- Home
- Agricultural Economics
- Animal and Food Sciences
- Biosystems and Agricultural Engineering
- Community and Leadership Development
- Entomology
- Extension and Education
- Extension Administration
- Forestry
- Horticulture
- Human Environmental Sciences
- Landscape Architecture
- Livestock Disease Diagnostic Center
- Plant Pathology
- Plant and Soil Sciences
- Veterinary Science
Search research reports:
Molecular Genetics of the Interaction between Corn and Corn Stalk Rot Fungi (Colletotrichum graminicola and Gibberella zeae)
L.J. Vaillancourt
Department of Plant Pathology
Non-Technical Summary
Stalk rot is one of the most economically important diseases of corn worldwide. Complete control is currently impossible, although damage can usually be reduced by use of hybrids with partial resistance to one or more of the causal fungi, and by minimizing plant stress. My long-term goal is to develop a detailed molecular and cellular understanding of the interactions between corn and corn stalk rot fungi so that we can manage stalk rot disease more effectively.
2010 Project Description
Industry estimates suggest that approximately 6 percent of the corn crop in the U.S. is lost to fungal stalk rot diseases annually. Resistance is available, but tends to break down during grain filling or under conditions that stress the plant. This makes management of this disease syndrome particularly challenging.
We are using a combination of molecular and cytological approaches to study and compare the relationship between pathogenicity of two important stalk rot fungi, Colletotrichum graminicola and Gibberella zeae and the nutritional and defense status of the host, and to understand more about how these fungi enter and colonize stalks. We have continued our studies of a nonpathogenic C. graminicola mutant that we identified during a large-scale screening experiment. The mutant is deficient in one component of the signal peptidase enzyme responsible for cleavage of signal peptides from proteins destined for transport through the endoplasmic reticulum system of the cell. The gene encoding this enzyme was named CPR1.
The hypothesis we are testing is that the mutant fails to suppress resistance responses in the host because it cannot secrete a specific suppressor of the host resistance response. We have been able to functionally demonstrate the existence of this suppressor: co-inoculation of the wild type up to 0.5 cm away from the mutant on maize leaf sheaths allows the mutant to develop normally in the host tissues, and application of culture filtrates from the wild type allows normal infection by the mutant. We are now focused on learning more about the nature of this suppressor.
We have continued our work to study the relationship of CPR1 to stress response, and we have found that the mutant is more sensitive to various stresses, in particular to oxidative stress. Thus we propose that CPR1 functions in the general stress response of C. graminicola. We are developing new tools to study the occurrence of stress in planta for our future research.
Meanwhile we have been working to develop F. graminearum as a model corn stalk rot pathosystem comparable to what we have already done for C. graminicola. We have perfected protocols and strains for conducting crosses and for making knockout mutants. We have produced various mutants of F. graminearum that we are testing for pathogenicity and response to stress. We continue to work on developing reliable pathogenicity bioassays on corn stalks and ears in the greenhouse, and we are currently evaluating various germplasm and timing to discover the effect.
A genome sequence has been available for F. graminearum for several years. During the past year, we have completed the genome of C. graminicola in collaboration with the Broad Institute. A high quality annotation was released in October.
2010 Impact
Our investigations have dramatically increased our understanding of how stalk rot fungi cause decay symptoms in their host plants, and how those symptoms relate to fungal infection and colonization. We developed a reproducible greenhouse assay for infection of corn stalks that we have shared now with many other labs. We have been able to show more parallels than previously suspected between infections of leaves and stalks by C. graminicola. We have identified a novel and previously unsuspected role for the protein secretion machinery, including the signal peptidase, in the establishment of biotrophic colonization and also in necrotrophic (rotting) development. We have uncovered evidence that C. graminicola produces a secreted suppressor of the corn resistance response, and we have developed a bioassay for that suppressor. Our work has supported the U.S. hybrid corn industry by developing more effective screening tools, and by helping to identify and characterize, novel sources of resistance for this disease.
Together C. graminicola and G. zeae are the most aggressive and problematic of the stalk rot fungi in the U.S. Germplasm with resistance to one type generally does not provide resistance to the other. By developing these fungi as model stalk rot pathosystems we have made it possible to conduct comparative analyses that may lead to more general understanding of factors important for stalk rots and in turn to more general therapies that will be effective against all stalk rot fungi.