ena-STUDY-USDA-ARS-27-11-2015-22:04:42:935-234
Degeneration of aflatoxin gene clusters in Aspergillus flavus from Africa and North America.
Aspergillus flavus is the primary causal agent of food and feed contamination with the toxic fungal metabolites aflatoxins. Aflatoxin-producing potential of A. flavus varies among genotypes and among vegetative compatibility groups (VCGs). The genes involved in aflatoxin biosynthesis are clustered together in a highly conserved order. Gene deletion and presence of single nucleotide polymorphisms (SNPs) in aflatoxin biosynthesis genes is often associated with inability to produce toxin by members of Aspergillus section Flavi. In order to identify mechanisms of atoxigenicity and understand degeneration of aflatoxin gene clusters in atoxigenic genotypes, aflatoxin gene clusters from 35 A. flavus genotypes from North America, West Africa and East Africa were sequenced and analyzed. Inability of some genotypes to produce aflatoxin resulted from the absence of the necessary biosynthetic genes, whereas in other genotypes, atoxigenicity originated from the degeneration through SNP formation. Comparative analysis of aflatoxin gene cluster leading to the degeneration should provide further insight into the mechanism of atoxigenicity in A. flavus and thus contribute to the diagnosis and monitoring of the biocontrol genotypes applied in the field.
Aspergillus flavus is the primary causal agent of food and feed contamination with the toxic fungal metabolites aflatoxins. Aflatoxin-producing potential of A. flavus varies among genotypes and among vegetative compatibility groups (VCGs). The genes involved in aflatoxin biosynthesis are clustered together in a highly conserved order. Gene deletion and presence of single nucleotide polymorphisms (SNPs) in aflatoxin biosynthesis genes is often associated with inability to produce toxin by members of Aspergillus section Flavi. In order to identify mechanisms of atoxigenicity and understand degeneration of aflatoxin gene clusters in atoxigenic genotypes, aflatoxin gene clusters from 35 A. flavus genotypes from North America, West Africa and East Africa were sequenced and analyzed. Inability of some genotypes to produce aflatoxin resulted from the absence of the necessary biosynthetic genes, whereas in other genotypes, atoxigenicity originated from the degeneration through SNP formation. Comparative analysis of aflatoxin gene cluster leading to the degeneration should provide further insight into the mechanism of atoxigenicity in A. flavus and thus contribute to the diagnosis and monitoring of the biocontrol genotypes applied in the field.