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Data_Sheet_2_New Insight Into Pathogenicity and Secondary Metabolism of the Plant Pathogen Penicillium expansum Through Deletion of the Epigenetic Reader SntB.PDF

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NIAID Data Ecosystem2026-03-11 收录
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https://figshare.com/articles/dataset/Data_Sheet_2_New_Insight_Into_Pathogenicity_and_Secondary_Metabolism_of_the_Plant_Pathogen_Penicillium_expansum_Through_Deletion_of_the_Epigenetic_Reader_SntB_PDF/12101925
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Penicillium expansum is one of the most harmful post-harvest pathogens of pomaceous fruits and the causal agent of blue rot disease. During infection, P. expansum produces the toxic secondary metabolites patulin and citrinin that can impact virulence and, further, render the fruit inedible. Several studies have shown that epigenetic machinery controls synthesis of secondary metabolites in fungi. In this regard, the epigenetic reader, SntB, has been reported to govern the production of multiple toxins in Aspergillus species, and impact virulence of plant pathogenic fungi. Here we show that deletion of sntB in P. expansum results in several phenotypic changes in the fungus including stunted vegetative growth, reduced conidiation, but enhanced germination rates as well as decreased virulence on Golden Delicious apples. In addition, a decrease in both patulin and citrinin biosynthesis in vitro and patulin in apples, was observed. SntB positively regulates expression of three global regulators of virulence and secondary metabolism (LaeA, CreA, and PacC) which may explain in part some of the phenotypic and virulence defects of the PeΔsntB strain. Lastly, results from this study revealed that the controlled environmental factors (low temperatures and high CO2 levels) to which P. expansum is commonly exposed during fruit storage, resulted in a significant reduction of sntB expression and consequent patulin and citrinin reduction. These data identify the epigenetic reader SntB as critical factor regulated in post-harvest pathogens under storage conditions and a potential target to control fungal colonization and decaying of stored fruit.

扩展青霉(Penicillium expansum)是危害仁果类水果最严重的采后病原菌之一,亦是蓝腐病的致病菌。在侵染过程中,扩展青霉会合成有毒次生代谢物棒曲霉素(patulin)与橘霉素(citrinin),这类物质不仅会影响病原菌的毒力,还会使果实丧失食用价值。多项研究已证实,表观遗传机制(epigenetic machinery)可调控真菌次生代谢产物的生物合成。其中,表观遗传阅读器(epigenetic reader)SntB已被报道能够调控曲霉属真菌多种毒素的产生,并影响植物病原真菌的毒力。本研究发现,在扩展青霉中敲除sntB基因后,该真菌会出现多种表型变化:营养生长受抑、产孢能力下降,但萌发率提升,同时在金冠苹果上的致病毒力显著降低。此外,体外培养条件下棒曲霉素与橘霉素的生物合成量,以及金冠苹果体内的棒曲霉素含量均出现下降。SntB可正向调控三个与毒力及次生代谢相关的全局调控因子LaeA、CreA与PacC的表达,这或许可以部分解释PeΔsntB突变株所出现的部分表型与毒力缺陷。最后,本研究结果显示,扩展青霉在果实贮藏期间通常会暴露于低温与高二氧化碳(CO₂)环境中,这类环境会显著降低sntB基因的表达水平,进而导致棒曲霉素与橘霉素的合成减少。上述数据表明,表观遗传阅读器SntB是采后病原菌在贮藏条件下受到调控的关键因子,同时也是调控贮藏果实真菌定殖与腐烂的潜在靶点。
创建时间:
2020-04-09
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