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 B(1) (AFB(1)), but elevated quantities of a new metabolite, deoxyAFB(1). To explain this result, we suggest that, in the absence of NorA, the AFB(1) reduction product, aflatoxicol, is produced and is readily dehydrated to deoxyAFB(1) in the acidic medium, enabling us to observe this otherwise minor toxin produced in wild-type A. flavus.
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