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Silencing of the aflatoxin gene cluster in a diploid strain of Aspergillus flavus is suppressed by ectopic aflR expression.
- Source :
-
Genetics [Genetics] 2007 Aug; Vol. 176 (4), pp. 2077-86. Date of Electronic Publication: 2007 Jun 11. - Publication Year :
- 2007
-
Abstract
- Aflatoxins are toxic secondary metabolites produced by a 70-kb cluster of genes in Aspergillus flavus. The cluster genes are coordinately regulated and reside as a single copy within the genome. Diploids between a wild-type strain and a mutant (649) lacking the aflatoxin gene cluster fail to produce aflatoxin or transcripts of the aflatoxin pathway genes. This dominant phenotype is rescued in diploids between a wild-type strain and a transformant of the mutant containing an ectopic copy of aflR, the transcriptional regulator of the aflatoxin biosynthetic gene cluster. Further characterization of the mutant showed that it is missing 317 kb of chromosome III, including the known genes for aflatoxin biosynthesis. In addition, 939 kb of chromosome II is present as a duplication on chromosome III in the region previously containing the aflatoxin gene cluster. The lack of aflatoxin production in the diploid was not due to a unique or a mis-expressed repressor of aflR. Instead a form of reversible silencing based on the position of aflR is likely preventing the aflatoxin genes from being expressed in 649 x wild-type diploids. Gene expression analysis revealed the silencing effect is specific to the aflatoxin gene cluster.
- Subjects :
- Base Sequence
DNA Primers genetics
DNA, Fungal genetics
DNA-Binding Proteins genetics
Diploidy
Fungal Proteins genetics
Gene Dosage
Gene Expression
Gene Silencing
Mutation
Sequence Deletion
Transcription Factors genetics
Transformation, Genetic
Aflatoxins genetics
Aspergillus flavus genetics
Genes, Fungal
Multigene Family
Subjects
Details
- Language :
- English
- ISSN :
- 0016-6731
- Volume :
- 176
- Issue :
- 4
- Database :
- MEDLINE
- Journal :
- Genetics
- Publication Type :
- Academic Journal
- Accession number :
- 17565943
- Full Text :
- https://doi.org/10.1534/genetics.107.073460