
Absence of the aflatoxin biosynthesis gene, norA , allows accumulation of deoxyaflatoxin B 1 in Aspergillus flavus cultures
Author(s) -
Ehrlich Kenneth C.,
Chang PerngKuang,
Scharfenstein Leslie L.,
Cary Jeffrey W.,
Crawford Jason M.,
Townsend Craig A.
Publication year - 2010
Publication title -
fems microbiology letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.899
H-Index - 151
eISSN - 1574-6968
pISSN - 0378-1097
DOI - 10.1111/j.1574-6968.2010.01914.x
Subject(s) - aspergillus flavus , aflatoxin , biosynthesis , gene cluster , metabolite , biochemistry , monooxygenase , aspergillus , toxin , mutant , biology , carcinogen , cytochrome p450 , chemistry , gene , microbiology and biotechnology , enzyme , food science
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 .