The Aspergillus nidulans esdC (early sexual development) gene is necessary for sexual development and is controlled by veA and a heterotrimeric G protein

• Published in: Fungal genetics and biology Vol. 45; no. 3; pp. 310 - 318
• Main Authors: Han, Kap-Hoon, Kim, Jong Hwa, Moon, Hosun, Kim, Serha, Lee, Sung-Suk, Han, Dong-Min, Jahng, Kwang-Yeop, Chae, Keon-Sang
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 01.03.2008
• Subjects: Amino Acid Sequence; amino acid sequences; Aspergillus nidulans; Aspergillus nidulans - genetics; Aspergillus nidulans - growth & development; Aspergillus nidulellus; Binding Sites - genetics; cell differentiation; esdC; esdC gene; FadA; Fungal Proteins - genetics; Fungal Proteins - physiology; G-proteins; gene expression; gene expression regulation; Gene Expression Regulation, Developmental; Gene Expression Regulation, Fungal; genes; Glycogen binding domain; Heterotrimeric GTP-Binding Proteins - genetics; Heterotrimeric GTP-Binding Proteins - physiology; introns; Introns - genetics; messenger RNA; Molecular Sequence Data; Mutation; nucleotide sequences; Sequence Homology, Amino Acid; Sexual development; veA gene; FadA; esdC; Sexual development; Aspergillus nidulans; Glycogen binding domain
• ISSN: 1087-1845; 1096-0937
• DOI: 10.1016/j.fgb.2007.09.008

The esdC ( early sexual development) gene was isolated by using an expressed sequence tag (EST) as a probe from a genomic library of the early sexual developmental stage mycelia of Aspergillus nidulans. The sequence analysis revealed that the esdC gene contains a 59 bp intron and encodes a 266 amino acid polypeptide with a calculated molecular weight of 29.4 kDa. The EsdC protein is conserved among filamentous fungi and has a domain with similarity to a glycogen binding domain conserved in the β subunit of the AMP-activated protein kinase (AMPK) complex. Although the esdD gene was expressed during asexual development, the expression reached its maximum at 10 h and decreased thereafter up to 50 h after the end of the induction of sexual development. In an esdC-null mutant under a veA + background, no sexual structures were formed at any condition examined. However, esdC overexpression did not lead to an induction of sexual development. In addition, to the effect of the esdC mutation on the sexual development, more conidiophores were formed in the esdC-null mutant than in a wild type. These results indicate that the esdC gene is necessary for sexual structure formation but its overexpression is not sufficient to enhance this process. Expression of the esdC gene throughout development was positively regulated by the veA gene. In addition, very little and no esdC transcript, respectively, was observed in an flbA-null mutant and in a fadA G42R mutant, and the esdC transcript level was higher in a fadA-null mutant and in a sfaD-null mutant than in a wild type, indicating that inactivation of FadA is necessary for positive regulation of esdC expression.