in mammals
title_fullStr Accumulation of GC donor splice signals in mammals
title_full_unstemmed Accumulation of GC donor splice signals in mammals
title_short Accumulation of GC donor splice signals in mammals
title_sort accumulation of gc donor splice signals in mammals
topic Discovery Notes
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2490688/
https://www.ncbi.nlm.nih.gov/pubmed/18613975
http://dx.doi.org/10.1186/1745-6150-3-30
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