Maize (Zea mays L.) susceptibility to ear rot by Aspergillus flavus (Link:Fr) and aflatoxin accumulation causes global economic and human health damage. Host plant resistance is an ideal solution, but commercial varieties lack sufficient resistance to solve the problem. Due to general lack of resistant maize germplasm, no currently available association mapping panels are expected to contain significant variation for the trait. A new association mapping panel containing the majority of aflatoxin accumulation resistant maize lines at the time of compilation is presented here along with genetic and phenotypic characterization data. Phenotypic data from testcrossed lines include aflatoxin levels, days to silking, and corn earworm [Helicoverpa zea (Boddie)] damage measured in seven environments and fungal biomass of kernels measured in three. In addition to identifying previously reported aflatoxin resistant lines, new resistant lines were discovered, which may be used for breeding improved germplasm. The Mexican landrace Tuxpeño is the progenitor or one main contributor for most of the resistant lines and likely the source of resistance, but a few other sources may allow additional novel resistance to be pyramided into future breeding lines. Genetic characterization of kinship, genetic diversity, and substructure analysis presented here will allow this resource to be used for association mapping of aflatoxin and identification of factors responsible for this challenging quantitative trait.

Maize (Zea mays L.) is a crop of global importance, but prone to contamination by aflatoxins produced by fungi in the genus Aspergillus. The development of resistant germplasm and the identification of genes contributing to resistance would aid in the reduction of the problem with a minimal need for intervention by farmers. Chitinolytic enzymes respond to attack by potential pathogens and have been demonstrated to increase insect and fungal resistance in plants. Here, all chitinase genes in the maize genome were characterized via sequence diversity and expression patterns. Recent evolution within this gene family was noted. Markers from within each gene were developed and used to map the phenotypic effect on resistance of each gene in up to four QTL mapping populations and one association panel. Seven chitinase genes were identified that had alleles associated with increased resistance to aflatoxin accumulation and A. flavus infection in field grown maize. The chitinase in bin 1.05 identified a new and highly significant QTL, while chitinase genes in bins 2.04 and 5.03 fell directly beneath the peaks of previously published QTL. The expression patterns of these genes corroborate possible grain resistance mechanisms. Markers from within the gene sequences or very closely linked to them are presented to aid in the use of marker assisted selection to improve this trait.

Contamination of maize (Zea mays L.) with aflatoxin, produced by the fungus Aspergillus flavus Link, has severe health and economic consequences. Efforts to reduce aflatoxin accumulation in maize have focused on identifying and selecting germplasm with natural host resistance factors, and several maize lines with significantly reduced aflatoxin accumulation have been identified. Past linkage mapping studies have identified quantitative trait loci (QTL) that consistently reduce aflatoxin levels in maize. In addition, an association mapping panel of 300 maize inbred lines was previously created specifically for the dissection of aflatoxin accumulation resistance. Here we report the results of a genome‐wide association study (GWAS) using this panel of testcrossed maize hybrids. Each of the inbred parents of the testcrossed hybrids was genotyped by sequencing to generate 261,184 robust single nucleotide polymorphisms (SNPs), and the entire panel was phenotyped for aflatoxin accumulation following inoculation with A. flavus in multilocation, replicated field trials. Results uncovered 107 SNPs associated with aflatoxin accumulation in one or more environments in the association panel at a probability level between 9.78 × 10−6 and 2.87 × 10−10. Eight SNP trait associations were found with a false discovery rate (FDR) of less than 10% (p < 3.83 × 10−7). These SNPs occur within the sequence of three uncharacterized genes. Variants in 25 other genomic regions showing high association values over more than one environment are also presented. These genomic regions are undergoing validation studies and will be of use to dissect the resistance to aflatoxin accumulation and improve this trait.

Mycotoxin contamination in corn (Zea mays L.) grain is a worldwide threat to safety of both human food and animal feed. A select group of inbred corn lines was evaluated in fi eld trials for ear rot caused by Aspergillus fl avus and Fusarium verticillioides and mycotoxin accumulation in grain. Our goal was to identify lines resistant to both fungi. In separate tests, 20 inbred lines were inoculated with either A. fl avus or F. verticillioides. Aft er harvest, ears were rated for rot and evaluated for levels of afl atoxin or fumonisin contamination. Inbred line Mp717 exhibited low grain afl atoxin contamination and it also had the lowest levels of fumonisin. Inbred line Mp317 has been shown previously to have low levels of F. verticillioides kernel infection and fumonisin contamination. Mp317 also had low levels of afl atoxin contamination in this study. Area of the ear rotted by F. verticillioides and A. fl avus was signifi cantly correlated to toxin production for both fumonisin (P = 0.0002; r = 0.74) and afl atoxin (P = 0.004; r = 0.61), indicating that inbreds exhibiting afl atoxin resistance may also be good sources of fumonisin resistance. Our method of quantifying ear rot may also be used to rapidly screen lines for A. fl avus resistance and subsequent afl atoxin accumulation in preliminary evaluations.

Isozyme, randomly amplified polymorphic DNA (RAPD), and simple sequence repeats (SSR) markers were used to generate a linkage map in an F2 and F3 watermelon [Citrullus lanatus (Thumb.) Matsum. & Nakai] population derived from a cross between the fusarium wilt (Fusarium oxysporum f. sp. niveum) susceptible `New Hampshire Midget' and resistant PI 296341-FR. A 112.9 cM RAPD-based map consisting of 26 markers spanning two linkage groups was generated with F2 data. With F3 data, a 139 cM RAPD-based map consisting of 13 markers covering five linkage groups was constructed. Isozyme and SSR markers were unlinked. About 40% to 48% of the RAPD markers were significantly skewed from expected Mendelian segregation ratios in both generations. Bulked segregant analysis and single-factor analysis of variance were employed to identify RAPD markers linked to fusarium wilt caused by races 1 and 2 of F. oxysporum f. sp. niveum. Current linkage estimates between the resistance trait and the marker loci were too large for effective use in a marker-assisted selection program.