Table_1_Disentangling Genetic Variation for Resistance and Endurance to Scuticociliatosis in Turbot Using Pedigree and Genomic Information.xlsx

Selective breeding for improving host responses to infectious pathogens is a promising option for disease control. In fact, disease resilience, the ability of a host to survive or cope with infectious challenge, has become a highly desirable breeding goal. However, resilience is a complex trait comp...

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Main Authors: María Saura, María J. Carabaño, Almudena Fernández, Santiago Cabaleiro, Andrea B. Doeschl-Wilson, Osvaldo Anacleto, Francesco Maroso, Adrián Millán, Miguel Hermida, Carlos Fernández, Paulino Martínez, Beatriz Villanueva
Format: Dataset
Language:unknown
Published: 2019
Subjects:
Online Access:https://doi.org/10.3389/fgene.2019.00539.s002
https://figshare.com/articles/Table_1_Disentangling_Genetic_Variation_for_Resistance_and_Endurance_to_Scuticociliatosis_in_Turbot_Using_Pedigree_and_Genomic_Information_xlsx/8241155
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spelling ftfrontimediafig:oai:figshare.com:article/8241155 2023-05-15T18:41:10+02:00 Table_1_Disentangling Genetic Variation for Resistance and Endurance to Scuticociliatosis in Turbot Using Pedigree and Genomic Information.xlsx María Saura María J. Carabaño Almudena Fernández Santiago Cabaleiro Andrea B. Doeschl-Wilson Osvaldo Anacleto Francesco Maroso Adrián Millán Miguel Hermida Carlos Fernández Paulino Martínez Beatriz Villanueva 2019-06-07T06:39:19Z https://doi.org/10.3389/fgene.2019.00539.s002 https://figshare.com/articles/Table_1_Disentangling_Genetic_Variation_for_Resistance_and_Endurance_to_Scuticociliatosis_in_Turbot_Using_Pedigree_and_Genomic_Information_xlsx/8241155 unknown doi:10.3389/fgene.2019.00539.s002 https://figshare.com/articles/Table_1_Disentangling_Genetic_Variation_for_Resistance_and_Endurance_to_Scuticociliatosis_in_Turbot_Using_Pedigree_and_Genomic_Information_xlsx/8241155 CC BY 4.0 CC-BY Genetics Genetic Engineering Biomarkers Developmental Genetics (incl. Sex Determination) Epigenetics (incl. Genome Methylation and Epigenomics) Gene Expression (incl. Microarray and other genome-wide approaches) Genome Structure and Regulation Genomics Genetically Modified Animals Livestock Cloning Gene and Molecular Therapy aquaculture disease resilience resistance endurance scuticociliatosis turbot Dataset 2019 ftfrontimediafig https://doi.org/10.3389/fgene.2019.00539.s002 2019-06-12T22:59:15Z Selective breeding for improving host responses to infectious pathogens is a promising option for disease control. In fact, disease resilience, the ability of a host to survive or cope with infectious challenge, has become a highly desirable breeding goal. However, resilience is a complex trait composed of two different host defence mechanisms, namely resistance (the ability of a host to avoid becoming infected or diseased) and endurance (the ability of an infected host to survive the infection). While both could be targeted for genetic improvement, it is currently unknown how they contribute to survival, as reliable estimates of genetic parameters for both traits obtained simultaneously are scarce. A difficulty lies in obtaining endurance phenotypes for genetic analyses. In this study, we present the results from an innovative challenge test carried out in turbot whose design allowed disentangling the genetic basis of resistance and endurance to Philasterides dicentrarchi, a parasite causing scuticociliatosis that leads to substantial economic losses in the aquaculture industry. A noticeable characteristic of the parasite is that it causes visual signs that can be used for disentangling resistance and endurance. Our results showed the existence of genetic variation for both traits (heritability = 0.26 and 0.12 for resistance and endurance, respectively) and for the composite trait resilience (heritability = 0.15). The genetic correlation between resistance and resilience was very high (0.90) indicating that both are at a large extent the same trait, but no significant genetic correlation was found between resistance and endurance. A total of 18,125 SNPs obtained from 2b-RAD sequencing enabled genome-wide association analyses for detecting QTLs controlling the three traits. A candidate QTL region on linkage group 19 that explains 33% of the additive genetic variance was identified for resilience. The region contains relevant genes related to immune response and defence mechanisms. Although no significant ... Dataset Turbot Frontiers: Figshare
institution Open Polar
collection Frontiers: Figshare
op_collection_id ftfrontimediafig
language unknown
topic Genetics
Genetic Engineering
Biomarkers
Developmental Genetics (incl. Sex Determination)
Epigenetics (incl. Genome Methylation and Epigenomics)
Gene Expression (incl. Microarray and other genome-wide approaches)
Genome Structure and Regulation
Genomics
Genetically Modified Animals
Livestock Cloning
Gene and Molecular Therapy
aquaculture
disease
resilience
resistance
endurance
scuticociliatosis
turbot
spellingShingle Genetics
Genetic Engineering
Biomarkers
Developmental Genetics (incl. Sex Determination)
Epigenetics (incl. Genome Methylation and Epigenomics)
Gene Expression (incl. Microarray and other genome-wide approaches)
Genome Structure and Regulation
Genomics
Genetically Modified Animals
Livestock Cloning
Gene and Molecular Therapy
aquaculture
disease
resilience
resistance
endurance
scuticociliatosis
turbot
María Saura
María J. Carabaño
Almudena Fernández
Santiago Cabaleiro
Andrea B. Doeschl-Wilson
Osvaldo Anacleto
Francesco Maroso
Adrián Millán
Miguel Hermida
Carlos Fernández
Paulino Martínez
Beatriz Villanueva
Table_1_Disentangling Genetic Variation for Resistance and Endurance to Scuticociliatosis in Turbot Using Pedigree and Genomic Information.xlsx
topic_facet Genetics
Genetic Engineering
Biomarkers
Developmental Genetics (incl. Sex Determination)
Epigenetics (incl. Genome Methylation and Epigenomics)
Gene Expression (incl. Microarray and other genome-wide approaches)
Genome Structure and Regulation
Genomics
Genetically Modified Animals
Livestock Cloning
Gene and Molecular Therapy
aquaculture
disease
resilience
resistance
endurance
scuticociliatosis
turbot
description Selective breeding for improving host responses to infectious pathogens is a promising option for disease control. In fact, disease resilience, the ability of a host to survive or cope with infectious challenge, has become a highly desirable breeding goal. However, resilience is a complex trait composed of two different host defence mechanisms, namely resistance (the ability of a host to avoid becoming infected or diseased) and endurance (the ability of an infected host to survive the infection). While both could be targeted for genetic improvement, it is currently unknown how they contribute to survival, as reliable estimates of genetic parameters for both traits obtained simultaneously are scarce. A difficulty lies in obtaining endurance phenotypes for genetic analyses. In this study, we present the results from an innovative challenge test carried out in turbot whose design allowed disentangling the genetic basis of resistance and endurance to Philasterides dicentrarchi, a parasite causing scuticociliatosis that leads to substantial economic losses in the aquaculture industry. A noticeable characteristic of the parasite is that it causes visual signs that can be used for disentangling resistance and endurance. Our results showed the existence of genetic variation for both traits (heritability = 0.26 and 0.12 for resistance and endurance, respectively) and for the composite trait resilience (heritability = 0.15). The genetic correlation between resistance and resilience was very high (0.90) indicating that both are at a large extent the same trait, but no significant genetic correlation was found between resistance and endurance. A total of 18,125 SNPs obtained from 2b-RAD sequencing enabled genome-wide association analyses for detecting QTLs controlling the three traits. A candidate QTL region on linkage group 19 that explains 33% of the additive genetic variance was identified for resilience. The region contains relevant genes related to immune response and defence mechanisms. Although no significant ...
format Dataset
author María Saura
María J. Carabaño
Almudena Fernández
Santiago Cabaleiro
Andrea B. Doeschl-Wilson
Osvaldo Anacleto
Francesco Maroso
Adrián Millán
Miguel Hermida
Carlos Fernández
Paulino Martínez
Beatriz Villanueva
author_facet María Saura
María J. Carabaño
Almudena Fernández
Santiago Cabaleiro
Andrea B. Doeschl-Wilson
Osvaldo Anacleto
Francesco Maroso
Adrián Millán
Miguel Hermida
Carlos Fernández
Paulino Martínez
Beatriz Villanueva
author_sort María Saura
title Table_1_Disentangling Genetic Variation for Resistance and Endurance to Scuticociliatosis in Turbot Using Pedigree and Genomic Information.xlsx
title_short Table_1_Disentangling Genetic Variation for Resistance and Endurance to Scuticociliatosis in Turbot Using Pedigree and Genomic Information.xlsx
title_full Table_1_Disentangling Genetic Variation for Resistance and Endurance to Scuticociliatosis in Turbot Using Pedigree and Genomic Information.xlsx
title_fullStr Table_1_Disentangling Genetic Variation for Resistance and Endurance to Scuticociliatosis in Turbot Using Pedigree and Genomic Information.xlsx
title_full_unstemmed Table_1_Disentangling Genetic Variation for Resistance and Endurance to Scuticociliatosis in Turbot Using Pedigree and Genomic Information.xlsx
title_sort table_1_disentangling genetic variation for resistance and endurance to scuticociliatosis in turbot using pedigree and genomic information.xlsx
publishDate 2019
url https://doi.org/10.3389/fgene.2019.00539.s002
https://figshare.com/articles/Table_1_Disentangling_Genetic_Variation_for_Resistance_and_Endurance_to_Scuticociliatosis_in_Turbot_Using_Pedigree_and_Genomic_Information_xlsx/8241155
genre Turbot
genre_facet Turbot
op_relation doi:10.3389/fgene.2019.00539.s002
https://figshare.com/articles/Table_1_Disentangling_Genetic_Variation_for_Resistance_and_Endurance_to_Scuticociliatosis_in_Turbot_Using_Pedigree_and_Genomic_Information_xlsx/8241155
op_rights CC BY 4.0
op_rightsnorm CC-BY
op_doi https://doi.org/10.3389/fgene.2019.00539.s002
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