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Univ. of Illinois, Dep. of Crop Sciences, Edward R. Madigan Lab., 1201 West Gregory, Urbana, IL 61801 and Kazan Inst. of Biology, Russian Academy of Sciences, Box 30, 420503, Kazan, Russia
Univ. of Illinois, Dep. of Crop Sciences Edward R. Madigan Lab., 1201 West Gregory, Urbana, IL 61801 and Suranaree Univ. of Technology, Inst. of Agric. Technology, 111 Univ. Avenue, Muang District, Nakhon Ratchasima 30000, Thailand
Univ. of Illinois, Dep. of Crop Sciences, Edward R. Madigan Lab., 1201 West Gregory, Urbana, IL 61801
* Corresponding author (widholm{at}uiuc.edu).
Studies of the activity levels of the fungal cell wall degradative enzyme, ß-l,3-glucanase, were carried out with Zea mays L. embryogenie callus cultures and kernels of genotypes with different abilities to resist aflatoxin formation on the ears. Dual-culture experiments of the aflatoxin forming fungus, Aspergillus flavus Link: Fr. with maize callus, demonstrated that the growth of A. flavus on plates was inhibited more by callus of a resistant genotype (Tex 6 x Mol7 denoted TxM) than by a sensitive genotype (Pa91). The inhibition correlated with the activity levels of ß-1,3-glucanase in the callus and in the culture medium. The presence of the fungus caused an increase in enzyme activity in TxM but not in Pa91 callus. Direct treatment of callus of both genotypes with A. flavus spores caused the amount of callose to increase within 30 min. An elevated ß-l,3-glucanase activity in maize kernels was also correlated with lower A. flavus infection observed in the resistant genotype (Tex 6) compared with a susceptible one (B73). Fungal inoculation of the ears increased the enzyme activities both in kernels in contact with and not in contact with the fungus. These studies indicate that ß-l,3-glucanase activity may have a role in the inhibition of growth of the A. flavus fungus, that maize embryogenic callus and kernels do respond to the presence of this nonpathogenic fungus, and that these systems might be useful in further plant-fungal interaction studies.
Received for publication September 19, 1997.
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