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ARS Home » Research » Publications at this Location » Publication #65617


item Leong, Sally

Submitted to: International Rice Genetics Symposium
Publication Type: Proceedings
Publication Acceptance Date: 2/15/1996
Publication Date: N/A
Citation: N/A

Interpretive Summary: Rice blast disease is the most important fungal disease of rice worldwide. Rice is the staple food for two thirds of the human population. We are trying to understand the details of how the rice blast fungus is recognized by rice plants that are resistant to blast. In order to improve our understanding of this host-parasite interaction, we have genetically identified and cloned using recombinant DNA methods a new gene from the fungus that controls this recognition event. We have also genetically identified the resistance gene in the host that specifically responds to pathogens carrying this gene. Through studies of these host and parasite genes and the cellular components that they specify, we hope to better understand how plants resist prevent rice blast disease. This information will allow us to strategically alter the plant to better resist this fungus.

Technical Abstract: Rice blast disease caused by Magnaporthe grisea is one of the most devastating diseases of rice worldwide (Zeigler et al 1994). Once a problem of moderate significance, crop losses associated with this disease have been magnified in recent times with the intensification of rice production. Thus we can expect increasing pressure from this disease as crop production is enhanced to meet the demands of a growing world population as rice is the staple food for two-thirds of the human population. Genetic resistance has been and continues to be the major method of disease control for blast. However, as with many diseases, M.grisea is able to rapidly overcome this resistance. Currently we have little understanding of the molecular basis of cultivar-specific interactions of M.grisea with rice. A M.grisea cultivar specificity gene toward rice cultivar CO39 was previously mapped to one arm of chromosome 1 between RFLP markers CH5-120H and 5-10-F(Smith and Leong 1993). These RFLP markers map 11.6 and 17.2 cM, respectively, on either side of AVRCO39.Using Achilles' cleavage methods, CH5-120H and 5-10-F were shown to be separated by 600 kb. A chromosome walk to avrCO39 was initiated from these flanking RJLP markers. Over 500 kb have been covered in 20 walking steps. Cosmid clones cosegregating with AVRCO39 have been identified and selected clones obtained from the walk were shown to confer avirulence on rice variety CO39 but not 51583 when introduced by transformation into the virulent M.grisea strain Guy11. The DNA conferring avirulence has been delimited to a 7.2 kb region. Preliminary hybridization studies to DNA of the virulent M.grisea strain Guyll using portions of the 7.2 kb region suggest that an alternate allele is not present, or if present has undergone extensive mutation.