School of Food and Biological Engineering, Hefei University of Technology, Hefei, 230009, China.
Chongqing Key Laboratory of Economic Plant Biotechnology, Collaborative Innovation Centre of Special Plant Industry in Chongqing, College of Forestry and Life Science, Institute of Special Plants, Chongqing University of Arts and Sciences, Yongchuan, 402160, China.
Mol Genet Genomics. 2020 Nov;295(6):1415-1429. doi: 10.1007/s00438-020-01710-9. Epub 2020 Jul 12.
Penicillium expansum is a destructive phytopathogen causing postharvest decay on many stored fruits. To develop effective and safe management strategies, it is important to investigate its pathogenicity-related mechanisms. In this study, a bioinformatic pipeline was constructed and 50 core effector genes were identified in P. expansum using multiple RNA-seq data sets and their putative functions were implicated by comparatively homologous analyses using pathogen-host interaction database. To functionally characterize P. expansum LysM domain proteins during infection, null mutants for the 15 uncharacterized putative LysM effectors were constructed and the fungal growth rate on either PDA or Cazpek medium or lesion expansion rate on the infected apple fruits was evaluated. The results showed the growth rate of knockout mutants from PeLysM5, PeLysM12 and PeLysM15 was retarded on PDA medium. No significant difference in growth rate was observed between wild type and all mutants on solid Cazpek medium. Nevertheless, the hypha of wild type displayed deeper yellow on the back of Cazpek medium than those of knockout mutants. On the infecting apples fruits, the knockout mutants from PeLysM5, PeLysM7, PeLysM8, PeLysM9, PeLysM10, PeLysM11, PeLysM14, PeLysM15, PeLysM16, PeLysM18 and PeLysM19 showed enhanced fungal virulence, with faster decaying on infected fruits than those from wild type. By contrast, the knockout mutation at PeLysM12 locus led to reduced lesion expansion rate on the infected apple fruits. In addition, P. expansum-apple interaction RNA-seq experiment was performed using apple fruit tissues infected by the wild type and knockout mutant ΔPeLysM15, respectively. Transcriptome analyses indicated that deletion of PeLysM15 could activate expression of several core effector genes, such as PEX2_055830, PEX2_036960 and PEX2_108150, and a chitin-binding protein, PEX2_064520. These results suggest PeLysM15 may play pivotal roles in fungal growth and development and involve pathogen-host interaction by modulating other effector genes' expression. Our results could provide solid data reference and good candidates for further pathogen-related studies in P. expansum.
扩展青霉是一种破坏性的植物病原菌,可导致许多储存水果的采后腐烂。为了制定有效的和安全的管理策略,研究其致病性相关机制非常重要。在本研究中,使用多个 RNA-seq 数据集构建了生物信息学管道,并鉴定了扩展青霉中的 50 个核心效应基因,通过使用病原体-宿主相互作用数据库进行比较同源分析,推测了它们的可能功能。为了在感染过程中对扩展青霉 LysM 结构域蛋白进行功能表征,构建了 15 个未鉴定的假定 LysM 效应物的缺失突变体,并评估了它们在 PDA 或 Cazpek 培养基上的真菌生长率或在感染苹果果实上的病斑扩展率。结果表明,PeLysM5、PeLysM12 和 PeLysM15 的敲除突变体在 PDA 培养基上的生长速度较慢。在固体 Cazpek 培养基上,野生型和所有突变体之间的生长率没有明显差异。然而,野生型的菌丝在 Cazpek 培养基背面比敲除突变体的菌丝颜色更深。在感染的苹果果实上,PeLysM5、PeLysM7、PeLysM8、PeLysM9、PeLysM10、PeLysM11、PeLysM14、PeLysM15、PeLysM16、PeLysM18 和 PeLysM19 的敲除突变体显示出增强的真菌毒力,在感染的果实上腐烂速度比野生型更快。相比之下,PeLysM12 基因座的敲除突变导致感染苹果果实上的病斑扩展率降低。此外,分别使用野生型和敲除突变体ΔPeLysM15 感染的苹果果实组织进行扩展青霉-苹果互作 RNA-seq 实验。转录组分析表明,PeLysM15 的缺失可激活 PEX2_055830、PEX2_036960 和 PEX2_108150 等几个核心效应基因的表达,以及一个几丁质结合蛋白 PEX2_064520 的表达。这些结果表明 PeLysM15 可能在真菌的生长和发育中发挥关键作用,并通过调节其他效应基因的表达参与病原体-宿主的相互作用。我们的结果可为扩展青霉的进一步病原体相关研究提供可靠的数据参考和良好的候选基因。