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A venom protein, Kazal-type serine protease inhibitor, of ectoparasitoid Pachycrepoideus vindemiae inhibits the hemolymph melanization of host Drosophila melanogaster.
Archives of Insect Biochemistry and Physiology ( IF 1.5 ) Pub Date : 2020-09-12 , DOI: 10.1002/arch.21736
Lei Yang 1 , Li-Ming Qiu 1 , Qi Fang 1 , Gong-Yin Ye 1
Affiliation  

Parasitic wasps inject various virulence factors into the host insects while laying eggs, among which the venom proteins, one of the key players in host insect/parasitoid relationships, act in host cellular and humoral immune regulation to ensure successful development of wasp progeny. Although the investigations into actions of venom proteins are relatively ample in larval parasitoids, their regulatory mechanisms have not been thoroughly understood in pupal parasitoids. Here, we identified a venom protein, Kazal‐type serine protease inhibitor, in the pupal ectoparasitoid Pachycrepoideus vindemiae (PvKazal). Sequence analysis revealed that PvKazal is packed by a signal peptide and a highly conserved “Kazal” domain. Quantitative polymerase chain reaction analysis recorded a higher transcript level of PvKazal in the venom apparatus relative to that in the carcass, and the PvKazal messenger RNA level appeared to reach a peak on day 5 posteclosion. Recombinant PvKazal strongly inhibited the hemolymph melanization of host Drosophila melanogaster. Additionally, the heterologous expression of PvKazal in transgenic Drosophila reduced the crystal cell numbers and blocked the melanization of host pupal hemolymph. Our present work underlying the roles of PvKazal undoubtedly increases the understanding of venom‐mediated host‐parasitoid crosstalk.

中文翻译:

外胚层类葡萄球菌Pachycrepoideus vindemiae的一种毒蛋白,Kazal型丝氨酸蛋白酶抑制剂,可抑制宿主果蝇的血淋巴黑色素化。

寄生黄蜂在产卵时向宿主昆虫注入各种毒力因子,其中毒蛋白是宿主昆虫/类寄生虫关系的关键角色之一,在宿主细胞和体液免疫调节中起作用,以确保黄蜂后代的成功发育。尽管对幼虫类寄生虫中毒蛋白作用的研究相对丰富,但它们的调控机制尚未在para类寄生虫中得到充分了解。在这里,我们在the外胚层类葡萄Pachycrepoideus vindemiae(PvKazal)中鉴定了一种毒蛋白,Kazal型丝氨酸蛋白酶抑制剂。序列分析表明,PvKazal被信号肽和高度保守的“ Kazal”结构域所包裹。定量聚合酶链反应分析记录了较高的转录水平PvKazal相对于在所述胎体的毒液装置,和PvKazal信使RNA水平上出现到达第5天posteclosion的峰。重组PvKazal强烈抑制寄主果蝇的血淋巴黑色素化。此外,PvKazal在转基因果蝇中的异源表达减少了晶体细胞数量并阻止了宿主p血淋巴的黑色素化。我们目前关于PvKazal角色的工作无疑增加了对毒液介导的宿主-拟寄生物串扰的了解。
更新日期:2020-10-12
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