TABLE 2.
Allele(s) | Function | Mutation effect | Reference(s) |
---|---|---|---|
aflR | Pathway-specific regulator of stc gene expression | 91 | |
ΔaflR | Loss of sterigmatocystin-aflatoxin production | 29, 92, 131 | |
Affects conidiation and sclerotial development | 25, 97, 108, 120 | ||
OEaflR | Early and increased mycotoxin production | 106 | |
brlA | Pathway-specific regulator of conidiogenesis genes | 31 | |
ΔbrlA | Abolishment of conidiation | 17, 58 | |
OEbrlA | Early onset of conidiation, including sporulation in submerged liquid culture; no effect on sterigmatocystin production | 8 | |
fluG | Involved in synthesis of extracellular, diffusible factor required for conidiation | 69 | |
ΔfluG | Aconidial; no sterigmatocystin production | 55 | |
OEfluG | Activates conidiation; early sterigmatocystin production observed in submerged liquid culture but not on plates | 55 | |
flbA | Encodes RGS-containing protein; active FlbA inactivates G-protein pathway | 70 | |
ΔflbA | Aconidial; no sterigmatocystin production | 55 | |
OEflbA | Premature sporulation, early sterigmatocystin production | 55 | |
fadA | α-Subunit of heterotrimeric G protein | 133 | |
ΔfadA and fadAG203R | Premature conidiation; early sterigmatocystin production | 55 | |
fadAG42R | Aconidial; no sterigmatocystin production | 55 | |
pkaA | cAMP-dependent PKA | 106 | |
ΔpkaA | Results in hypersporulation; aberrant sterigmatocystin production | 106 | |
OE pkaA | Decreased conidiation; no sterigmatocystin production | 106 | |
ΔpkaA ΔflbA | Double deletion mutant; partially restores some sporulation; restores sterigmatocystin production | 106 | |
ΔpkaA fadAG42R | Partially restores sporulation but not sterigmatocystin production | 106 | |
sfaD | β-Subunit of heterotrimeric G-protein | 99 | |
ΔsfaD | Increased sporulation | 105 |
Δ indicates the gene has been deleted. OE indicates the gene is overexpressed. fadAG203R is the dominant negative fadA allele. fadAG42R is the dominant activated fadA allele.