A novel cascade allows Metarhizium robertsii to distinguish cuticle and hemocoel microenvironments during infection of insects.

A novel cascade allows Metarhizium robertsii to distinguish cuticle and hemocoel microenvironments during infection of insects.
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一种新颖的级联使得绿僵菌能够在昆虫感染过程中区分角质层和血腔微环境。

DOI:
10.1371/journal.pbio.3001360
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发表时间:
2021-08
期刊:
影响因子:
9.8
通讯作者:
Fang W
Fang W
中科院分区:
生物学1区
文献类型:
--
作者:
Zhang X;Meng Y;Huang Y;Zhang D;Fang W

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病原真菌在感染过程中对动态的微环境做出精确的反应,但其潜在的机制尚不清楚。昆虫致病真菌罗伯茨绿僵菌与一些主要的植物和哺乳动物病原真菌在致病机理上相似,是研究真菌致病机理的代表性真菌。在这里,我们报告了一种新的级联反应,它调节了罗伯茨分枝杆菌在发病过程中对两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,COH1蛋白的表达是由于组蛋白脱乙酰酶HDAC1和组蛋白3乙酰转移酶HAT1导致的表观遗传抑制的减少。COH1与COH2相互作用降低COH2的稳定性,这下调了角质层穿透基因,上调了血腔定植基因。我们的工作极大地促进了对昆虫真菌致病性的深入了解。病原真菌在感染过程中对动态微环境做出精确的反应,但其潜在的机制尚不清楚。这项研究确定了昆虫真菌病原体中的一个调节级联,它作为开关来打开或关闭基因,以响应两个不同的宿主微环境:昆虫角质层和血腔。
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. Pathogenic fungi respond precisely to dynamic microenvironments during infection, but the underlying mechanisms are not well understood. This study identifies a regulatory cascade in a fungal pathogen of insects that acts as a switch to turn genes on or off in response to two distinct host microenvironments; the insect cuticle and the hemocoel.
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