Manipulation of host ecdysteroid hormone levels facilitates infection by the fungal insect pathogen, Metarhizium rileyi
Manipulation of host ecdysteroid hormone levels facilitates infection by the fungal insect pathogen, Metarhizium rileyi
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控制宿主蜕皮类固醇激素水平有利于真菌昆虫病原体莱氏绿僵菌的感染
DOI：
10.1111/1462-2920.15454
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发表时间：
2021
影响因子：
5.1
通讯作者：
Fan Yanhua
中科院分区：
文献类型：
--
作者：
Zhu Shengan;Feng Xueyao;Keyhani Nemat O.;Liu Yu;Jin Dan;Tong Sheng;Pei Yan;Fan Yanhua
昆虫病原真菌如绿僵菌和白僵菌是广泛使用的昆虫生物防治剂。然而，人们对区分这两种真菌病原体感染目标宿主的机制的遗传或酶促因素知之甚少。已知这些生物体的感染会增加生长和蜕皮激素、蜕皮激素的水平，蜕皮激素还调节许多先天免疫途径的表达。 rileyi，但不是 B.bassiana，显然进化出了一种可以灭活蜕皮激素的蜕皮类固醇-22-氧化酶 (MrE22O)。我们发现，与野生型菌株相比，MrE22O 的缺失会损害毒力，宿主中的蜕皮激素滴度增加，这与抗菌基因表达的增加有关。与各自的野生型亲本菌株相比，M.riley菌株经过工程改造，过表达MrE22O（MrE22OOE），并在B.bassiana（Bb::MrE220OE）中反式表达，结果显示毒力增强，宿主免疫反应减弱。这些结果表明，蜕皮激素在介导真菌感染反应中发挥着重要作用，并且一些昆虫病原真菌已经进化出针对这种激素作为促进感染的手段的机制。
Entomopathogenic fungi such asMetarhizium rileyiandBeauveria bassianaare widely used insect biological control agents. Little, however, is known concerning genetic or enzymatic factors that differentiate the mechanisms employed by these two fungal pathogens to infect target hosts. Infection by either of these organisms is known to increase levels of the growth and molting hormone, ecdysone, which also regulates the expression of a number of innate immune pathways.M. rileyi, but notB.bassiana, has apparently evolved an ecdysteroid‐22‐oxidase (MrE22O) that inactivate ecdysone. We show that deletion ofMrE22Oimpaired virulence compared with the wild‐type strain, with an increase in ecdysone titer seen in hosts that was coupled to an increase in the expression of antimicrobial genes. AnM.rileyistrain engineered to overexpressMrE22O(MrE22OOE), as well as trans‐expression inB.bassiana(Bb::MrE220OE) resulted, in strains displaying enhanced virulence and dampening of host immune responses compared with their respective wild‐type parental strains. These results indicate that ecdysone plays an important role in mediating responses to fungal infection and that some insect pathogenic fungi have evolved mechanisms for targeting this hormone as a means for facilitating infection.