Suppression and enhancement of the Aspergillus nidulans medusa mutation by altered dosage of the bristle and stunted genes.

Asexual reproduction in Aspergillus nidulans is characterized by the orderly differentiation of multicellular reproductive structures (conidiophores) and chains of uninucleate conidia (spores). Mutations in the developmental modifier medusa (medA) result in aberrant conidiophores with branching chains of reiterated reproductive cells (metulae), delayed conidial differentiation and frequent reinitiation of secondary conidiophores. We show that incorrect morphology is in part a consequence of modified bristle (brlA) and abacus (abaA) expression, key regulators of the core genetic pathway directing conidial differentiation. First, correct temporal expression of both brlA transcripts (brlA alpha and brlA beta) requires MedAp. Second, MedAp functions as a coactivator required for normal levels of abaA expression. Finally, we show that wild-type morphology results from a finely tuned balance in the expression of brlA, medA and the developmental modifier stunted (stuA). One extra copy of brlA suppresses medA mutations and restores normal abaA mRNA abundance. In contrast, an extra copy of stuA in a medA- strain results in an enhanced medusoid phenotype with extensive metulae proliferation and nearly complete absence of conidia. abaA and brlA alpha transcription are completely repressed in these strains. In general, low stuA:brlA ratios promoted conidiation while high ratios caused proliferation of unicellular sterigmata and inhibited conidiation.