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The Potential for pathogenicity was present in the ancestor of the Ascomycete subphylum Pezizomycotina

BACKGROUND: Previous studies in Ascomycetes have shown that the function of gene families of which the size is considerably larger in extant pathogens than in non-pathogens could be related to pathogenicity traits. However, by only comparing gene inventories in extant species, no insights can be gai...

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Autores principales: Sánchez-Rodríguez, Aminael, Martens, Cindy, Engelen, Kristof, Van de Peer, Yves, Marchal, Kathleen
Formato: Texto
Lenguaje:English
Publicado: BioMed Central 2010
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3087541/
https://www.ncbi.nlm.nih.gov/pubmed/20964831
http://dx.doi.org/10.1186/1471-2148-10-318
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author Sánchez-Rodríguez, Aminael
Martens, Cindy
Engelen, Kristof
Van de Peer, Yves
Marchal, Kathleen
author_facet Sánchez-Rodríguez, Aminael
Martens, Cindy
Engelen, Kristof
Van de Peer, Yves
Marchal, Kathleen
author_sort Sánchez-Rodríguez, Aminael
collection PubMed
description BACKGROUND: Previous studies in Ascomycetes have shown that the function of gene families of which the size is considerably larger in extant pathogens than in non-pathogens could be related to pathogenicity traits. However, by only comparing gene inventories in extant species, no insights can be gained into the evolutionary process that gave rise to these larger family sizes in pathogens. Moreover, most studies which consider gene families in extant species only tend to explain observed differences in gene family sizes by gains rather than by losses, hereby largely underestimating the impact of gene loss during genome evolution. RESULTS: In our study we used a selection of recently published genomes of Ascomycetes to analyze how gene family gains, duplications and losses have affected the origin of pathogenic traits. By analyzing the evolutionary history of gene families we found that most gene families with an enlarged size in pathogens were present in an ancestor common to both pathogens and non-pathogens. The majority of these families were selectively maintained in pathogenic lineages, but disappeared in non-pathogens. Non-pathogen-specific losses largely outnumbered pathogen-specific losses. CONCLUSIONS: We conclude that most of the proteins for pathogenicity were already present in the ancestor of the Ascomycete lineages we used in our study. Species that did not develop pathogenicity seemed to have reduced their genetic complexity compared to their ancestors. We further show that expansion of gained or already existing families in a species-specific way is important to fine-tune the specificities of the pathogenic host-fungus interaction.
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spelling pubmed-30875412011-05-05 The Potential for pathogenicity was present in the ancestor of the Ascomycete subphylum Pezizomycotina Sánchez-Rodríguez, Aminael Martens, Cindy Engelen, Kristof Van de Peer, Yves Marchal, Kathleen BMC Evol Biol Research Article BACKGROUND: Previous studies in Ascomycetes have shown that the function of gene families of which the size is considerably larger in extant pathogens than in non-pathogens could be related to pathogenicity traits. However, by only comparing gene inventories in extant species, no insights can be gained into the evolutionary process that gave rise to these larger family sizes in pathogens. Moreover, most studies which consider gene families in extant species only tend to explain observed differences in gene family sizes by gains rather than by losses, hereby largely underestimating the impact of gene loss during genome evolution. RESULTS: In our study we used a selection of recently published genomes of Ascomycetes to analyze how gene family gains, duplications and losses have affected the origin of pathogenic traits. By analyzing the evolutionary history of gene families we found that most gene families with an enlarged size in pathogens were present in an ancestor common to both pathogens and non-pathogens. The majority of these families were selectively maintained in pathogenic lineages, but disappeared in non-pathogens. Non-pathogen-specific losses largely outnumbered pathogen-specific losses. CONCLUSIONS: We conclude that most of the proteins for pathogenicity were already present in the ancestor of the Ascomycete lineages we used in our study. Species that did not develop pathogenicity seemed to have reduced their genetic complexity compared to their ancestors. We further show that expansion of gained or already existing families in a species-specific way is important to fine-tune the specificities of the pathogenic host-fungus interaction. BioMed Central 2010-10-21 /pmc/articles/PMC3087541/ /pubmed/20964831 http://dx.doi.org/10.1186/1471-2148-10-318 Text en Copyright ©2010 Sánchez-Rodríguez 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 Research Article
Sánchez-Rodríguez, Aminael
Martens, Cindy
Engelen, Kristof
Van de Peer, Yves
Marchal, Kathleen
The Potential for pathogenicity was present in the ancestor of the Ascomycete subphylum Pezizomycotina
title The Potential for pathogenicity was present in the ancestor of the Ascomycete subphylum Pezizomycotina
title_full The Potential for pathogenicity was present in the ancestor of the Ascomycete subphylum Pezizomycotina
title_fullStr The Potential for pathogenicity was present in the ancestor of the Ascomycete subphylum Pezizomycotina
title_full_unstemmed The Potential for pathogenicity was present in the ancestor of the Ascomycete subphylum Pezizomycotina
title_short The Potential for pathogenicity was present in the ancestor of the Ascomycete subphylum Pezizomycotina
title_sort potential for pathogenicity was present in the ancestor of the ascomycete subphylum pezizomycotina
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3087541/
https://www.ncbi.nlm.nih.gov/pubmed/20964831
http://dx.doi.org/10.1186/1471-2148-10-318
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