Postgraduate Program in Genetics, Department of Genetics, Federal University of Paraná, Centro Politécnico, Jardim das Américas, 81531-990, Curitiba, Paraná State, Brazil.
Martin Luther University Halle-Wittenberg, Faculty of Natural Sciences III, Institute for Agricultural and Nutritional Sciences, Chair for Phytopathology and Plant Protection, Betty-Heimann-Str. 3; D-06120 Halle (Saale), Germany.
Phytopathology. 2020 Sep;110(9):1530-1540. doi: 10.1094/PHYTO-04-20-0114-R. Epub 2020 Jul 20.
Fungal pathogenicity is governed by environmental factors, with nitrogen playing a key role in triggering pathogenic development. Spores germinating on the plant cuticle are exposed to a nitrogen-free environment, and reprograming of nitrogen metabolism is required for bridging the time needed to gain access to the nitrogen sources of the host. Although degradation of endogenous purine bases efficiently generates ammonium and may allow the fungus to bridge the preinvasion nitrogen gap, the roles of the purine degradation pathway and of the key genes encoding allantoicase and urease are largely unknown in plant pathogenic fungi. To investigate the roles of the allantoicase and urease genes and of the maize anthracnose fungus in pathogenic development, we generated : and : fusion strains as well as allantoicase- and urease-deficient mutants. Virulence assays, live cell, and differential interference contrast imaging, chemical complementation and employment of a urease inhibitor showed that the purine degradation genes and are required for bridging nitrogen deficiency at early phases of the infection process and for full virulence. Application of the urease inhibitor acetohydroxamic acid did not only protect maize from infection, but also interfered with the infection process of the wheat powdery mildew fungus f. sp. , the maize and broad bean rusts and , and the potato late blight pathogen . Our data strongly suggest that inhibition of the purine degradation pathway might represent a novel approach to control plant pathogenic fungi and oomycetes.
真菌的致病性受环境因素控制,其中氮起着触发致病发育的关键作用。在植物表皮上发芽的孢子暴露在无氮环境中,需要重新编程氮代谢,以弥合获得宿主氮源所需的时间。虽然降解内源性嘌呤碱基可以有效地产生铵,并且可能允许真菌弥合入侵前的氮缺口,但嘌呤降解途径的作用以及编码尿酸酶和尿囊素酶的关键基因在植物病原真菌中的作用在很大程度上是未知的。为了研究玉米炭疽病真菌中尿酸酶和尿囊素酶基因和的作用,我们生成了和融合菌株以及尿酸酶和尿囊素酶缺陷突变体。毒力测定、活细胞和相差干涉对比成像、化学互补和使用尿酸酶抑制剂表明,嘌呤降解基因和在感染过程的早期阶段弥合氮缺乏以及完全毒力方面是必需的。尿酸酶抑制剂乙酰羟肟酸的应用不仅保护了玉米免受感染,而且还干扰了小麦白粉菌 f. sp. 的感染过程,玉米和菜豆锈病和,以及马铃薯晚疫病病原菌。我们的数据强烈表明,抑制嘌呤降解途径可能代表一种控制植物病原真菌和卵菌的新方法。