Submitted to: Plant Physiology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 10/20/2000
Publication Date: N/A
Citation: Interpretive Summary: Fusarium head scab of wheat is a devastating disease resulting in billions of dollars lost in wheat yield and quality. The Fusarium fungus penetrates the wheat head (spike) causing seed abortion and toxin accumulation. Among U.S. wheat there is little to no resistance to this disease. However, the Chinese variety Sumai shows good resistance. Little is known about how resistance and susceptibility occur in wheat in response to the Fusarium fungus. The objectives of this study were to evaluate the spread of the fungus in resistant and susceptible wheat cultivars. We also determined whether plant genes associated with plant disease responses were induced to high levels during infection. The fungus was inoculated into the developing middle seeds of the wheat spike and initial spread was monitored. After 48 hours the inoculated spikes were divided into three sections, the lower 1/3, middle 1/3, and upper 1/3, and expression of plant defense response genes were evaluated. The results showed that within the initial 48 hours the fungus did not spread beyond the middle 1/3 of the spike. However, plant defense response gene expression was induced through the wheat spike. No differences were noted between the susceptible and resistant genotypes for fungal spread and expression of plant defense response genes. These results are important because they prove that induction of high levels of plant defense response genes in wheat does not require the presence of the pathogen and that a signal molecule from the fungus-plant interaction probably moves from the infection site to induce gene expression in uninfected tissue. Identification of a signal molecule that induces defense response gene expression in wheat spikes may lead to effective method for controlling this disease.
Technical Abstract: Fusarium head blight (FHB) of wheat is a crippling disease that causes severe economic losses in many of the wheat growing regions of the world. Our group is studying the interactions between wheat spikes and F. graminearum during infection. Microscopy of inoculated glumes revealed that the fungus appeared to penetrate through stomata, exhibited subcuticular growth along stomatal rows, colonized glume parenchyma cells and sporulate within 48 to 76 hours after infection (hai). No major differences in the timing of these events were found between Sumai 3 (resistant) and Wheaton (susceptible) genotypes. To study the host response to infection, we examined the expression of six defense response genes (peroxidase, PR-1, PR-2, PR-3, PR-4, and PR-5) in resistant (Sumai 3) and susceptible (Wheaton) genotypes during the initial 48 hai. In both genotypes, transcripts of the six defense response genes accumulated as early as 6 to 12 hai and peaked at 36 to 48 hai. Greater and earlier PR-4 and PR-5 transcript accumulation was observed in Sumai 3 as compared to Wheaton. These data indicated that wheat responds to infection by inducing a set of defense response genes. In a companion study, we examined whether infection induced a systemic response of the defense response genes. We found that infected plants of both resistant (Sumai 3) and susceptible (Wheaton) genotypes induced defense response genes in uninfected portions of the wheat spike, indicating that wheat mounts a systemic response to infection. Our results provide the first documentation of the infection pathways on wheat glumes and provide the first look at the host response at the molecular level.