Unraveling Genomic Complexity at a Quantitative Disease Resistance Locus in Maize. Issue 1 (9th July 2014)

• Record Type: Journal Article
• Authors: Jamann, Tiffany M; Poland, Jesse A; Kolkman, Judith M; Smith, Laurie G; Nelson, Rebecca J
• Is Part Of: Genetics. Volume 198:Issue 1(2014)
• Page Start: 333
• Page End: 344
• Publication Date: 2014-07-09
• Subjects: quantitative disease resistance -- northern leaf blight -- Setosphaeria turcica -- multiple disease resistance -- Stewart's wilt -- Genetics of Immunity; Genetics -- Periodicals; 576.5
• DOI: 10.1534/genetics.114.167486
• Languages: English
• ISSNs: 0016-6731

Abstract

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 pan1 . We tested mutant alleles and found that pan1 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 pan1, a gene conditioning susceptibility for NLB, may underlie the QTL.