The velvet genes are conserved in ascomycetous fungi and function as global regulators of differentiation and secondary metabolism. Here, we characterized one of the velvet genes, designated FgVelB, in the plant-pathogenic fungus Fusarium graminearum, which causes fusarium head blight in cereals and produces mycotoxins within plants. FgVelB-deleted (DFgVelB) strains produced fewer aerial mycelia with less pigmentation than those of the wildtype (WT) during vegetative growth. Under sexual development conditions, the DFgVelB strains produced no fruiting bodies but retained male fertility, and conidiation was threefold higher compared with the WT strain. Production of trichothecene and zearalenone was dramatically reduced compared with the WT strain. In addition, the DFgVelB strains were incapable of colonizing host plant tissues. Transcript analyses revealed that FgVelB was highly expressed during the sexual development stage, and may be regulated by a mitogen-activated protein kinase cascade. Microarray analysis showed that FgVelB affects regulatory pathways mediated by the mating-type loci and a G-protein alpha subunit, as well as primary and secondary metabolism. These results suggest that FgVelB has diverse biological functions, probably by acting as a member of a possible velvet protein complex, although identification of the FgVelB-FgVeA complex and the determination of its roles require further investigation.

Gibberella zeae (anamorph, Fusarium graminearum) is an important pathogen of cereal crops found in many regions of the world. In this study, we have characterized two auxotrophic strains, designated S4B1279 and S4B3008, which were discovered from a collection of insertional mutants of G. zeae generated by restriction enzyme-mediated integration (REMI). Both mutant strains exhibited pleiotropic phenotypic changes that include reduction of mycelial growth and virulence and abolished sexual reproduction. Molecular analysis of the REMI mutants has shown that the auxotrophy of S4B1279 is due to a mutation of the ARG2 gene encoding an acetylglutamate synthase, and the auxotrophy of S4B3008 is due to a mutation of the ADE5 gene encoding a phosphoribosylamine-glycine ligase. Subsequent gene disruption and complementation studies have confirmed the functions for ARG2 and ADE5, respectively, in G. zeae. Our study has demonstrated the feasibility of using the REMI technique in studying G. zeae virulence mechanisms, in addition to providing two new selectable markers allowing genetic transformation of the fungus.