El Hajj Assaf Christelle, Snini Selma P, Tadrist Souria, Bailly Sylviane, Naylies Claire, Oswald Isabelle P, Lorber Sophie, Puel Olivier
Toxalim (Research Centre in Food Toxicology), Université de Toulouse, INRA, ENVT, INP-Purpan, UPS, 31027 Toulouse, France.
Flanders Research Institute for Agricultural, Fisheries and Food (ILVO), Technology and Food Science Unit, Melle 9090, Belgium.
Mol Plant Pathol. 2018 Mar 8;19(8):1971-83. doi: 10.1111/mpp.12673.
Penicillium expansum, 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 P. expansum remains unknown. A null mutant PeΔveA strain and a complemented PeΔveA:veA strain were generated in P. expansum and their pathogenicity on apples was studied. Like the wild-type and the complemented strains, the null mutant PeΔveA strain was still able to sporulate and to colonize apples, but at a lower rate. However, it could not form coremia either in vitro or in vivo, thus limiting its dissemination from natural substrates. The impact of veA on the expression of genes encoding proteins involved in the production of patulin, citrinin and other secondary metabolites was evaluated. The disruption of veA 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 PeΔveA 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 P. expansum and modulates its secondary metabolism.
扩展青霉是青霉病的致病因子,除了其他次生代谢产物外,还会产生棒曲霉素和桔霉素这两种霉菌毒素。次生代谢与真菌发育相关,真菌发育会对众多生物和非生物外部触发因素做出反应。全局转录因子VeA在许多真菌物种的次生代谢和分化过程的协调中起着关键作用。VeA在扩展青霉中的具体作用尚不清楚。在扩展青霉中构建了一个缺失突变体PeΔveA菌株和一个互补的PeΔveA:veA菌株,并研究了它们对苹果的致病性。与野生型和互补菌株一样,缺失突变体PeΔveA菌株仍然能够产孢并在苹果上定殖,但定殖率较低。然而,它在体外或体内都不能形成分生孢子座,因此限制了其从天然基质中的传播。评估了veA对编码参与棒曲霉素、桔霉素和其他次生代谢产物合成的蛋白质的基因表达的影响。veA的破坏极大地降低了合成培养基上棒曲霉素和桔霉素的产量,这与参与这两种霉菌毒素生物合成的所有基因的显著下调有关。此外,缺失突变体PeΔveA菌株在苹果上不能产生棒曲霉素。基因表达分析揭示了对次生代谢的全局影响,因为35个骨干基因中的15个在两种不同培养基上表现出差异调节。这些发现支持了VeA有助于扩展青霉的致病性并调节其次生代谢的假设。