Absence of the aflatoxin biosynthesis gene, norA, allows accumulation of deoxyaflatoxin B1 in Aspergillus flavus cultures

Abstract

Biosynthesis of the highly toxic and carcinogenic aflatoxins in select Aspergillus species from the common intermediate O-methylsterigmatocystin has been postulated to require only the cytochrome P450 monooxygenase, OrdA (AflQ). We now provide evidence that the aryl alcohol dehydrogenase NorA (AflE) encoded by the aflatoxin biosynthetic gene cluster in Aspergillus flavus affects the accumulation of aflatoxins in the final steps of aflatoxin biosynthesis. Mutants with inactive norA produced reduced quantities of aflatoxin B1 (AFB1), but elevated quantities of a new metabolite, deoxyAFB 1. To explain this result, we suggest that, in the absence of NorA, the AFB1 reduction product, aflatoxicol, is produced and is readily dehydrated to deoxyAFB1 in the acidic medium, enabling us to observe this otherwise minor toxin produced in wild-type A. flavus. © 2010 Federation of European Microbiological Societies. Published by Blackwell Publishing Ltd.