Aflatoxins, a group of polyketide-derived furanocoumarins  are the most toxic and carcinogenic compounds among the known mycotoxins. Aflatoxins are polyketide-derived secondary metabolites produced via the following conversion path: acetate → polyketide → anthraquinones → xanthones → aflatoxins. The genes involved in the major conversion steps from early precursors to aflatoxins and their functions are as following (1) aflA (fas-2), aflB (fas-1), and aflC (pksA) are involved in the conversion of acetate to NOR.(2) aflD (nor-1), aflE (norA), and aflF (norB) are involved in the conversion of NOR to AVN.aflG (avnA) gene encodes a cytochrome P450 monooxygenase that converts AVN to HAVN.aflH (adhA) is involved in conversion of HAVN to AVF. aflI (avfA) encodes an oxidase for conversion of AVF to VHA.aflJ (estA) is involved in the conversion of VHA to VAL.aflK (vbs) is involved in the conversion of VAL to VERB.aflL (verB) is involved in the conversion of VERB to VERA.aflM (ver-1) and aflN (verA) are involved in the conversion of VERA to DMST.aflO (omtB, dmtA) is involved in the conversion of DMST to ST and of DMDHST to DHST.aflQ (ordA) is involved in the conversion of OMST to AFB1 and AFG1 and of DMDHST to AFB2 and AFG2.

Morespecifically, aflR gene is involved in transcription activation and aflS (aflJ) gene is involved in regulation of aflatoxin biosynthesis.

aflR is the ninth gene of the aflatoxin biosynthesis cluster. It encodes a Cys6Zn2 transcription factor needed for AFT production (Payne et al., 1993). .

Composition of AflR: Among the different regions, the AflR N-terminal region is the DNA-binding domain, including: the Nuclear Localization Domain (NLD) that ensures AflR transfer from cytoplasm to nucleus (Ehrlich et al., 1998) and the linker region that is possibly involved in DNA-binding specificity.

The specific DNA sequence is composed of 11 bp: 5'-TCGSWNNSCGR-3' (with S: Guanine (G) or Cytosine (C); W: Adenine (A) or Thymine (T) and R: A or G) with the strongest binding site being 5'-WCGSNNNSCGA-3'. These AflR binding sites are usually localized at 200 bp (mainly in the promoter region) prior to the aflatoxin genes translation start point (tsp) except for aflT and avfA (Ehrlich, 2009). There is upstream of the aflR gene transcription start point (TSP), a partial AflR binding site, suggesting an autoregulation. In the same intergenic region, other binding sites from various DNA-binding proteins suggest that many regulation systems may impact aflR expression.

Price et al., (2006) studied 40% of the A. parasiticus transcriptome in a wild type strain and its ∆aflR mutant which lacks the capacity to produce AFT. They revealed that most of the aflatoxin gene in the cluster were down regulated in the mutant (except for aflF, I ,Ma, N and Na) (Price et al., 2006).

aflR is the ninth gene of the aflatoxin biosynthesis cluster. It encodes a Cys6Zn2 transcription factor needed for AFT production (Payne et al., 1993). .

Composition of AflR: Among the different regions, the AflR N-terminal region is the DNA-binding domain, including: the Nuclear Localization Domain (NLD) that ensures AflR transfer from cytoplasm to nucleus (Ehrlich et al., 1998) and the linker region that is possibly involved in DNA-binding specificity.

The specific DNA sequence is composed of 11 bp: 5'-TCGSWNNSCGR-3' (with S: Guanine (G) or Cytosine (C); W: Adenine (A) or Thymine (T) and R: A or G) with the strongest binding site being 5'-WCGSNNNSCGA-3'. These AflR binding sites are usually localized at 200 bp (mainly in the promoter region) prior to the aflatoxin genes translation start point (tsp) except for aflT and avfA (Ehrlich, 2009). There is upstream of the aflR gene transcription start point (TSP), a partial AflR binding site, suggesting an autoregulation. In the same intergenic region, other binding sites from various DNA-binding proteins suggest that many regulation systems may impact aflR expression.

Price et al., (2006) studied 40% of the A. parasiticus transcriptome in a wild type strain and its ∆aflR mutant which lacks the capacity to produce AFT. They revealed that most of the aflatoxin gene in the cluster were down regulated in the mutant (except for aflF, I ,Ma, N and Na) (Price et al., 2006).