Altered Transcript Abundances of Aspergillus Flavus and Transgenic Maize Overexpressing a Bacterial Glutamate Dehydrogenase (GDH) Reduces Aflatoxin Contamination of Grain.
Poster Number 818
Tuesday, November 5, 2013
Tampa Convention Center, East Hall, Third Floor
David A. Lightfoot, Southern Illinois University Carbondale, Carbondale, IL and Ahmad Fakhoury, PSAS, SIUC, Carbondale, IL
Aspergillus flavus is a filamentous fungus that causes an ear and kernel rot in maize (Zea mays L.). Ear rots are often associated with the accumulation of aflatoxin in the infected plant. The ability of A. flavus to produce aflatoxin depends on the nature and the composition of the substrate. Transgenic maize lines expressing a bacterial NADPH dependent gdhA (glutamate dehydrogenase) gene showed increased nitrogen metabolism with an overall increase in some amino acids in the ear. Previous studies showed that A. flavus exhibits decreased conidiation and aflatoxin accumulation on GDH+ maize lines. The aim here was to use microarray studies to assess changes in the expression patterns of A. flavus genes on GDH+ maize. Used was artificial inoculation in the field of dough stage maize kernels of inbred ‘H99’ transgenic or non transgenic with gdhA. The mRNA was isolated after harvest. Increased by more than 2 fold on GDH+ maize were 747 A. flavus transcripts, only 27 decreased. Hydrolases (EC 3.-), kinases (EC 7.-) and ABC transporters (non-enymatic) were the major protein families increased. No effect on toxin pathway genes was detected. No maize transcripts were increased by GDH+, though 95 were reduced significantly by two fold or more. Reduced by GDH were transcripts encoding trehalase, branched chain amino acids, primary carbon metabolism and polyphenol synthesis. Metabolites increased by the reduced transcripts in GDH+ maize included cellulose to lignin ratios; non-branched side chain amino acids; and some toxic products of special nitrogen metabolism. Therefore, the gdhA gene was inferred to confer partial resistance to A. flavus by repressing pathways in a way that lead to altered compositions, stronger cell walls and increased defense metabolite concentrations, pathways different from endogenous resistance mechanisms discovered to date.