Fusarium pseudograminearum (Fp), the causative fungal pathogen of the diseases Fusarium crown rot, is an important constraint to cereals production in many countries including Australia. Fp produces a number of secondary metabolites throughout its life cycle. One of these metabolites, the cyclic lipopeptide fusaristatin A, is encoded by a specific gene cluster containing a polyketide synthase and a three-module non-ribosomal peptide synthetase. However, a recent survey of Fp populations across Australia suggests that this cluster may only be present in a subset of isolates from Western Australia (WA). In this study, we screened 319 Fp isolates from WA and 110 Fp isolates from the Australian eastern states of New South Wales, Victoria, Queensland and South Australia to examine the distribution of this gene cluster among Australian Fp populations. The fusaristatin A gene cluster was found to be present in ~50% of Fp isolates from WA but completely absent in Fp isolates from eastern states. To determine its potential function, mutants of the fusaristatin A gene cluster were generated by disrupting the non-ribosomal peptide synthetase and polyketide synthase genes simultaneously in two different parental backgrounds. The mutants showed increased growth rates and were significantly more aggressive than their respective parental strains on wheat in crown rot pathogenicity assays. This suggested that fusaristatin A has a negative effect on fungal development and aggressiveness. The possible reasons for the geographically restricted presence of the fusaristatin A gene cluster and its role in fungal biology are discussed.

中文翻译：

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Fusaristatin A的生产会对小麦病原体Fusarium pseudograminearum的生长和侵略性产生负面影响。

镰刀菌冠腐病的病原真菌病原体镰刀菌（Fp）是包括澳大利亚在内的许多国家的谷物生产的重要制约因素。Fp在其整个生命周期中都会产生许多次级代谢产物。这些代谢产物之一，环状脂肽富沙地他汀A，是由含有聚酮化合物合酶和三模块非核糖体肽合成酶的特定基因簇编码的。但是，最近对整个澳大利亚的Fp种群进行的调查表明，该簇仅可能存在于来自西澳大利亚州（WA）的分离株中。在这项研究中，我们筛选了WA的319 Fp分离株和新南威尔士州，维多利亚州，昆士兰州和南澳大利亚州的澳大利亚东部各州的110 Fp分离株，以检查该基因簇在澳大利亚Fp人群中的分布。发现fusaristatin A基因簇存在于WA的Fp分离株的约50％中，但在东部各州的Fp分离株中完全不存在。为了确定其潜在功能，通过在两个不同的亲本背景下同时破坏非核糖体肽合成酶和聚酮化合物合酶基因，生成了fusristatin A基因簇的突变体。在冠腐病致病性分析中，这些突变体显示出更高的生长速率，并且比其各自的亲本菌株对小麦的侵袭性更强。这表明fusristatin A对真菌发育和侵略性具有负面影响。讨论了fusristatin A基因簇在地理上受限制的可能原因及其在真菌生物学中的作用。