Pathogenic fungi precisely respond to dynamic microenvironments during infection, but the underlying mechanisms are not well understood. The insect pathogenic fungus Metarhizium robertsii is a representative fungus in which to study broad themes of fungal pathogenicity as it resembles some major plant and mammalian pathogenic fungi in its pathogenesis. Here we report on a novel cascade that regulates response of M. robertsii to 2 distinct microenvironments during its pathogenesis. On the insect cuticle, the transcription factor COH2 activates expression of cuticle penetration genes. In the hemocoel, the protein COH1 is expressed due to the reduction in epigenetic repression conferred by the histone deacetylase HDAC1 and the histone 3 acetyltransferase HAT1. COH1 interacts with COH2 to reduce COH2 stability, and this down-regulates cuticle penetration genes and up-regulates genes for hemocoel colonization. Our work significantly advances the insights into fungal pathogenicity in insects.

中文翻译：

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一种新的级联允许罗伯氏绿僵菌在昆虫感染期间区分角质层和血腔微环境。

病原真菌在感染过程中对动态微环境做出精确反应，但其潜在机制尚不清楚。昆虫病原真菌绿僵菌是研究真菌致病性广泛主题的代表性真菌，因为它在发病机制上类似于一些主要的植物和哺乳动物病原真菌。在这里，我们报告了一种新的级联反应，该级联反应在其发病过程中调节 M. robertsii 对 2 个不同微环境的反应。在昆虫角质层上，转录因子 COH2 激活角质层穿透基因的表达。在血腔中，由于组蛋白去乙酰化酶 HDAC1 和组蛋白 3 乙酰转移酶 HAT1 赋予的表观遗传抑制减少，因此表达了蛋白质 COH1。COH1 与 COH2 相互作用以降低 COH2 的稳定性，这会下调角质层渗透基因并上调血腔定植基因。我们的工作显着提高了对昆虫真菌致病性的认识。