Recent studies have identified key genes that control the symbiotic interaction between Epichloë festucae and Lolium perenne. Here we report on the identification of specific E. festucae genes that control host infection. Deletion of setB, which encodes a homologue of the H3K36 histone methyltransferase Set2/KMT3, reduced histone H3K36 trimethylation and led to severe defects in colony growth and hyphal development. The E. festucae ΔclrD mutant, which lacks the gene encoding the homologue of the H3K9 methyltransferase KMT1, displays similar developmental defects. Both mutants are completely defective in their ability to infect L. perenne. Alleles that complement the culture and plant phenotypes of both mutants also complement the histone methylation defects. Co‐inoculation of either ΔsetB or ΔclrD with the wild‐type strain enables these mutants to colonize the host. However, successful colonization by the mutants resulted in death or stunting of the host plant. Transcriptome analysis at the early infection stage identified four fungal candidate genes, three of which encode small‐secreted proteins, that are differentially regulated in these mutants compared to wild type. Deletion of crbA, which encodes a putative carbohydrate binding protein, resulted in significantly reduced host infection rates by E. festucae.

中文翻译：

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组蛋白 H3K9 和 H3K36 甲基转移酶对草共生真菌 Epichloë festucae 宿主感染能力的调节

最近的研究已经确定了控制Epichloë festucae和Lolium perenne之间共生相互作用的关键基因。在这里，我们报告了控制宿主感染的特定E.festucae基因的鉴定。的删除组B，其编码H3K36组蛋白甲基SET2 / KMT3，减少组蛋白H3K36三甲基化的同系物，并导致集落生长和菌丝发育严重缺陷。在E. festucae Δ clrD突变体，其缺少编码所述H3K9的同源物的基因的甲基KMT1，显示类似的发育缺陷。两种突变体在感染L. perenne的能力方面都存在完全缺陷. 补充两种突变体的培养物和植物表型的等位基因也补充了组蛋白甲基化缺陷。Δ setB或 Δ clrD与野生型菌株的共同接种使这些突变体能够在宿主中定殖。然而，突变体的成功定植导致宿主植物死亡或发育迟缓。早期感染阶段的转录组分析确定了四个真菌候选基因，其中三个编码小分泌蛋白，与野生型相比，这些突变体在这些突变体中受到不同的调控。编码假定的碳水化合物结合蛋白的crbA 的缺失导致E. festucae 的宿主感染率显着降低。