Unraveling Genomic Complexity at a Quantitative Disease Resistance Locus in Maize
Identifieur interne : 000545 ( Ncbi/Merge ); précédent : 000544; suivant : 000546Unraveling Genomic Complexity at a Quantitative Disease Resistance Locus in Maize
Auteurs : Tiffany M. Jamann [États-Unis] ; Jesse A. Poland [États-Unis] ; Judith M. Kolkman ; Laurie G. Smith [États-Unis] ; Rebecca J. Nelson [États-Unis]Source :
- Genetics [ 0016-6731 ] ; 2014.
Abstract
Multiple disease resistance has important implications for plant fitness, given the selection pressure that many pathogens exert directly on natural plant populations and indirectly via crop improvement programs. Evidence of a locus conditioning resistance to multiple pathogens was found in bin 1.06 of the maize genome with the allele from inbred line “Tx303” conditioning quantitative resistance to northern leaf blight (NLB) and qualitative resistance to Stewart’s wilt. To dissect the genetic basis of resistance in this region and to refine candidate gene hypotheses, we mapped resistance to the two diseases. Both resistance phenotypes were localized to overlapping regions, with the Stewart’s wilt interval refined to a 95.9-kb segment containing three genes and the NLB interval to a 3.60-Mb segment containing 117 genes. Regions of the introgression showed little to no recombination, suggesting structural differences between the inbred lines Tx303 and “B73,” the parents of the fine-mapping population. We examined copy number variation across the region using next-generation sequencing data, and found large variation in read depth in Tx303 across the region relative to the reference genome of B73. In the fine-mapping region, association mapping for NLB implicated candidate genes, including a putative zinc finger and
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DOI: 10.1534/genetics.114.167486
PubMed: 25009146
PubMed Central: 4174945
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<front><div type="abstract" xml:lang="en"><p>Multiple disease resistance has important implications for plant fitness, given the selection pressure that many pathogens exert directly on natural plant populations and indirectly via crop improvement programs. Evidence of a locus conditioning resistance to multiple pathogens was found in bin 1.06 of the maize genome with the allele from inbred line “Tx303” conditioning quantitative resistance to northern leaf blight (NLB) and qualitative resistance to Stewart’s wilt. To dissect the genetic basis of resistance in this region and to refine candidate gene hypotheses, we mapped resistance to the two diseases. Both resistance phenotypes were localized to overlapping regions, with the Stewart’s wilt interval refined to a 95.9-kb segment containing three genes and the NLB interval to a 3.60-Mb segment containing 117 genes. Regions of the introgression showed little to no recombination, suggesting structural differences between the inbred lines Tx303 and “B73,” the parents of the fine-mapping population. We examined copy number variation across the region using next-generation sequencing data, and found large variation in read depth in Tx303 across the region relative to the reference genome of B73. In the fine-mapping region, association mapping for NLB implicated candidate genes, including a putative zinc finger and <italic>pan1</italic>
. We tested mutant alleles and found that <italic>pan1</italic>
is a susceptibility gene for NLB and Stewart’s wilt. Our data strongly suggest that structural variation plays an important role in resistance conditioned by this region, and <italic>pan1</italic>
, a gene conditioning susceptibility for NLB, may underlie the QTL.</p>
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<front><journal-meta><journal-id journal-id-type="nlm-ta">Genetics</journal-id>
<journal-id journal-id-type="iso-abbrev">Genetics</journal-id>
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<article-categories><subj-group subj-group-type="heading"><subject>Investigations</subject>
<subj-group><subject>Genetics of Immunity</subject>
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<title-group><article-title>Unraveling Genomic Complexity at a Quantitative Disease Resistance Locus in Maize</article-title>
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<contrib-group><contrib contrib-type="author"><name><surname>Jamann</surname>
<given-names>Tiffany M.</given-names>
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<xref ref-type="aff" rid="aff1">*</xref>
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<contrib contrib-type="author"><name><surname>Poland</surname>
<given-names>Jesse A.</given-names>
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<xref ref-type="aff" rid="aff2"><sup>†</sup>
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<xref ref-type="aff" rid="aff3"><sup>‡</sup>
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<contrib contrib-type="author"><name><surname>Kolkman</surname>
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<xref ref-type="aff" rid="aff4"><sup>§</sup>
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<aff id="aff1"><label>*</label>
School of Integrative Plant Science, Cornell University, Ithaca, New York 14853</aff>
<aff id="aff2"><label>†</label>
U.S. Department of Agriculture–Agricultural Research Service, Hard Winter Wheat Genetics Research Unit, Manhattan, Kansas 66502</aff>
<aff id="aff3"><label>‡</label>
Department of Agronomy, Kansas State University, Manhattan, Kansas 66506</aff>
<aff id="aff4"><label>§</label>
Section of Cell and Developmental Biology, Division of Biological Sciences, University of California at San Diego, La Jolla, California 92093</aff>
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<author-notes><corresp id="cor1"><label>1</label>
Corresponding author: 303G Plant Science Bldg., 236 Tower Rd., Cornell University, Ithaca, NY 14853. E-mail: <email>rjn7@cornell.edu</email>
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<abstract><p>Multiple disease resistance has important implications for plant fitness, given the selection pressure that many pathogens exert directly on natural plant populations and indirectly via crop improvement programs. Evidence of a locus conditioning resistance to multiple pathogens was found in bin 1.06 of the maize genome with the allele from inbred line “Tx303” conditioning quantitative resistance to northern leaf blight (NLB) and qualitative resistance to Stewart’s wilt. To dissect the genetic basis of resistance in this region and to refine candidate gene hypotheses, we mapped resistance to the two diseases. Both resistance phenotypes were localized to overlapping regions, with the Stewart’s wilt interval refined to a 95.9-kb segment containing three genes and the NLB interval to a 3.60-Mb segment containing 117 genes. Regions of the introgression showed little to no recombination, suggesting structural differences between the inbred lines Tx303 and “B73,” the parents of the fine-mapping population. We examined copy number variation across the region using next-generation sequencing data, and found large variation in read depth in Tx303 across the region relative to the reference genome of B73. In the fine-mapping region, association mapping for NLB implicated candidate genes, including a putative zinc finger and <italic>pan1</italic>
. We tested mutant alleles and found that <italic>pan1</italic>
is a susceptibility gene for NLB and Stewart’s wilt. Our data strongly suggest that structural variation plays an important role in resistance conditioned by this region, and <italic>pan1</italic>
, a gene conditioning susceptibility for NLB, may underlie the QTL.</p>
</abstract>
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