Insights Into Disease Resistance: Genetic Architecture, Genes, And Pleiotropy In Maize

Abstract

The genes and mechanisms underlying quantitative disease resistance remain largely elusive. The objective of this dissertation was to resolve the structure of multiple disease resistance loci, explore the dynamics that shape the genome at those loci, and identify genes associated with plant defense. In order to do this, both locus-specific and genome-wide approaches were taken, as each resistance locus has a unique resistance profile and mechanism(s) of resistance. Bins 1.02 and 1.06 of the maize genome carry loci of interest conditioning multiple disease resistance. The two loci differ in allelic diversity, pathogen specificity, and mechanism of resistance. The locus in bin 1.06 is particularly interesting, as it has been characterized as yield-stabilizing and exhibits signs of genome plasticity. I have used fine-mapping, association mapping, expression evidence, and mutant analysis to dissect these loci, identify candidate genes, and demonstrate the role of candidate genes in plant defense. Each locus was unique, although common themes arose. Both loci may have multiple underlying genes, demonstrating that the genetic architecture of disease resistance is complex. Resistance to multiple diseases appears to be due to linkage, although there may be a role for pleiotropy at both loci. Fine-mapping narrowed the intervals, and was complemented by association mapping and expression analysis to evaluate candidate genes. A putative remorin was implicated by fine-mapping and expression analysis; roughsheath2-interacting KH domain protein (rik) and pangloss1 (pan1) were identified through fine-mapping and association mapping. rik was later eliminated as a candidate for the QTL of interest through fine-mapping and association mapping. Mutants were used to confirm the role of candidate genes in plant defense, including for pan1 and the putative remorin. Based on these results, pan1 was inferred to be a susceptibility gene for NLB and Stewart's wilt, and increased resistance was correlated with decreased expression. Susceptibility conditioned by wild-type pan1 could be due to a passive mechanism, such as altered anatomical structures, or an active process, such as actin re-organization during pathogen attack. To test genome-wide association mapping candidate genes, mutants were identified and evaluated for NLB phenotype. Approximately 37% of the 123 families tested differed in disease phenotype from the background line. One of these was the putative remorin gene, which was inferred to contribute to resistance. Overall, I have examined candidate genes, explored genomic structure at these loci, and demonstrated a role for pan1 in resistance to multiple diseases.