摘要
Penicillium expansum is a globally significant postharvest pathogen causing substantial economic losses in fruit and vegetable production. Despite the importance of this pathogen to global food security, the regulatory roles of transcription factors - particularly APSES family members - remain poorly characterized in P. expansum . Here, we identified PeStuA, a homolog of the key APSES member StuA, in P. expansum . Targeted deletion of PeStuA resulted in three independent deletion mutants. These mutants exhibited decreased biomass and the lack of the ability to form conidiophores and conidia, accompanied by significantly reduced expression of genes encoding fungal development regulators (BrlA, AabA, WetA, and VosA), confirming the role of PeStuA in fungal growth and development. PeStuA also influences the metabolism of P. expansum in terms of carbon and nitrogen sources. Notably, although Δ PeStuA mutants completely lost patulin production capacity in vitro , only a few genes within the patulin cluster were significantly down-regulated in expression, implying potential new regulatory mechanisms governing patulin production in P. expansum . Furthermore, the Δ PeStuA mutants presented significantly decreased pathogenicity on apple fruits. RNA sequencing analysis demonstrated the global regulatory role of PeStuA in spore development, primary metabolism and secondary metabolism during P. expansum infecting apple hosts. Overall, this study reveals the role of PeStuA and offers new perspectives on the molecular basis of P. expansum , providing a theoretical foundation for developing strategies against fruit diseases and patulin pollution it poses.
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