Generation of Multicellular Structures in Aspergillus Grant uri icon



  • 9508088 Miller The long term goal of this project is to address mechanistic questions concerning the orderly differentiation and spatial organization of diverse cell types into morphologies specific for a tissue or developmental state. Conidiation in the filamentous fungus Aspergillus nidulans offers the unique opportunity to investigate molecular mechanisms that control multicellular development in eukaryotes. Conidiation is characterized by its highly synchronous nature and the spatial organization of a limited number of differentiated cell types. A genetic hierarchy consisting of five essential regulatory genes controls 1) the transition from multinucleate filamentous growth to uninucleate budding growth, the assembly of a multicellular reproductive structure (conidiophore)and 3) the production of dormant conidia (spores). Complex regulatory interactions provide a mechanism for establishing overlapping spatiotemporal gradients in the transcription factors which, in turn, coordinately activate hundreds of conidiation specific genes. The objectives of this proposal are to begin elucidating mechanisms that integrate spatiotemporal control of developmental gene expression with alterations in cell cycle regulation. Dr. Miller is approaching this problem through a molecular analysis of the modifier genes Medusa (medA) and Stunted (stuA). The medA protein is required for commitment to the developmental program, functioning as a co- activator of a subset of target genes. The stuA protein belongs to a family of transcription factors that control cell cycle progression and fungal development. The specific objectives are to 1) identify, isolate and characterize regulatory gene(s) required for competence dependent stuA transcription, one of the earliest events of the developmental program; 2) identify and characterize gene(s) required for early induction dependent, brlA-independent medA transcription; 3) functionally characterize the medA and stuA proteins; 4) isol ate stuA target genes and 5) characterize extragenic suppressors of stuA mutations and extragenic mutations that mimic the Stunted phenotype. ***

date/time interval

  • October 1, 1995 - September 30, 1999

total award amount

  • 300,000