Niehaus Eva-Maria, Kim Hee-Kyoung, Münsterkötter Martin, Janevska Slavica, Arndt Birgit, Kalinina Svetlana A, Houterman Petra M, Ahn Il-Pyung, Alberti Ilaria, Tonti Stefano, Kim Da-Woon, Sieber Christian M K, Humpf Hans-Ulrich, Yun Sung-Hwan, Güldener Ulrich, Tudzynski Bettina
Institute of Biology and Biotechnology of Plants, Molecular Biology and Biotechnology of Fungi, Westfälische Wilhelms-Universität Münster, Münster, Germany.
Department of Medical Biotechnology, Soonchunhyang University, Asan, Republic of Korea.
PLoS Pathog. 2017 Oct 26;13(10):e1006670. doi: 10.1371/journal.ppat.1006670. eCollection 2017 Oct.
Fusarium fujikuroi causes bakanae ("foolish seedling") disease of rice which is characterized by hyper-elongation of seedlings resulting from production of gibberellic acids (GAs) by the fungus. This plant pathogen is also known for production of harmful mycotoxins, such as fusarins, fusaric acid, apicidin F and beauvericin. Recently, we generated the first de novo genome sequence of F. fujikuroi strain IMI 58289 combined with extensive transcriptional, epigenetic, proteomic and chemical product analyses. GA production was shown to provide a selective advantage during infection of the preferred host plant rice. Here, we provide genome sequences of eight additional F. fujikuroi isolates from distant geographic regions. The isolates differ in the size of chromosomes, most likely due to variability of subtelomeric regions, the type of asexual spores (microconidia and/or macroconidia), and the number and expression of secondary metabolite gene clusters. Whilst most of the isolates caused the typical bakanae symptoms, one isolate, B14, caused stunting and early withering of infected seedlings. In contrast to the other isolates, B14 produced no GAs but high amounts of fumonisins during infection on rice. Furthermore, it differed from the other isolates by the presence of three additional polyketide synthase (PKS) genes (PKS40, PKS43, PKS51) and the absence of the F. fujikuroi-specific apicidin F (NRPS31) gene cluster. Analysis of additional field isolates confirmed the strong correlation between the pathotype (bakanae or stunting/withering), and the ability to produce either GAs or fumonisins. Deletion of the fumonisin and fusaric acid-specific PKS genes in B14 reduced the stunting/withering symptoms, whereas deletion of the PKS51 gene resulted in elevated symptom development. Phylogenetic analyses revealed two subclades of F. fujikuroi strains according to their pathotype and secondary metabolite profiles.
藤仓镰孢菌会引发水稻的恶苗病（“疯长苗”病），其特征是由于该真菌产生赤霉素（GAs）导致幼苗过度伸长。这种植物病原体还以产生有害的霉菌毒素而闻名，比如镰刀菌素、镰刀菌酸、杀顶孢菌素F和白僵菌素。最近，我们首次生成了藤仓镰孢菌菌株IMI 58289的从头基因组序列，并结合了广泛的转录组、表观遗传组、蛋白质组和化学产物分析。研究表明，在感染其首选宿主植物水稻的过程中，赤霉素的产生提供了一种选择性优势。在此，我们提供了另外8个来自不同地理区域的藤仓镰孢菌分离株的基因组序列。这些分离株在染色体大小上存在差异，很可能是由于端粒下区域的变异性、无性孢子（微分生孢子和/或大分生孢子）的类型，以及次级代谢产物基因簇的数量和表达情况不同。虽然大多数分离株会引发典型的恶苗病症状，但有一个分离株B14会导致受感染幼苗发育迟缓并过早枯萎。与其他分离株不同的是，B14在感染水稻期间不产生赤霉素，但会产生大量伏马菌素。此外，它与其他分离株的不同之处在于，它有另外三个聚酮合酶（PKS）基因（PKS40、PKS43、PKS51），并且没有藤仓镰孢菌特有的杀顶孢菌素F（NRPS31）基因簇。对更多田间分离株的分析证实了致病型（恶苗病或发育迟缓/枯萎）与产生赤霉素或伏马菌素的能力之间存在很强的相关性。在B14中删除伏马菌素和镰刀菌酸特异性的PKS基因可减轻发育迟缓/枯萎症状，而删除PKS51基因则导致症状加重。系统发育分析根据藤仓镰孢菌菌株的致病型和次级代谢产物谱揭示了两个亚分支。
