The transcription factor BrlA plays a central role in the production of asexual spores (conidia) in the fungus Aspergillus nidulans. BrlA levels are controlled by signal transducers known collectively as UDAs. Furthermore, it governs the expression of CDP regulators, which control most of the morphological transitions leading to the production of conidia. In response to the emergence of fungal cells in the air, the main stimulus triggering conidiation, UDA mutants such as the flbB deletant fail to induce brlA expression. Nevertheless, ΔflbB colonies conidiate profusely when they are cultured on a medium containing high H2PO4- concentrations, suggesting that the need for FlbB activity is bypassed. We used this phenotypic trait and an UV-mutagenesis procedure to isolate ΔflbB mutants unable to conidiate under these stress conditions. Transformation of mutant FLIP166 with a wild-type genomic library led to the identification of the putative transcription factor SocA as a multicopy suppressor of the FLIP (Fluffy, aconidial, In Phosphate) phenotype. Deregulation of socA altered both growth and developmental patterns. Sequencing of the FLIP166 genome enabled the identification and characterization of PmtCP282L as the recessive mutant form responsible for the FLIP phenotype. Overall, results validate this strategy for identifying genes/mutations related to the control of conidiation.
Keywords: asexual development; conidiation; filamentous fungi; mutagenesis; protein O-mannosylation; signal transduction; transcriptional regulation.