Impact of veA on the development, aggressiveness, dissemination and secondary metabolism of Penicillium expansum : Role of veA in Penicillium expansum

Abstract

<p id="d5414990e289"> <i>Penicillium expansum</i>, the causal agent of blue mould disease, produces the mycotoxins patulin and citrinin amongst other secondary metabolites. Secondary metabolism is associated with fungal development, which responds to numerous biotic and abiotic external triggers. The global transcription factor VeA plays a key role in the coordination of secondary metabolism and differentiation processes in many fungal species. The specific role of VeA in <i>P. expansum</i> remains unknown. A null mutant PeΔ <i>veA</i> strain and a complemented PeΔ <i>veA</i>: <i>veA</i> strain were generated in <i>P. expansum</i> and their pathogenicity on apples was studied. Like the wild‐type and the complemented strains, the null mutant PeΔ <i>veA</i> strain was still able to sporulate and to colonize apples, but at a lower rate. However, it could not form coremia either <i>in vitro</i> or <i>in vivo</i>, thus limiting its dissemination from natural substrates. The impact of <i>veA</i> on the expression of genes encoding proteins involved in the production of patulin, citrinin and other secondary metabolites was evaluated. The disruption of <i>veA</i> drastically reduced the production of patulin and citrinin on synthetic media, associated with a marked down‐regulation of all genes involved in the biosynthesis of the two mycotoxins. Moreover, the null mutant PeΔ <i>veA</i> strain was unable to produce patulin on apples. The analysis of gene expression revealed a global impact on secondary metabolism, as 15 of 35 backbone genes showed differential regulation on two different media. These findings support the hypothesis that VeA contributes to the pathogenicity of <i>P. expansum</i> and modulates its secondary metabolism. </p>