Asexual development (conidiation for higher fungi) is the most common reproductive mode of many fungi; yet, its regulatory mechanisms remain to be understood. In this study, we carried out a multi-copy based genetic screen in the absence of the repressor of conidiation sfgA, which is designed to identify a new set of negative regulator(s) of conidiation. Among over 100,000 colonies, 45 transformants showing altered conidiation were isolated, of which 10 defined the nsdDgene (AN3152), a key activator of sexual fruiting. The others have defined AN7507, AN2009, AN1652, AN5833 and AN9141. A series of verification, genetic and mycotoxin analyses revealed that only NsdD is a true negative regulator of brlA (an essential activator of conidiation) and conidiation, and that NsdD acts downstream of fluGand flbA~E, but upstream of brlA. The removal of NsdD was sufficient to cause hyper-active conidiation even in liquid submerged culture, as well as early and prolonged activation of brlA, suggesting that NsdD is indeed a key repressor of brlA and conidiation. Moreover, the deletion of nsdDresults in hyper-active conidiation and altered production of mycotoxins in the opportunistic human pathogen Aspergillus fumigatus and the aflatoxin-producing human/plant pathogen Aspergillus flavus. Importantly, we have discovered that nsdDencodes two differentially expressed mRNAs and polypeptides (b and a). Finally, the subsequent transient promoter analysis using the brlA promoter::luciferase fusion constructs have revealed that NsdD negatively regulates the brlAb promoter activity. In summary, NsdD is a key negative regulator of conidiation acting direct upstream of brlA in A. nidulans, and couples conidiation and mycotoxin biosynthesis in Aspergilli.
Full conference title:
27th Fungal Genetics Conference
- Fungal Genetics Conference 27th (2013)