|Harris Coward, Pamela|
Submitted to: Applied Microbiology and Biotechnology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 6/6/2007
Publication Date: 7/24/2007
Citation: Cary, J.W., OBrian, G.R., Nielsen, D.M., Nierman, W., Harris-Coward, P.Y., Yu, J., Bhatnagar, D., Cleveland, T.E., Payne, G.A., Calvo, A.M. 2007. Elucidation of veA-dependent genes associated with aflatoxin and sclerotial production in Aspergillus flavus by functional genomics. Applied Microbiology and Biotechnology. 76:1107-1118. Interpretive Summary: This work describes experiments that have been conducted in an effort to better understand the genetic mechanisms that control aflatoxin production and growth and development in Aspergillus flavus. Aflatoxins are toxic and carcinogenic compounds often produced by the fungi, Aspergillus flavus, during growth on crops such as corn, peanuts, cottonseed, and treenuts. Because of the potential health risks, aflatoxin contamination of food and feed crops is also of great economic importance to farmers who cannot sell their crops due to strict domestic and international regulatory guidelines with regards to aflatoxin contamination. We have succeeded identifying a gene, designated veA, from A. flavus that when inactivated stops the fungus from producing aflatoxin and also structures known as sclerotia that help the fungus to survive in the field under adverse conditions. Using DNA microarray technology, we have identified a number of genes from A. flavus that appear to be under the control of the VeA protein and as such may be involved in aflatoxin or sclerotia production. We can now characterize these genes and determine their role in aflatoxin/sclerotia production. This will provide us with more information on the mechanisms responsible for production of aflatoxin and A. flavus development. This in turn will help in devising strategies for eliminating fungal toxin contamination of food and feed crops.
Technical Abstract: The aflatoxin-producing fungi, Aspergillus flavus and A. parasiticus, form structures called sclerotia that allow for survival under adverse conditions. Deletion of the veA gene in A. flavus and A. parasiticus blocks production of aflatoxin, as well as sclerotial formation. We used microarray technology to identify genes differentially expressed in wild-type veA and veA mutant strains that could be involved in aflatoxin production and sclerotial development in A. flavus. The DNA microarray analysis revealed 684 genes whose expression changed significantly over time, 136 of these were differentially expressed between the two strains, including 27 genes that demonstrated a significant difference in expression both between strains and over time. A group of 115 genes showed greater expression in the wild type than in the veA mutant strain. We identified a subgroup of veA-dependent genes that exhibited time-dependent expression profiles similar to those of known aflatoxin biosynthetic genes or that were candidates for involvement in sclerotial production in the wild type.