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How Athila retrotransposons survive in the Arabidopsis genome

BACKGROUND: Transposable elements are selfish genetic sequences which only occasionally provide useful functions to their host species. In addition, models of mobile element evolution assume a second type of selfishness: elements of different familes do not cooperate, but they independently fight fo...

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Detalles Bibliográficos
Autores principales: Marco, Antonio, Marín, Ignacio
Formato: Texto
Lenguaje:English
Publicado: BioMed Central 2008
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2410132/
https://www.ncbi.nlm.nih.gov/pubmed/18479510
http://dx.doi.org/10.1186/1471-2164-9-219
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author Marco, Antonio
Marín, Ignacio
author_facet Marco, Antonio
Marín, Ignacio
author_sort Marco, Antonio
collection PubMed
description BACKGROUND: Transposable elements are selfish genetic sequences which only occasionally provide useful functions to their host species. In addition, models of mobile element evolution assume a second type of selfishness: elements of different familes do not cooperate, but they independently fight for their survival in the host genome. RESULTS: We show that recombination events among distantly related Athila retrotransposons have led to the generation of new Athila lineages. Their pattern of diversification suggests that Athila elements survive in Arabidopsis by a combination of selfish replication and of amplification of highly diverged copies with coding potential. Many Athila elements are non-autonomous but still conserve intact open reading frames which are under the effect of negative, purifying natural selection. CONCLUSION: The evolution of these mobile elements is far more complex than hitherto assumed. Strict selfish replication does not explain all the patterns observed.
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spelling pubmed-24101322008-06-05 How Athila retrotransposons survive in the Arabidopsis genome Marco, Antonio Marín, Ignacio BMC Genomics Research Article BACKGROUND: Transposable elements are selfish genetic sequences which only occasionally provide useful functions to their host species. In addition, models of mobile element evolution assume a second type of selfishness: elements of different familes do not cooperate, but they independently fight for their survival in the host genome. RESULTS: We show that recombination events among distantly related Athila retrotransposons have led to the generation of new Athila lineages. Their pattern of diversification suggests that Athila elements survive in Arabidopsis by a combination of selfish replication and of amplification of highly diverged copies with coding potential. Many Athila elements are non-autonomous but still conserve intact open reading frames which are under the effect of negative, purifying natural selection. CONCLUSION: The evolution of these mobile elements is far more complex than hitherto assumed. Strict selfish replication does not explain all the patterns observed. BioMed Central 2008-05-14 /pmc/articles/PMC2410132/ /pubmed/18479510 http://dx.doi.org/10.1186/1471-2164-9-219 Text en Copyright © 2008 Marco and Marín; 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 Research Article
Marco, Antonio
Marín, Ignacio
How Athila retrotransposons survive in the Arabidopsis genome
title How Athila retrotransposons survive in the Arabidopsis genome
title_full How Athila retrotransposons survive in the Arabidopsis genome
title_fullStr How Athila retrotransposons survive in the Arabidopsis genome
title_full_unstemmed How Athila retrotransposons survive in the Arabidopsis genome
title_short How Athila retrotransposons survive in the Arabidopsis genome
title_sort how athila retrotransposons survive in the arabidopsis genome
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2410132/
https://www.ncbi.nlm.nih.gov/pubmed/18479510
http://dx.doi.org/10.1186/1471-2164-9-219
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