Professor, Botany and Plant Pathology
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| Office: | Cordley 3069 |
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| Phone: | (541)-737-5293 |
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Pub Med | | Keywords: | Host-Parasite Interactions; Host-Specific Toxins; Disease Resistance |
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Education
Ph.D. 1983, Purdue University
Research
Our laboratory is interested in understanding the physiological changes that occur in a plant host that results in the expression of either disease resistance or susceptibility. Largely due to its genetic tractability, significant advances have and continue to be made in our understanding of mechanisms that regulate plant disease resistance. However, far less is understood about plant disease susceptibility, the underlying event upon which the resistance response is predicated. We have been investigating a disease called Victoria Blight of oats. In this disease, susceptibility is conferred by a single dominant gene at the
Vb locus. The disease is caused by,
Cochliobolus victoriae, which is pathogenic because of its production of the cyclized peptide, victorin. Victorin, either through a direct or indirect interaction with the product of the
Vb gene, appears to signal host disease susceptibility because all isolates that produce victorin are pathogenic but only toward dominant Vb oat genotypes. Homozygous recessive genotypes (
vb,vb) are resistant to all isolates of the fungus. Consequently, Victoria Blight presents a genetically-tractable disease interaction where characterization of the
Vb gene should lead to significant insights into mechanisms of plant disease susceptibility. In addition, various genetic approaches have indicated that the
Vb disease susceptibility gene is either tightly linked or identical with the
Pc2 gene, which confers resistance to a different pathogen. This suggests that signaling events that lead to susceptibility may share components in common with disease resistance responses. Significantly, we have found that victorin induces a form of cell death in oats, which displays the characteristics of
programmed
cell
death (PCD). PCD has been associated with resistance in the form of the hypersensitive response (HR) and is increasingly being associated with disease susceptibility. Thus, understanding the function of the
Vb gene should provide insight into mechanisms of both disease susceptibility and resistance and an event apparently common to both, the regulation of PCD.
Previously, the victorin response had only been identified in Avena sativa (oats), an allohexaploid with a large, complicated, poorly-characterized genome, making genetic characterization difficult. However, we recently identified victorin-responsive Arabidopsis genotypes in a variety of diverse ecotypes. In all cases, as in oats, the victorin response is conferred by a single, dominant gene that maps to a single locus we have named LOV (for Locus Orchestrating Victorin effects). In addition to its genetic similarity, all of the responses to victorin that have been characterized in Arabidopsis to this point also appear similar to those evoked in oats including, perhaps most importantly, that LOV appears to condition susceptibility to C. victoriae. Current efforts in the laboratory are employing an integrated approach including biochemical, physiological, cell biological and now genetic approaches to understanding the nature of disease susceptibility and PCD in plants.
