QTL Mapping for Resistance to Cankers Induced by Pseudomonas syringae pv. actinidiae (Psa) in a Tetraploid Actinidia chinensis Kiwifruit Population

Polyploidy is a key driver of significant evolutionary changes in plant species. The genus Actinidia (kiwifruit) exhibits multiple ploidy levels, which contribute to novel fruit traits, high yields and resistance to the canker-causing dieback disease incited by Pseudomonas syringae pv. actinidiae (P...

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Published inPathogens (Basel) Vol. 9; no. 11; p. 967
Main Authors Tahir, Jibran, Brendolise, Cyril, Hoyte, Stephen, Lucas, Marielle, Thomson, Susan, Hoeata, Kirsten, McKenzie, Catherine, Wotton, Andrew, Funnell, Keith, Morgan, Ed, Hedderley, Duncan, Chagné, David, Bourke, Peter M., McCallum, John, Gardiner, Susan E., Gea, Luis
Format Journal Article
LanguageEnglish
Published Switzerland MDPI AG 20.11.2020
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Abstract Polyploidy is a key driver of significant evolutionary changes in plant species. The genus Actinidia (kiwifruit) exhibits multiple ploidy levels, which contribute to novel fruit traits, high yields and resistance to the canker-causing dieback disease incited by Pseudomonas syringae pv. actinidiae (Psa) biovar 3. However, the genetic mechanism for resistance to Psa observed in polyploid kiwifruit is not yet known. In this study we performed detailed genetic analysis of a tetraploid Actinidia chinensis var. chinensis population derived from a cross between a female parent that exhibits weak tolerance to Psa and a highly Psa-resistant male parent. We used the capture-sequencing approach across the whole kiwifruit genome and generated the first ultra-dense maps in a tetraploid kiwifruit population. We located quantitative trait loci (QTLs) for Psa resistance on these maps. Our approach to QTL mapping is based on the use of identity-by-descent trait mapping, which allowed us to relate the contribution of specific alleles from their respective homologues in the male and female parent, to the control of Psa resistance in the progeny. We identified genes in the diploid reference genome whose function is suggested to be involved in plant defense, which underly the QTLs, including receptor-like kinases. Our study is the first to cast light on the genetics of a polyploid kiwifruit and suggest a plausible mechanism for Psa resistance in this species.
AbstractList Polyploidy is a key driver of significant evolutionary changes in plant species. The genus Actinidia (kiwifruit) exhibits multiple ploidy levels, which contribute to novel fruit traits, high yields and resistance to the canker-causing dieback disease incited by Pseudomonas syringae pv. actinidiae (Psa) biovar 3. However, the genetic mechanism for resistance to Psa observed in polyploid kiwifruit is not yet known. In this study we performed detailed genetic analysis of a tetraploid Actinidia chinensis var. chinensis population derived from a cross between a female parent that exhibits weak tolerance to Psa and a highly Psa-resistant male parent. We used the capture-sequencing approach across the whole kiwifruit genome and generated the first ultra-dense maps in a tetraploid kiwifruit population. We located quantitative trait loci (QTLs) for Psa resistance on these maps. Our approach to QTL mapping is based on the use of identity-by-descent trait mapping, which allowed us to relate the contribution of specific alleles from their respective homologues in the male and female parent, to the control of Psa resistance in the progeny. We identified genes in the diploid reference genome whose function is suggested to be involved in plant defense, which underly the QTLs, including receptor-like kinases. Our study is the first to cast light on the genetics of a polyploid kiwifruit and suggest a plausible mechanism for Psa resistance in this species.
Polyploidy is a key driver of significant evolutionary changes in plant species. The genus Actinidia (kiwifruit) exhibits multiple ploidy levels, which contribute to novel fruit traits, high yields and resistance to the canker-causing dieback disease incited by Pseudomonas syringae pv. actinidiae (Psa) biovar 3. However, the genetic mechanism for resistance to Psa observed in polyploid kiwifruit is not yet known. In this study we performed detailed genetic analysis of a tetraploid Actinidia chinensis var. chinensis population derived from a cross between a female parent that exhibits weak tolerance to Psa and a highly Psa-resistant male parent. We used the capture-sequencing approach across the whole kiwifruit genome and generated the first ultra-dense maps in a tetraploid kiwifruit population. We located quantitative trait loci (QTLs) for Psa resistance on these maps. Our approach to QTL mapping is based on the use of identity-by-descent trait mapping, which allowed us to relate the contribution of specific alleles from their respective homologues in the male and female parent, to the control of Psa resistance in the progeny. We identified genes in the diploid reference genome whose function is suggested to be involved in plant defense, which underly the QTLs, including receptor-like kinases. Our study is the first to cast light on the genetics of a polyploid kiwifruit and suggest a plausible mechanism for Psa resistance in this species.
Polyploidy is a key driver of significant evolutionary changes in plant species. The genus Actinidia (kiwifruit) exhibits multiple ploidy levels, which contribute to novel fruit traits, high yields and resistance to the canker-causing dieback disease incited by Pseudomonas syringae pv. actinidiae (Psa) biovar 3. However, the genetic mechanism for resistance to Psa observed in polyploid kiwifruit is not yet known. In this study we performed detailed genetic analysis of a tetraploid Actinidia chinensis var. chinensis population derived from a cross between a female parent that exhibits weak tolerance to Psa and a highly Psa-resistant male parent. We used the capture-sequencing approach across the whole kiwifruit genome and generated the first ultra-dense maps in a tetraploid kiwifruit population. We located quantitative trait loci (QTLs) for Psa resistance on these maps. Our approach to QTL mapping is based on the use of identity-by-descent trait mapping, which allowed us to relate the contribution of specific alleles from their respective homologues in the male and female parent, to the control of Psa resistance in the progeny. We identified genes in the diploid reference genome whose function is suggested to be involved in plant defense, which underly the QTLs, including receptor-like kinases. Our study is the first to cast light on the genetics of a polyploid kiwifruit and suggest a plausible mechanism for Psa resistance in this species.Polyploidy is a key driver of significant evolutionary changes in plant species. The genus Actinidia (kiwifruit) exhibits multiple ploidy levels, which contribute to novel fruit traits, high yields and resistance to the canker-causing dieback disease incited by Pseudomonas syringae pv. actinidiae (Psa) biovar 3. However, the genetic mechanism for resistance to Psa observed in polyploid kiwifruit is not yet known. In this study we performed detailed genetic analysis of a tetraploid Actinidia chinensis var. chinensis population derived from a cross between a female parent that exhibits weak tolerance to Psa and a highly Psa-resistant male parent. We used the capture-sequencing approach across the whole kiwifruit genome and generated the first ultra-dense maps in a tetraploid kiwifruit population. We located quantitative trait loci (QTLs) for Psa resistance on these maps. Our approach to QTL mapping is based on the use of identity-by-descent trait mapping, which allowed us to relate the contribution of specific alleles from their respective homologues in the male and female parent, to the control of Psa resistance in the progeny. We identified genes in the diploid reference genome whose function is suggested to be involved in plant defense, which underly the QTLs, including receptor-like kinases. Our study is the first to cast light on the genetics of a polyploid kiwifruit and suggest a plausible mechanism for Psa resistance in this species.
Polyploidy is a key driver of significant evolutionary changes in plant species. The genus (kiwifruit) exhibits multiple ploidy levels, which contribute to novel fruit traits, high yields and resistance to the canker-causing dieback disease incited by pv. (Psa) biovar 3. However, the genetic mechanism for resistance to Psa observed in polyploid kiwifruit is not yet known. In this study we performed detailed genetic analysis of a tetraploid var. population derived from a cross between a female parent that exhibits weak tolerance to Psa and a highly Psa-resistant male parent. We used the capture-sequencing approach across the whole kiwifruit genome and generated the first ultra-dense maps in a tetraploid kiwifruit population. We located quantitative trait loci (QTLs) for Psa resistance on these maps. Our approach to QTL mapping is based on the use of identity-by-descent trait mapping, which allowed us to relate the contribution of specific alleles from their respective homologues in the male and female parent, to the control of Psa resistance in the progeny. We identified genes in the diploid reference genome whose function is suggested to be involved in plant defense, which underly the QTLs, including receptor-like kinases. Our study is the first to cast light on the genetics of a polyploid kiwifruit and suggest a plausible mechanism for Psa resistance in this species.
Author Brendolise, Cyril
Gea, Luis
Hoeata, Kirsten
Thomson, Susan
Gardiner, Susan E.
Morgan, Ed
McCallum, John
Chagné, David
Hoyte, Stephen
Bourke, Peter M.
Wotton, Andrew
Funnell, Keith
Tahir, Jibran
Hedderley, Duncan
Lucas, Marielle
McKenzie, Catherine
AuthorAffiliation 7 Plant Sciences Group, Department of Plant Sciences, Wageningen University and Research, Droevendaalsesteeg 1, P.O. Box 386, 6700 AJ Wageningen, The Netherlands; peter.bourke@wur.nl
5 The New Zealand Institute for Plant and Food Research Limited, 412 No 1 Road, RD2, Te Puke 3182, New Zealand; Kirsten.hoeata@plantandfood.co.nz (K.H.); Catherine.mckenzie@plantandfood.co.nz (C.M.)
4 The New Zealand Institute for Plant and Food Research Limited, Lincoln 7608, New Zealand; susan.thomson@plantandfood.co.nz
6 The New Zealand Institute for Plant & Food Research Limited, Private Bag 11030, Manawatu Mail Centre, Palmerston North 4442, New Zealand; Andrew.Wotton@plantandfood.co.nz (A.W.); Keith.Funnell@plantandfood.co.nz (K.F.); Ed.Morgan@plantandfood.co.nz (E.M.); duncan.hedderley@plantandfood.co.nz (D.H.); David.Chagne@plantandfood.co.nz (D.C.)
3 Breeding Department, Enza Zaden, 1602 DB Enkhuizen, The Netherlands; m.lucas@enzazaden.nl
1 The New Zealand Institute for Plant and Food Research Limited,
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Keywords chromosome pairing
polygenic resistance
perennials
polyploid genetics
QTLs
bacterial pathogen
kiwifruit
Language English
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Snippet Polyploidy is a key driver of significant evolutionary changes in plant species. The genus Actinidia (kiwifruit) exhibits multiple ploidy levels, which...
Polyploidy is a key driver of significant evolutionary changes in plant species. The genus (kiwifruit) exhibits multiple ploidy levels, which contribute to...
Polyploidy is a key driver of significant evolutionary changes in plant species. The genus Actinidia (kiwifruit) exhibits multiple ploidy levels, which...
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SubjectTerms Actinidia
Actinidia chinensis
alleles
Artificial chromosomes
bacterial pathogen
Canker
Datasets
Dieback
Diploids
diploidy
exhibitions
females
Flowers & plants
Food quality
fruit characteristics
Gene mapping
Genetic analysis
Genetic crosses
Genetics
Genomes
Genotype & phenotype
Haplotypes
Homology
Horticulture
Kinases
Kiwifruit
light
males
Mapping
pathogens
perennials
phosphotransferases (kinases)
Plant species
Ploidy
polygenic resistance
polyploid genetics
Polyploidy
Population
Progeny
Pseudomonas
Pseudomonas syringae
Pseudomonas syringae pv. actinidiae
QTLs
Quantitative trait loci
tetraploidy
yields
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Title QTL Mapping for Resistance to Cankers Induced by Pseudomonas syringae pv. actinidiae (Psa) in a Tetraploid Actinidia chinensis Kiwifruit Population
URI https://www.ncbi.nlm.nih.gov/pubmed/33233616
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https://www.proquest.com/docview/2464193472
https://www.proquest.com/docview/2498310716
https://pubmed.ncbi.nlm.nih.gov/PMC7709049
https://doaj.org/article/fef4c64d88784011b1b469fb3164b63a
Volume 9
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