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Department of Plant Pathology, Box 7567, North Carolina State University, Raleigh, North Carolina 27695-7567
D.R. Georgianna
Department of Plant Pathology, Box 7567, North Carolina State University, Raleigh, North Carolina 27695-7567, and Functional Genomics Graduate Program, Box 7567, North Carolina State University, Raleigh, North Carolina 27695-7567
J.R. Wilkinson
Department of Biochemistry and Molecular Biology, Box 9650, Mississippi State University, Mississippi State, Mississippi 39762
J. Yu
USDA/ARS, Southern Regional Research Center, New Orleans, Louisiana 70124
H.K. Abbas
USDA/ARS, Crop Genetics & Production Research Unit, Stoneville, Mississippi 38776
D. Bhatnagar
T.E. Cleveland
USDA/ARS, Southern Regional Research Center, New Orleans, Louisiana 70124
W. Nierman
The Institute for Genomic Research, 9712 Medical Center Drive, Rockville, Maryland 20850
G.A. Payne 1
Department of Plant Pathology, Box 7567, North Carolina State University, Raleigh, North Carolina 27695-7567
The molecular regulation of aflatoxin biosynthesis is complex and influenced by several environmental conditions; one of these is temperature. Aflatoxins are produced optimally at 2830 C, and production decreases as temperatures approach 37 C, the optimum temperature for fungal growth. To better characterize the influence of temperature on aflatoxin biosynthesis, we monitored the accumulation of aflatoxin and the expression of more than 5000 genes in Aspergillus flavus at 28 C and 37 C. A total of 144 genes were expressed differentially (P < 0.001) between the two temperatures. Among the 103 genes more highly expressed at 28 C, approximately 25% were involved in secondary metabolism and about 30% were classified as hypothetical. Genes encoding a catalase and superoxide dismutase were among those more highly expressed at 37 C. As anticipated we also found that all the aflatoxin biosynthetic genes were much more highly expressed at 28 C relative to 37 C. To our surprise expression of the pathway regulatory genes aflR and aflS, as well as aflR antisense, did not differ between the two temperatures. These data indicate that the failure of A. flavus to produce aflatoxin at 37 C is not due to lack of transcription of aflR or aflS. One explanation is that AFLR is nonfunctional at high temperatures. Regardless, the factor(s) sensing the elevated temperatures must be acute. When aflatoxin-producing cultures are transferred to 37 C they immediately stop producing aflatoxin.
Key words: AFLR, biosynthesis, micro-arrays
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