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Paleo-evolutionary plasticity of plant disease resistance genes

BACKGROUND: The recent access to a large set of genome sequences, combined with a robust evolutionary scenario of modern monocot (i.e. grasses) and eudicot (i.e. rosids) species from their founder ancestors, offered the opportunity to gain insights into disease resistance genes (R-genes) evolutionar...

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Autores principales: Zhang, Rongzhi, Murat, Florent, Pont, Caroline, Langin, Thierry, Salse, Jerome
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2014
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4234491/
https://www.ncbi.nlm.nih.gov/pubmed/24617999
http://dx.doi.org/10.1186/1471-2164-15-187
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author Zhang, Rongzhi
Murat, Florent
Pont, Caroline
Langin, Thierry
Salse, Jerome
author_facet Zhang, Rongzhi
Murat, Florent
Pont, Caroline
Langin, Thierry
Salse, Jerome
author_sort Zhang, Rongzhi
collection PubMed
description BACKGROUND: The recent access to a large set of genome sequences, combined with a robust evolutionary scenario of modern monocot (i.e. grasses) and eudicot (i.e. rosids) species from their founder ancestors, offered the opportunity to gain insights into disease resistance genes (R-genes) evolutionary plasticity. RESULTS: We unravel in the current article (i) a R-genes repertoire consisting in 7883 for monocots and 15758 for eudicots, (ii) a contrasted R-genes conservation with 23.8% for monocots and 6.6% for dicots, (iii) a minimal ancestral founder pool of 384 R-genes for the monocots and 150 R-genes for the eudicots, (iv) a general pattern of organization in clusters accounting for more than 60% of mapped R-genes, (v) a biased deletion of ancestral duplicated R-genes between paralogous blocks possibly compensated by clusterization, (vi) a bias in R-genes clusterization where Leucine-Rich Repeats act as a ‘glue’ for domain association, (vii) a R-genes/miRNAs interome enriched toward duplicated R-genes. CONCLUSIONS: Together, our data may suggest that R-genes family plasticity operated during plant evolution (i) at the structural level through massive duplicates loss counterbalanced by massive clusterization following polyploidization; as well as at (ii) the regulation level through microRNA/R-gene interactions acting as a possible source of functional diploidization of structurally retained R-genes duplicates. Such evolutionary shuffling events leaded to CNVs (i.e. Copy Number Variation) and PAVs (i.e. Presence Absence Variation) between related species operating in the decay of R-genes colinearity between plant species.
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spelling pubmed-42344912014-11-19 Paleo-evolutionary plasticity of plant disease resistance genes Zhang, Rongzhi Murat, Florent Pont, Caroline Langin, Thierry Salse, Jerome BMC Genomics Research Article BACKGROUND: The recent access to a large set of genome sequences, combined with a robust evolutionary scenario of modern monocot (i.e. grasses) and eudicot (i.e. rosids) species from their founder ancestors, offered the opportunity to gain insights into disease resistance genes (R-genes) evolutionary plasticity. RESULTS: We unravel in the current article (i) a R-genes repertoire consisting in 7883 for monocots and 15758 for eudicots, (ii) a contrasted R-genes conservation with 23.8% for monocots and 6.6% for dicots, (iii) a minimal ancestral founder pool of 384 R-genes for the monocots and 150 R-genes for the eudicots, (iv) a general pattern of organization in clusters accounting for more than 60% of mapped R-genes, (v) a biased deletion of ancestral duplicated R-genes between paralogous blocks possibly compensated by clusterization, (vi) a bias in R-genes clusterization where Leucine-Rich Repeats act as a ‘glue’ for domain association, (vii) a R-genes/miRNAs interome enriched toward duplicated R-genes. CONCLUSIONS: Together, our data may suggest that R-genes family plasticity operated during plant evolution (i) at the structural level through massive duplicates loss counterbalanced by massive clusterization following polyploidization; as well as at (ii) the regulation level through microRNA/R-gene interactions acting as a possible source of functional diploidization of structurally retained R-genes duplicates. Such evolutionary shuffling events leaded to CNVs (i.e. Copy Number Variation) and PAVs (i.e. Presence Absence Variation) between related species operating in the decay of R-genes colinearity between plant species. BioMed Central 2014-03-12 /pmc/articles/PMC4234491/ /pubmed/24617999 http://dx.doi.org/10.1186/1471-2164-15-187 Text en Copyright © 2014 Zhang 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 credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
spellingShingle Research Article
Zhang, Rongzhi
Murat, Florent
Pont, Caroline
Langin, Thierry
Salse, Jerome
Paleo-evolutionary plasticity of plant disease resistance genes
title Paleo-evolutionary plasticity of plant disease resistance genes
title_full Paleo-evolutionary plasticity of plant disease resistance genes
title_fullStr Paleo-evolutionary plasticity of plant disease resistance genes
title_full_unstemmed Paleo-evolutionary plasticity of plant disease resistance genes
title_short Paleo-evolutionary plasticity of plant disease resistance genes
title_sort paleo-evolutionary plasticity of plant disease resistance genes
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4234491/
https://www.ncbi.nlm.nih.gov/pubmed/24617999
http://dx.doi.org/10.1186/1471-2164-15-187
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