Location: Food and Feed Safety ResearchTitle: Aspergillus flavus VelB acts distinctly from VeA in conidiation and may coordinate with FluG to modulate sclerotial production) Author
Submitted to: Fungal Genetics and Biology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 8/18/2013
Publication Date: 8/29/2013
Citation: Chang, P-K., Scharfenstein, L.L., Li, P., Ehrlich, K. 2013. Aspergillus flavus VelB acts distinctly from VeA in conidiation and may coordinate with FluG to modulate sclerotial production. Fungal Genetics and Biology. 58-59:71-79. Interpretive Summary: The carcinogenic aflatoxin produced by the yellow green mold Aspergillus flavus is tightly linked to fungal differentiation. To better understand molecular mechanisms that regulate the processes, we knocked out two genes that are known to control light-dependent production of spores and secondary metabolites in other fungi. Impairment of these genes severely decreased spore production in the dark and also abolished aflatoxin formation regardless of illumination conditions. This information, used along with other preventive strategies, may help to reduce aflatoxin contamination of crops in the field.
Technical Abstract: Asexual and sexual differentiation in Aspergillus nidulans involve complex control by a number of factors and is light-dependent. The velvet protein, VeA, in A. nidulans is a negative regulator of conidiation and a positive regulator of sexual development. It forms a complex with VelB and LaeA to coordinate sexual development and secondary metabolite production in response to growth in the dark. VelB also forms a complex with VosA, another velvet protein, to repress asexual conidiation in the dark. The role of another velvet protein, VelC, is not yet defined. Since, unlike A. nidulans, Aspergillus flavus normally only reproduces and disseminates asexually in nature, we hypothesized that the roles of VeA, VelB, and VelC in A. flavus are different from those in A. nidulans. Deletion of veA or velB severely impaired conidiation in the dark but not in the light. In these mutants further deletion of a gene for a protein that regulates mycelial growth, fluG, resulted in a marked decrease in conidiation even in the light. Both types of mutants were unable to produce aflatoxins regardless of illumination conditions. In contrast, velC deletion strains developed normally and produced aflatoxins. Complementation of the 'veA and 'velB strains with respective gene remediated the aforementioned defects. Overexpression of veA in the 'velB strain remediated the defect in conidiation in the dark but not the lack of aflatoxin production although the aflatoxin pathway regulatory gene alfR expressed in the strains are at levels comparable to that of the wild-type strain. Overexpression of velB in the 'veA strain failed to restore conidiation or aflatoxin production. Yeast two-hybrid assays confirmed that VeA, VelB and LaeA form a complex and suggested that FluG is likely an interacting partner. Concerted interactions of A. flavus VeA and VelB with LaeA are critical for conidiation and aflatoxin biosynthesis in the dark.