Conidiation of the filamentous ascomycete Aspergillus nidulans follows a developmental program of cell differentiation which culminates in the production of spore-bearing structures called conidiophores. This developmental program serves as model system for the study of cellular differentiation and inhibition of proliferative growth pathways. The flbD gene product has been proposed to function in an initiation pathway which leads to development. Strains which harbor a deletion of the flbD locus exhibit a fluffy phenotype associated with delayed conidiation and uncontrolled proliferative growth. In order to further understand the pathways in which flbD functions, a screen for mutations which suppress the phenotype of a flbD null mutant were sought. Twenty such mutations were isolated which restore wild-type timing of conidiation to a strain harboring a flbD deletion. These mutations map to two linkage groups designated sfd,A and sfdB. Strains harboring mutations in sfdA or sfdB have been shown to exhibit a reduced growth phenotype on agar plates and unlike wild-type strains, are capable of forming conidiophores in submerged culture. The N-terminal region of FlbD is very similar to the DNA binding regions of the Myb family of transcription factors including the protooncogene c-myb. We show here that FlbD activates transcription from a yeast reporter gene containing consensus c-myb binding sites as upstream activating sequences. Partial funding for this work is provided by NIH National Research Service Award Number 1 F32 GM20072-01 to E.M.K.
Fungal Genet. Newsl. 46 (Supl):
Full conference title:
Fungal Genetics Conference 20th
- Fungal Genetics Conference 20th (1999)