Data_Sheet_1_Biosynthesis of Fusapyrone Depends on the H3K9 Methyltransferase, FmKmt1, in Fusarium mangiferae.pdf

The phytopathogenic fungus Fusarium mangiferae belongs to the Fusarium fujikuroi species complex (FFSC). Members of this group cause a wide spectrum of devastating diseases on diverse agricultural crops. F. mangiferae is the causal agent of the mango malformation disease (MMD) and as such detrimental for agriculture in the southern hemisphere. During plant infection, the fungus produces a plethora of bioactive secondary metabolites (SMs), which most often lead to severe adverse defects on plants health. Changes in chromatin structure achieved by posttranslational modifications (PTM) of histones play a key role in regulation of fungal SM biosynthesis. Posttranslational tri-methylation of histone 3 lysine 9 (H3K9me3) is considered a hallmark of heterochromatin and established by the SET-domain protein Kmt1. Here, we show that FmKmt1 is involved in H3K9me3 in F. mangiferae. Loss of FmKmt1 only slightly though significantly affected fungal hyphal growth and stress response and is required for wild type-like conidiation. While FmKmt1 is largely dispensable for the biosynthesis of most known SMs, removal of FmKMT1 resulted in an almost complete loss of fusapyrone and deoxyfusapyrone, γ-pyrones previously only known from Fusarium semitectum. Here, we identified the polyketide synthase (PKS) FmPKS40 to be involved in fusapyrone biosynthesis, delineate putative cluster borders by co-expression studies and provide insights into its regulation.

病原性植物真菌Fusarium mangiferae隶属于Fusarium fujikuroi物种复合群（FFSC）。该复合群成员可引发多种农业作物上的广泛而毁灭性的病害。F. mangiferae是芒果变形病（MMD）的病原体，对南半球农业造成了严重的损害。在植物感染过程中，该真菌产生大量生物活性次生代谢物（SMs），这些代谢物通常会导致植物健康出现严重的负面缺陷。通过组蛋白的翻译后修饰（PTM）实现的染色质结构变化，在真菌SM生物合成调控中发挥着关键作用。组蛋白3赖氨酸9的翻译后三甲基化（H3K9me3）被视为异染色质的标志，由SET结构域蛋白Kmt1所确立。在本研究中，我们揭示了FmKmt1在F. mangiferae中的H3K9me3作用。FmKmt1的缺失仅对真菌菌丝生长和应激反应产生轻微但显著的影响，并且对于野生型类似的分生孢子形成是必需的。虽然FmKmt1对于大多数已知SMs的生物合成并非不可或缺，但FmKMT1的去除导致 Fusapyrone和deoxyfusapyrone（γ-吡喃酮，此前仅见于Fusarium semitectum）几乎完全丧失。在此，我们确定了多聚酮合成酶（PKS）FmPKS40参与Fusapyrone的生物合成，通过共表达研究划定了潜在的簇边界，并对其调控机制提供了洞见。