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ARS Home » Southeast Area » New Orleans, Louisiana » Southern Regional Research Center » Food and Feed Safety Research » Research » Publications at this Location » Publication #183857
Title: The Aflatoxin Pathway Regulator AFLR Induces Gene Transcription Inside and Outside of the Aflatoxin Biosynthetic Cluster

Author
item PRICE, MICHAEL - NCSU
item Yu, Jiujiang
item NIERMAN, WILLIAM - TIGR
item KIM, H - TIGR
item PRITCHARD, BETHAN - NCSU
item JACOBUS, CARRIE - NCSU
item Bhatnagar, Deepak
item Cleveland, Thomas
item PAYNE, GARY - NCSU

Submitted to: Federation of European Microbiological Societies Microbiology Letters
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 11/15/2005
Publication Date: 2/1/2006
Citation: Price, M.S., Yu, J., Nierman, W.C., Kim, H.S., Pritchard, B., Jacobus, C.A., Bhatnagar, D., Cleveland, T.E., Payne, G.A. 2006. The aflatoxin pathway regulator AflR induces gene transcription inside and outside of the aflatoxin biosynthetic cluster. Federation of European Microbiological Societies Microbiology Letters. 255:275-279.

Interpretive Summary: Aflatoxins are toxic and cancer-inducing compounds produced by fungal mold, such as Aspergillus flavus and A. parasiticus. These compounds contaminate our food source such as corn, cotton, peanut and tree nuts when the fungus infects crops. Discovery of all of the genes responsible for aflatoxin formation is absolutely necessary for the control or elimination of aflatoxin contamination in food and feed. The information obtained through genetic studies is significant and important for devising strategies to control aflatoxin contamination through genetic engineering of commercial crops.

Technical Abstract: Transcriptional profiling comparing wild type and delta aflR strains of Aspergillus parasiticus grown under conditions conducive for aflatoxin production identified only 23 up-regulated genes in the wild type. These included 20 genes in the biosynthetic cluster, and 3 additional genes (nadA, hlyC, and niiA), all with AflR binding sites.