Extragenic Suppressors of Loss-of-Function Mutations in the Aspergillus FlbA Regulator of G-Protein Signaling Domain Protein

Corresponding author: Thomas H. Adams, Department of Biology, Texas A&M University, College Station, TX 77843-3258., tom{at}bio.tamu.edu (E-mail)

Communicating editor: R. H. DAVIS

We showed previously that two genes, bA and fadA, have a major role in determining the balance between growth, sporulation, and mycotoxin (sterigmatocystin; ST) production by the filamentous fungus Aspergillus nidulans. fadA encodes the subunit for a heterotrimeric G-protein, and continuous activation of FadA blocks sporulation and ST production while stimulating growth. bA encodes an A. nidulans regulator of G-protein signaling (RGS) domain protein that antagonizes FadA-mediated signaling to allow development. To better understand FlbA function and other aspects of FadA-mediated growth control, we have isolated and characterized mutations in four previously undefined genes designated as sfaA, sfaC, sfaD, and sfaE (suppressors of flbA), and a new allele of fadA (fadA^R205H), all of which suppress a bA loss-of-function mutation (bA98). These suppressors overcome bA losses of function in both sporulation and ST biosynthesis. fadA^R205H, sfaC67, sfaD82, and sfaE83 mutations are dominant to wild type whereas sfaA1 is semidominant. sfaA1 also differs from other suppressor mutations in that it cannot suppress a bA deletion mutation (and is therefore allele specific) whereas all the dominant suppressors can bypass complete loss of bA. Only sfaE83 suppressed dominant activating mutations in fadA, indicating that sfaE may have a unique role in fadA-bA interactions. Finally, none of these suppressor mutations bypassed uG loss-of-function mutations in development-specific activation.

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