A SNP associated with alternative splicing of <it>RPT5b </it>causes unequal redundancy between <it>RPT5a </it>and <it>RPT5b </it>among <it>Arabidopsis thaliana </it>natural variation

<p>Abstract</p> <p>Background</p> <p>The proteasome subunit RPT5, which is essential for gametophyte development, is encoded by two genes in <it>Arabidopsis thaliana</it>; <it>RPT5a </it>and <it>RPT5b</it>. We showed previously that &...

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Main Authors: Guerche Philippe, Bonhomme Sandrine, Lécureuil Alain, Guyon-Debast Anouchka, Gallois Jean-Luc
Format: Article
Language:English
Published: BMC 2010-08-01
Series:BMC Plant Biology
Online Access:http://www.biomedcentral.com/1471-2229/10/158
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spelling doaj-54491a196a49428d91ee2711224c58422020-11-25T00:26:06ZengBMCBMC Plant Biology1471-22292010-08-0110115810.1186/1471-2229-10-158A SNP associated with alternative splicing of <it>RPT5b </it>causes unequal redundancy between <it>RPT5a </it>and <it>RPT5b </it>among <it>Arabidopsis thaliana </it>natural variationGuerche PhilippeBonhomme SandrineLécureuil AlainGuyon-Debast AnouchkaGallois Jean-Luc<p>Abstract</p> <p>Background</p> <p>The proteasome subunit RPT5, which is essential for gametophyte development, is encoded by two genes in <it>Arabidopsis thaliana</it>; <it>RPT5a </it>and <it>RPT5b</it>. We showed previously that <it>RPT5a </it>and <it>RPT5b </it>are fully redundant in the Columbia (Col-0) accession, whereas in the Wassilewskia accession (Ws-4), <it>RPT5b </it>does not complement the effect of a strong <it>rpt5a </it>mutation in the male gametophyte, and only partially complements <it>rpt5a </it>mutation in the sporophyte. <it>RPT5b<sup>Col-0 </sup></it>and <it>RPT5b<sup>Ws-4 </sup></it>differ by only two SNPs, one located in the promoter and the other in the seventh intron of the gene.</p> <p>Results</p> <p>By exploiting natural variation at <it>RPT5b </it>we determined that the SNP located in <it>RPT5b </it>intron seven, rather than the promoter SNP, is the sole basis of this lack of redundancy. In Ws-4 this SNP is predicted to create a new splicing branchpoint sequence that induces a partial mis-splicing of the pre-mRNA, leading to the introduction of a Premature Termination Codon. We characterized 5 accessions carrying this A-to-T substitution in intron seven and observed a complete correlation between this SNP and both a 10 to 20% level of the <it>RPT5b </it>pre-mRNA mis-splicing and the lack of ability to complement an <it>rpt5a </it>mutant phenotype.</p> <p>Conclusion</p> <p>The accession-dependent unequal redundancy between <it>RPT5a </it>and <it>RPT5b </it>genes illustrates an example of evolutionary drifting between duplicated genes through alternative splicing.</p> http://www.biomedcentral.com/1471-2229/10/158
collection DOAJ
language English
format Article
sources DOAJ
author Guerche Philippe
Bonhomme Sandrine
Lécureuil Alain
Guyon-Debast Anouchka
Gallois Jean-Luc
spellingShingle Guerche Philippe
Bonhomme Sandrine
Lécureuil Alain
Guyon-Debast Anouchka
Gallois Jean-Luc
A SNP associated with alternative splicing of <it>RPT5b </it>causes unequal redundancy between <it>RPT5a </it>and <it>RPT5b </it>among <it>Arabidopsis thaliana </it>natural variation
BMC Plant Biology
author_facet Guerche Philippe
Bonhomme Sandrine
Lécureuil Alain
Guyon-Debast Anouchka
Gallois Jean-Luc
author_sort Guerche Philippe
title A SNP associated with alternative splicing of <it>RPT5b </it>causes unequal redundancy between <it>RPT5a </it>and <it>RPT5b </it>among <it>Arabidopsis thaliana </it>natural variation
title_short A SNP associated with alternative splicing of <it>RPT5b </it>causes unequal redundancy between <it>RPT5a </it>and <it>RPT5b </it>among <it>Arabidopsis thaliana </it>natural variation
title_full A SNP associated with alternative splicing of <it>RPT5b </it>causes unequal redundancy between <it>RPT5a </it>and <it>RPT5b </it>among <it>Arabidopsis thaliana </it>natural variation
title_fullStr A SNP associated with alternative splicing of <it>RPT5b </it>causes unequal redundancy between <it>RPT5a </it>and <it>RPT5b </it>among <it>Arabidopsis thaliana </it>natural variation
title_full_unstemmed A SNP associated with alternative splicing of <it>RPT5b </it>causes unequal redundancy between <it>RPT5a </it>and <it>RPT5b </it>among <it>Arabidopsis thaliana </it>natural variation
title_sort snp associated with alternative splicing of <it>rpt5b </it>causes unequal redundancy between <it>rpt5a </it>and <it>rpt5b </it>among <it>arabidopsis thaliana </it>natural variation
publisher BMC
series BMC Plant Biology
issn 1471-2229
publishDate 2010-08-01
description <p>Abstract</p> <p>Background</p> <p>The proteasome subunit RPT5, which is essential for gametophyte development, is encoded by two genes in <it>Arabidopsis thaliana</it>; <it>RPT5a </it>and <it>RPT5b</it>. We showed previously that <it>RPT5a </it>and <it>RPT5b </it>are fully redundant in the Columbia (Col-0) accession, whereas in the Wassilewskia accession (Ws-4), <it>RPT5b </it>does not complement the effect of a strong <it>rpt5a </it>mutation in the male gametophyte, and only partially complements <it>rpt5a </it>mutation in the sporophyte. <it>RPT5b<sup>Col-0 </sup></it>and <it>RPT5b<sup>Ws-4 </sup></it>differ by only two SNPs, one located in the promoter and the other in the seventh intron of the gene.</p> <p>Results</p> <p>By exploiting natural variation at <it>RPT5b </it>we determined that the SNP located in <it>RPT5b </it>intron seven, rather than the promoter SNP, is the sole basis of this lack of redundancy. In Ws-4 this SNP is predicted to create a new splicing branchpoint sequence that induces a partial mis-splicing of the pre-mRNA, leading to the introduction of a Premature Termination Codon. We characterized 5 accessions carrying this A-to-T substitution in intron seven and observed a complete correlation between this SNP and both a 10 to 20% level of the <it>RPT5b </it>pre-mRNA mis-splicing and the lack of ability to complement an <it>rpt5a </it>mutant phenotype.</p> <p>Conclusion</p> <p>The accession-dependent unequal redundancy between <it>RPT5a </it>and <it>RPT5b </it>genes illustrates an example of evolutionary drifting between duplicated genes through alternative splicing.</p>
url http://www.biomedcentral.com/1471-2229/10/158
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