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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 #94459
Title: REPRESSOR-AFLR INTERACTION MODULATES AFLATOXIN BIOSYNTHESIS IN ASPERGILLUS PARASITICUS

Author
item Chang, Perng Kuang
item Yu, Jiujiang
item Bhatnagar, Deepak
item Cotty, Peter
item BENNETT, JOAN - DCMB,TULANE UNIV.N.O.
item Cleveland, Thomas

Submitted to: Mycopathologia
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 3/20/2000
Publication Date: N/A
Citation: N/A

Interpretive Summary: Aflatoxins are toxic and carcinogenic compounds produced by the fungi A. parasiticus and A. flavus when these fungi invade crops such as corn, cotton seed, peanut and tree nuts. These molds do not have a sexual reproductive cycle. Aspergilli have filamentous structure called mycelia and normally produce asexual spores for dissemination. They also produce mycelial aggregates called sclerotia. Sclerotia are resistant to unfavorable conditions and are capable of remaining dormant for long periods of time. Sclerotia are therefore considered as the survival structures of the fungi. The relationship between aflatoxin biosynthesis of these fungi and sclerotial production is an emerging field for scientists to study toxin production and fungal development. Our efforts have been focused on the regulatory relationship between aflatoxin biosynthesis and sclerotial production in A. parasiticus. In this study, we have demonstrated that specific genetic modification of A. parasiticus results in an increase in the production of aflatoxin precursors, which also alters not only the quantities of sclerotial production but also the shape and size of the sclerotia. These results represent the first genetic evidence of possible link between aflatoxin production and fungal survival.

Technical Abstract: The relationship between aflatoxin biosynthesis and sclerotial development in Aspergillus parasiticus SRRC 2043 was examined by overexpressing a region of aflR, that encoded the transcription activation domain (aflRC). This portion was fused to the promoter of the A. parasiticus nitrite reductase gene, niiA, to give the expression construct, niiA::aflRC. Transformants that contained one copy of niiA::aflRC at the niaD locus, and copies of niiA:aflRC at both the niaD and aflR loci restored aflatoxin biosynthesis in aflatoxin non-permissive nitrate medium to varying degrees. The transformants containing one niiA:aflRC at the niaD locus and another niiA:aflRC at the aflR locus exhibited pigmented phenotype similar to aflR transformants that contained an additional copy of intact aflR integrated into the niaD locus. Increased production of aflatoxin precursors in the niiA::aflRC transformants, as well as in the transformants with intact aflR was associated with a decrease in sclerotial size and an elongation in sclerotial shape. For the niiA::aflRC transformants grown on PDA, the higher copy number of the integrated niiA::aflRC was correlated with increased expression of both aflRC and native aflR. Since the niiA::aflRC gene does not encode a DNA-binding domain, these results suggest that a putative repressor which interacts with the aflR gene product may be involved in aflatoxin biosynthesis and sclerotial development.