Theses and Dissertations

Issuing Body

Mississippi State University


Williams, W. Paul

Committee Member

Baldwin, Brian S.

Committee Member

Dubien, Janice

Committee Member

Warburton, Marilyn Louise

Committee Member

Krakowsky, Matthew D.

Date of Degree


Document Type

Dissertation - Open Access



Degree Name

Doctor of Philosophy (Ph.D)


College of Agriculture and Life Sciences


Department of Plant and Soil Sciences


Pre-harvest contamination of maize grain with aflatoxin is a chronic problem worldwide and particularly in the southeastern U.S. Aflatoxin is a mycotoxin produced by the fungus Aspergillus flavus, an opportunistic ear-rot pathogen of maize (Zea mays). Resistance to aflatoxin accumulation is heritable, and resistant germplasm-lines are available. These lines are derived from “exotic” genetic backgrounds and were released as sources of resistance, not parental inbreds. However, all current sources of resistance are quantitative, which complicates conventional efforts to introgress resistance alleles from unadapted but resistant donor lines to adapted but susceptible recipient lines. Mapping quantitative trait loci (QTL) and their linked markers enables targeted introgression of the desired alleles via marker-assisted selection. Quantitative trait loci were identified in two F2:3 mapping populations, derived from crossing resistant inbreds Mp715 and Mp717 to a common susceptible parent (Va35). The Mp715 x Va35 population was phenotyped for aflatoxin accumulation under artificial inoculation in replicated field trials at Mississippi State (MSU) in 2015 and 2016. The Mp717 x Va35 population was phenotyped at MSU and Lubbock, TX in 2016. Populations were genotyped using simple sequence repeat (SSR) and single nucleotide polymorphism (SNP) markers and linkage maps created in JoinMap4. To locate QTL, linkage maps, genotypes, and phenotypes were analyzed jointly in QTL Cartographer 2.5 using composite interval mapping (CIM) and multiple interval mapping (MIM) procedures. Five QTL with the beneficial allele contributed by Mp715 were identified during CIM in bins 5.01, 6.06, 7.03 10.04 and 10.05. Three QTL with the beneficial allele contributed by Mp717 were identified during CIM in bins 3.07/3.08, 7.02/7.03, and 10.05. In both populations, QTL were identified with the beneficial allele contributed by Va35. Those QTL did not co-locate across populations but four of the six were on chromosome 1. Significant QTL effects from CIM were used as the initial model terms in MIM, where all QTL effects were fit simultaneously and their gene-action and epistatic interactions estimated.