The Physiology and Host Genetics of Quantitative Resistance in Maize to the Fungal Pathogen Cochliobolus heterostrophus.

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Title: The Physiology and Host Genetics of Quantitative Resistance in Maize to the Fungal Pathogen Cochliobolus heterostrophus.
Author: Belcher, Araby Ruth
Advisors: Margaret E. Daub, Committee Member
James B. Holland, Committee Member
Peter J. Balint-Kurti, Committee Chair
Abstract: Quantitative disease resistance, despite widespread use, remains poorly understood. A previous project in the NCSU Maize Disease Resistance Genetics lab has generated 253 near-isogenic lines (NILs) in the background of the historically important maize inbred line B73. B73, although of excellent overall agronomic quality, is highly resistant to a number of common maize diseases. Each NIL is genetically differentiated by its combination of 1-5 of 12 total introgressed regions from the multiple disease-resistant parent NC250P. These 12 NC250P introgressions were selected for study as, following an initial B73 x NC250P cross, they had been retained by a program of recurrent backcrossing to B73 and selection for resistance to the fungal maize pathogen Cochliobolus heterostrophus, causal agent of southern corn leaf blight (SLB). Prior research also evaluated the effect of each NC250P introgression in conferring quantitative resistance or susceptibility against SLB. Introgressions having an effect can be designated as disease resistance quantitative trait loci, or “dQTLs†. Presented here is a 2-phase study with the ultimate aim of characterizing the physiological basis for the effect on disease severity of these NC250P-derived SLB dQTLs. The first phase attempts to determine more precisely how infection is altered by the two largest-effect introgressions, termed dQTL 3.04 and dQTL 6.01 (or 3B and 6A). To do so, it uses growth chamber juvenile plant trials to compare the interactions between C. heterostrophus and 6 select lines - B73, the major-gene resistant line B73rhm (also a B73-background NIL), and four NILs with varying combinations of dQTLs 3.04 and 6.01 - by quantifying spore germination and penetration efficiency, hyphal growth, and host expression of the pathogenesis related genes PR1 and PR5. The second phase investigates dQTL disease specificity by field testing 236 NILs for adult plant resistance to 5 fungal maize pathogens. Based on the results of the first phase, host genotype was not a significant factor for germination or penetration efficiency (P≥0.27). None of the resistance loci had an effect on hyphal growth at 24 hours post-inoculation (hpi), but dQTL 6.01 NILs did have significantly less fungal growth at 48hpi (α=0.05). PR1 and PR5 were significantly upregulated at 15 and 24hpi in all lines (P≤0.01), although relative PR gene expression between lines did not uniformly correspond with the presence of any resistance locus or with the relative resistance between NILs. Moreover, using data from a previous B73rhm1 x NC250A (sister line of NC250P and allelic to NC250P for dQTL 6.01) to test for allelism between rhm and dQTL 6.01, it was determined that the gene underlying dQTL 6.01 is almost certainly rhm itself. In the second phase experiments, correlations for resistance to any given disease pair were low across the NIL population (0.067 ≤ |r| ≤ 0.535). However, eight of the twelve NC250P introgressions represented in the NILs were shown to have significant multiple disease resistance effects (P≤0.058 for all significant effects). A dQTL in bin 3.04 had a significant effect on resistance for 4 diseases; and the dQTLs in bins 2.06, 5.07-5.09, and 6.01 had significant effects on 3 diseases. The dQTLs in bins 3.00-3.01, 9.01, 9.02-9.03, and 10.02 had significant effects on resistance for 2 diseases. The combined results of these experiments, by adding to the current knowledge of the timing and specificity of quantitative disease resistance effects within the infection court, can be used to both 1) help plant breeders better deploy quantitative resistance genes through an increased understanding of their effects and 2) provide quantitative resistance and multiple disease resistance gene candidates for future fine-mapping and cloning efforts.
Date: 2009-08-12
Degree: MS
Discipline: Plant Pathology

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