Submitted to: Molecular Plant Microbe Interactions
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 5/15/2000
Publication Date: N/A
Citation: N/A Interpretive Summary: Corn diseases cause millions of dollars of losses each year. Identifying and understanding resistance mechanisms to these diseases can ultimately help move resistance traits into non- resistant varieties. Molecular biological methods were used to identify the mechanisms of resistance in a mutant resistant line. A novel resistance mechanism was identified. Knowing what this resistance mechanism is should help in the development of disease resistant commercial varieties of corn using conventional breeding or molecular biological methods. Disease resistant material is expected to result in savings to growers, end users, and consumers.
Technical Abstract: The maize rhml mutation resists Bipolaris maydis by producing small necrotic lesions surrounded by chlorotic haloes. Both rhml and wild type lesions contained viable fungus, but sporulation was inhibited on rhml. Chitinase, PR1, and peroxidase protein levels differed little between rhml and wild type with or without B. maydis infection. Global mRNA profiles surveyed using the CuraGen GeneCalling mRNA differential display technology revealed hundreds of cDNA fragments two-fold or more induced or suppressed in rhml and wild type plants following B. maydis infection. Nonetheless between rhml and wild type, however, only 0.4% to 0.7% of the cDNA fragments were two-fold or more differentially expressed. Among these few differentially expressed genes, and supported by northern blots, was beta-glucosidase Glu l, whose mRNA accumulated to higher levels after B. maydis infection of rhml than wild type. Glu l is thought to function in defense by releasing antimicrobial compounds from glucosyl conjugates, such as hydroxamic acids like DIMBOA from DIMBOA-glucoside. While aglycone DIMBOA levels were observed to be higher in four rhml alleles relative to wild types, double mutants of rhml and bxl, a hydroxamic acid deficient mutant, revealed that rhml resistance is expressed in the bxl genetic background and is, therefore, hydroxamic acid independent.