Three non-allelic, asporogenous mutants of Aspergillus nidulans that are blocked at an early stage of development (PRN mutants) each overproduce a set of phenolic metabolites. These same mutants also overproduce an activity, of yet unknown chemical nature, that induces sexual sporulation and inhibits asexual sporulation of wild type. Other studies suggest that this activity, called psi, is a hormone precursor that can be processed to the hormone by wild type, but not by PRN mutants.
The specific aims of this proposal are: 1. To determine the chemical identity of the phenolic metabolites overproduced by PRN mutants and establish that some of these are intermediates of a metabolic pathway blocked at specific steps by PRN mutations. 2. To determine the chemical nature of psi factor, the relationship of psi to the co-accumulated phenolic metabolites, and the metabolic fate of psi in fungal tissues. 3. To isolate and characterize mutants that underproduce psi and mutants that do not respond to psi. 4. To clone the genes involved in the biosynthesis of and response to psi. These clones will be used as probes to determine at what developmental stage and in which tissues the corresponding mRNAs are present. The cloned genes will also be used to create null mutations in these genes by gene disruption. The long-term goal of this work is to understand the nature of the switch mechanism that initiates differentiation in Aspergillus and possibly in other organisms.
