title: A remorin gene is implicated in quantitative disease resistance in maize.
abstract: Quantitative disease resistance is used by plant breeders to improve host resistance. We demonstrate a role for a maize remorin ( ZmREM6.3 ) in quantitative resistance against northern leaf blight using high-resolution fine mapping, expression analysis, and mutants. This is the first evidence of a role for remorins in plant-fungal interactions. Quantitative disease resistance (QDR) is important for the development of crop cultivars and is particularly useful when loci also confer multiple disease resistance. Despite its widespread use, the underlying mechanisms of QDR remain largely unknown. In this study, we fine-mapped a known quantitative trait locus (QTL) conditioning disease resistance on chromosome 1 of maize. This locus confers resistance to three foliar diseases: northern leaf blight (NLB), caused by the fungus Setosphaeria turcica; Stewart's wilt, caused by the bacterium Pantoea stewartii; and common rust, caused by the fungus Puccinia sorghi. The Stewart's wilt QTL was confined to a 5.26-Mb interval, while the rust QTL was reduced to an overlapping 2.56-Mb region. We show tight linkage between the NLB QTL locus and the loci conferring resistance to Stewart's wilt and common rust. Pleiotropy cannot be excluded for the Stewart's wilt and the common rust QTL, as they were fine-mapped to overlapping regions. Four positional candidate genes within the 243-kb NLB interval were examined with expression and mutant analysis: a gene with homology to an F-box gene, a remorin gene (ZmREM6.3), a chaperonin gene, and an uncharacterized gene. The F-box gene and ZmREM6.3 were more highly expressed in the resistant line. Transposon tagging mutants were tested for the chaperonin and ZmREM6.3, and the remorin mutant was found to be more susceptible to NLB. The putative F-box is a strong candidate, but mutants were not available to test this gene. Multiple lines of evidence strongly suggest a role for ZmREM6.3 in quantitative disease resistance.
authors: School of Integrative Plant Science, Cornell University, Ithaca, NY, 14853, USA. tjamann@illinois.edu.|Department of Crop Sciences, University of Illinois, Urbana, IL, 61801, USA. tjamann@illinois.edu.
authors: Tiffany M
authors: TM
authors: Jamann
authors: School of Integrative Plant Science, Cornell University, Ithaca, NY, 14853, USA.|Department of Plant Pathology, University of Wisconsin-Madison, Madison, WI, 53706, USA.
authors: Xingyu
authors: X
authors: Luo
authors: School of Integrative Plant Science, Cornell University, Ithaca, NY, 14853, USA.
authors: Laura
authors: L
authors: Morales
authors: School of Integrative Plant Science, Cornell University, Ithaca, NY, 14853, USA.
authors: Judith M
authors: JM
authors: Kolkman
authors: School of Integrative Plant Science, Cornell University, Ithaca, NY, 14853, USA.|Department of Plant Pathology and Microbiology, National Taiwan University, Taipei, Taiwan.
authors: Chia-Lin
authors: CL
authors: Chung
authors: School of Integrative Plant Science, Cornell University, Ithaca, NY, 14853, USA.
authors: Rebecca J
authors: RJ
authors: Nelson
mesh_terms: D001203:Ascomycota / Q000472:pathogenicity; D001487:Basidiomycota / Q000472:pathogenicity; D002352:Carrier Proteins / Q000235:genetics*; D002874:Chromosome Mapping; D060467:Disease Resistance / Q000235:genetics*; D008040:Genetic Linkage; D005838:Genotype; D010750:Phosphoproteins / Q000235:genetics*; D010802:Phylogeny; D010935:Plant Diseases / Q000235:genetics* / Q000382:microbiology; D018515:Plant Leaves / Q000382:microbiology; D010940:Plant Proteins / Q000235:genetics*; D020641:Polymorphism, Single Nucleotide; D040641:Quantitative Trait Loci; D003313:Zea mays / Q000235:genetics* / Q000382:microbiology
chemical_list: D002352:Carrier Proteins; D010750:Phosphoproteins; D010940:Plant Proteins; C103794:remorin