Implication of VelB in the development, pathogenicity, and secondary metabolism of Penicillium expansum

Penicillium expansum is the main cause of blue mold disease and the main producer of patulin in apple-derived products. This fungus also produces a wide variety of secondary metabolites, including citrinin and chaetoglobosin A. Secondary metabolism is regulated by global transcription factors that are affected by environmental signals. The light-dependent global transcription factor VelB, a member of the velvet complex, plays an important role in the regulation of secondary metabolism and fungal development in many fungal species. However, the specific roles of VelB in P. expansum remain unknown. A Pe∆velB mutant and a complemented Pe∆velB:velB strain were generated to investigate the role of VelB in pathogenicity and secondary metabolism. The Pe∆velB mutant colonized apples, but at a lower rate than the wild type and complemented strains. Conidiation was significantly reduced in the Pe∆velB strain. Under light conditions, the Pe∆velB strain showed a reduced level of spore viability. Deletion of the velB gene strongly inhibited the production of patulin, citrinin, and chaetoglobosin A on synthetic media or in planta, but increased the production of fumarylalanine; these changes were associated with down-regulation or upregulation of the genes involved in their respective biosynthesis. Analysis of the global secondary metabolism of the Pe∆velB strain revealed that 22 backbone genes were modulated. In addition, genes involved in siderophore biosynthesis, ergosterol biosynthesis, and nitrate assimilation were also upregulated in the PeΔvelB strain. Taken together, our results demonstrate that VelB is involved in the development, pathogenicity, and secondary metabolism of P. expansum. •VelB positively controls citrinin, chaetoglobosin A, and patulin production.•Fumarylalanine production is negatively controlled by VelB.•VelB represses iron uptake, nitrate assimilation and ergosterol biosynthesis.•Conidiation and spore viability are positively regulated by VelB.