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The filamentous fungus  Aspergillus nidulans  primarily reproduces by forming asexual spores called conidia and produces the mycotoxin sterigmatocystin (ST), the penultimate precursor of aflatoxins. It has been known that asexual development and ST production are tightly co-regulated by various regulatory inputs. Here, we report that the novel regulator AslA with a C 2 H 2  domain oppositely regulates development and ST biosynthesis. Nullifying  aslA  resulted in defective conidiation and reduced expression of  brlA  encoding a key activator of asexual development, which indicates that AslA functions as an upstream activator of  brlA  expression.  aslA  deletion additionally caused enhanced ST production and expression of  aflR  encoding a transcriptional activator for ST biosynthetic genes, suggesting that AslA functions as an upstream negative regulator of  aflR . Cellular and molecular studies showed that AslA has a trans-activation domain and is localized in the nuclei of vegetative and developing cells but not in spores, indicating that AslA is likely a transcription factor. Introduction of the  aslA  homologs from distantly-related aspergilli complemented the defects caused by  aslA  null mutation in  A. nidulans , implying a functional conservancy of AslA. We propose that AslA is a novel regulator that may act at the split control point of the developmental and metabolic pathways.

Differential Control of Asexual Development and Sterigmatocystin Biosynthesis by a Novel Regulator in Aspergillus nidulans