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Identification of Alleles Conferring Resistance to Gray Leaf Spot in Maize Derived from its Wild Progenitor Species Teosinte
Author(s) -
Len Jill R.,
Krakowsky Matthew,
Goodman Major,
FlintGarcia Sherry,
BalintKurti Peter J.
Publication year - 2016
Publication title -
crop science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.76
H-Index - 147
eISSN - 1435-0653
pISSN - 0011-183X
DOI - 10.2135/cropsci2014.07.0468
Subject(s) - biology , cercospora , germplasm , population , leaf spot , allele , single nucleotide polymorphism , genotype , inbred strain , agronomy , genetics , botany , gene , demography , sociology
ABSTRACT Gray leaf spot (GLS; causal agent Cercospora zeae‐maydis and Cercospora zeina ) is an important maize ( Zea mays L.) disease in the United States. Current control methods for GLS include using resistant cultivars, crop rotation, chemical applications, and conventional tillage to reduce inoculum levels. Teosinte ( Z. mays subsp. parviglumis ) is the wild progenitor of maize and easily forms hybrids with current maize inbreds. The aims of this study were to identify alleles from teosinte that, when introduced into temperate maize germplasm, conferred significant levels of GLS resistance. A population of 693 BC 4 S 2 near isogenic lines (NILs), developed by crossing nine different teosinte accessions into the background of the maize inbred B73, were evaluated for GLS resistance in replicated field trials over 2 yr. Six markers significantly associated with GLS resistance were identified using 768 single nucleotide polymorphism (SNP) markers used to genotype this population. Twenty‐seven individual NILs that differed significantly from B73 for GLS resistance and that carried teosinte introgressions at the significantly associated SNPs at bins 2.04, 3.06, 4.07, 5.03, 8.06, and 9.03 were selected for follow‐up studies. F 2:3 populations were developed by crossing each selected NIL to B73 followed by self‐pollinating the progeny twice. These F 2:3 populations were evaluated for GLS resistance and genotyped at the loci of interest. In most cases, single‐marker analysis validated predicted allelic substitution effects from the original NIL populations.