Fusarium verticillioides GBB1, a gene encoding heterotrimeric G protein beta subunit, is associated with fumonisin B biosynthesis and hyphal development but not with fungal virulence.

SUMMARY: Fusarium verticillioides (Sacc.) Nirenberg (teleomorph Gibberella moniliformis Wineland) is a maize pathogen that causes ear rots and stalk rots. The fungus also produces a group of mycotoxins, fumonisins, on infected ears, which cause considerable health and economic concerns for humans and animals worldwide. To date, our understanding of the molecular mechanisms associated with fungal virulence and fumonisin biosynthesis in F. verticillioides is limited. In this study, GBB1, a gene encoding a putative beta subunit of a heterotrimeric G protein, was disrupted and the effects on fumonisin biosynthesis and virulence were evaluated. A GBB1 deletion mutant (Deltagbb1) showed no significant differences in radial growth and mycelial mass but produced significantly less fumonisin B(1 )(FB(1)) than its wild-type progenitor. HPLC analysis showed that Deltagbb1 produced less than 10 p.p.m. FB(1) while the wild-type produced over 140 p.p.m. when strains were grown on cracked corn kernels. Reduced expression of the key FB(1 )biosynthetic genes, FUM1 and FUM8, in Deltagbb1 provides further evidence that GBB1 is involved in FB(1) regulation. Stalk rot virulence, as measured by mean lesion length and by area, was not significantly different in Deltagbb1 compared with the wild-type, suggesting that GBB1 does not regulate virulence in F. verticillioides. Developmentally, hyphae of Deltagbb1 do not deviate from the original axis of polarity established upon germ tube emergence in contrast to wild-type hyphae that meander on and off axis as they grow. Complementation of Deltagbb1 with GBB1 restored FB(1) production and hyphal growth to wild-type. The results of this study demonstrate that heterotrimeric G protein beta subunit plays an important role in regulation of FB(1) biosynthesis and hyphal growth, but not virulence in F. verticillioides.