Cargando…
Quantitative trait loci and transcriptome signatures associated with avian heritable resistance to Campylobacter
Campylobacter is the leading cause of bacterial foodborne gastroenteritis worldwide. Handling or consumption of contaminated poultry meat is a key risk factor for human campylobacteriosis. One potential control strategy is to select poultry with increased resistance to Campylobacter. We associated h...
Autores principales: | , , , , , , , , , , , , , , , , |
---|---|
Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group UK
2021
|
Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7804197/ https://www.ncbi.nlm.nih.gov/pubmed/33436657 http://dx.doi.org/10.1038/s41598-020-79005-7 |
_version_ | 1783636108805931008 |
---|---|
author | Psifidi, Androniki Kranis, Andreas Rothwell, Lisa M. Bremner, Abi Russell, Kay Robledo, Diego Bush, Stephen J. Fife, Mark Hocking, Paul M. Banos, Georgios Hume, David A. Kaufman, Jim Bailey, Richard A. Avendano, Santiago Watson, Kellie A. Kaiser, Pete Stevens, Mark. P. |
author_facet | Psifidi, Androniki Kranis, Andreas Rothwell, Lisa M. Bremner, Abi Russell, Kay Robledo, Diego Bush, Stephen J. Fife, Mark Hocking, Paul M. Banos, Georgios Hume, David A. Kaufman, Jim Bailey, Richard A. Avendano, Santiago Watson, Kellie A. Kaiser, Pete Stevens, Mark. P. |
author_sort | Psifidi, Androniki |
collection | PubMed |
description | Campylobacter is the leading cause of bacterial foodborne gastroenteritis worldwide. Handling or consumption of contaminated poultry meat is a key risk factor for human campylobacteriosis. One potential control strategy is to select poultry with increased resistance to Campylobacter. We associated high-density genome-wide genotypes (600K single nucleotide polymorphisms) of 3000 commercial broilers with Campylobacter load in their caeca. Trait heritability was modest but significant (h(2) = 0.11 ± 0.03). Results confirmed quantitative trait loci (QTL) on chromosomes 14 and 16 previously identified in inbred chicken lines, and detected two additional QTLs on chromosomes 19 and 26. RNA-Seq analysis of broilers at the extremes of colonisation phenotype identified differentially transcribed genes within the QTL on chromosome 16 and proximal to the major histocompatibility complex (MHC) locus. We identified strong cis-QTLs located within MHC suggesting the presence of cis-acting variation in MHC class I and II and BG genes. Pathway and network analyses implicated cooperative functional pathways and networks in colonisation, including those related to antigen presentation, innate and adaptive immune responses, calcium, and renin–angiotensin signalling. While co-selection for enhanced resistance and other breeding goals is feasible, the frequency of resistance-associated alleles was high in the population studied and non-genetic factors significantly influenced Campylobacter colonisation. |
format | Online Article Text |
id | pubmed-7804197 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-78041972021-01-13 Quantitative trait loci and transcriptome signatures associated with avian heritable resistance to Campylobacter Psifidi, Androniki Kranis, Andreas Rothwell, Lisa M. Bremner, Abi Russell, Kay Robledo, Diego Bush, Stephen J. Fife, Mark Hocking, Paul M. Banos, Georgios Hume, David A. Kaufman, Jim Bailey, Richard A. Avendano, Santiago Watson, Kellie A. Kaiser, Pete Stevens, Mark. P. Sci Rep Article Campylobacter is the leading cause of bacterial foodborne gastroenteritis worldwide. Handling or consumption of contaminated poultry meat is a key risk factor for human campylobacteriosis. One potential control strategy is to select poultry with increased resistance to Campylobacter. We associated high-density genome-wide genotypes (600K single nucleotide polymorphisms) of 3000 commercial broilers with Campylobacter load in their caeca. Trait heritability was modest but significant (h(2) = 0.11 ± 0.03). Results confirmed quantitative trait loci (QTL) on chromosomes 14 and 16 previously identified in inbred chicken lines, and detected two additional QTLs on chromosomes 19 and 26. RNA-Seq analysis of broilers at the extremes of colonisation phenotype identified differentially transcribed genes within the QTL on chromosome 16 and proximal to the major histocompatibility complex (MHC) locus. We identified strong cis-QTLs located within MHC suggesting the presence of cis-acting variation in MHC class I and II and BG genes. Pathway and network analyses implicated cooperative functional pathways and networks in colonisation, including those related to antigen presentation, innate and adaptive immune responses, calcium, and renin–angiotensin signalling. While co-selection for enhanced resistance and other breeding goals is feasible, the frequency of resistance-associated alleles was high in the population studied and non-genetic factors significantly influenced Campylobacter colonisation. Nature Publishing Group UK 2021-01-12 /pmc/articles/PMC7804197/ /pubmed/33436657 http://dx.doi.org/10.1038/s41598-020-79005-7 Text en © The Author(s) 2021 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. |
spellingShingle | Article Psifidi, Androniki Kranis, Andreas Rothwell, Lisa M. Bremner, Abi Russell, Kay Robledo, Diego Bush, Stephen J. Fife, Mark Hocking, Paul M. Banos, Georgios Hume, David A. Kaufman, Jim Bailey, Richard A. Avendano, Santiago Watson, Kellie A. Kaiser, Pete Stevens, Mark. P. Quantitative trait loci and transcriptome signatures associated with avian heritable resistance to Campylobacter |
title | Quantitative trait loci and transcriptome signatures associated with avian heritable resistance to Campylobacter |
title_full | Quantitative trait loci and transcriptome signatures associated with avian heritable resistance to Campylobacter |
title_fullStr | Quantitative trait loci and transcriptome signatures associated with avian heritable resistance to Campylobacter |
title_full_unstemmed | Quantitative trait loci and transcriptome signatures associated with avian heritable resistance to Campylobacter |
title_short | Quantitative trait loci and transcriptome signatures associated with avian heritable resistance to Campylobacter |
title_sort | quantitative trait loci and transcriptome signatures associated with avian heritable resistance to campylobacter |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7804197/ https://www.ncbi.nlm.nih.gov/pubmed/33436657 http://dx.doi.org/10.1038/s41598-020-79005-7 |
work_keys_str_mv | AT psifidiandroniki quantitativetraitlociandtranscriptomesignaturesassociatedwithavianheritableresistancetocampylobacter AT kranisandreas quantitativetraitlociandtranscriptomesignaturesassociatedwithavianheritableresistancetocampylobacter AT rothwelllisam quantitativetraitlociandtranscriptomesignaturesassociatedwithavianheritableresistancetocampylobacter AT bremnerabi quantitativetraitlociandtranscriptomesignaturesassociatedwithavianheritableresistancetocampylobacter AT russellkay quantitativetraitlociandtranscriptomesignaturesassociatedwithavianheritableresistancetocampylobacter AT robledodiego quantitativetraitlociandtranscriptomesignaturesassociatedwithavianheritableresistancetocampylobacter AT bushstephenj quantitativetraitlociandtranscriptomesignaturesassociatedwithavianheritableresistancetocampylobacter AT fifemark quantitativetraitlociandtranscriptomesignaturesassociatedwithavianheritableresistancetocampylobacter AT hockingpaulm quantitativetraitlociandtranscriptomesignaturesassociatedwithavianheritableresistancetocampylobacter AT banosgeorgios quantitativetraitlociandtranscriptomesignaturesassociatedwithavianheritableresistancetocampylobacter AT humedavida quantitativetraitlociandtranscriptomesignaturesassociatedwithavianheritableresistancetocampylobacter AT kaufmanjim quantitativetraitlociandtranscriptomesignaturesassociatedwithavianheritableresistancetocampylobacter AT baileyricharda quantitativetraitlociandtranscriptomesignaturesassociatedwithavianheritableresistancetocampylobacter AT avendanosantiago quantitativetraitlociandtranscriptomesignaturesassociatedwithavianheritableresistancetocampylobacter AT watsonkelliea quantitativetraitlociandtranscriptomesignaturesassociatedwithavianheritableresistancetocampylobacter AT kaiserpete quantitativetraitlociandtranscriptomesignaturesassociatedwithavianheritableresistancetocampylobacter AT stevensmarkp quantitativetraitlociandtranscriptomesignaturesassociatedwithavianheritableresistancetocampylobacter |