A Metalloprotease Homolog Venom Protein From a Parasitoid Wasp Suppresses the Toll Pathway in Host Hemocytes.

Zhe Lin,Yang Hu,Jian-Cheng Li,Rui-Juan Wang,Zhiqiang Lu,Olga Volovych,Zi-Yun Lu,Jie Du,Yang Cheng,Zhen Zou

doi:10.3389/fimmu.2018.02301

Abstract

Parasitoid wasps depend on a variety of maternal virulence factors to ensure successful parasitism. Encapsulation response carried out by host hemocytes is one of the major host immune responses toward limiting endoparasitoid wasp offspring production. We found that VRF1, a metalloprotease homolog venom protein identified from the endoparasitoid wasp, Microplitis mediator, could modulate egg encapsulation in its host, the cotton bollworm, Helicoverpa armigera. Here, we show that the VRF1 proenzyme is cleaved after parasitism, and that the C-terminal fragment containing the catalytic domain enters host hemocytes 6 h post-parasitism. Furthermore, using yeast two-hybrid and pull-down assays, VRF1 is shown to interact with the H. armigera NF-κB factor, Dorsal. We also show that overexpressed of VRF1 in an H. armigera cell line cleaved Dorsal in vivo. Taken together, our results have revealed a novel mechanism by which a component of endoparasitoid wasp venom interferes with the Toll signaling pathway in the host hemocytes.

Highlights

Insects have efficient cellular and humoral immune mechanisms that protect them from invasion by microbes and parasites
We found that venom regulatory factor-1 (VRF1), a metalloprotease homolog venom protein identified from the endoparasitoid wasp, Microplitis mediator, could modulate egg encapsulation in its host, the cotton bollworm, Helicoverpa armigera
Our integrative analysis of RNA-seq and proteomic data identified 25 metalloproteases in M. mediator venom apparatus, which belongs to M12B and M13 metalloproteases (Supplementary Data 1)

Summary

Introduction

Insects have efficient cellular and humoral immune mechanisms that protect them from invasion by microbes and parasites. Cellular encapsulation of endoparasitoid wasp offspring is an effective and general defense response of hosts [1]. Drosophila parasitized by Leptopilina has been used as a classical parasitism model to understand the insect immune system. Injection of Leptopilina eggs into the host insect triggers the encapsulation processes, including recognition by plasmatocytes and cell-layer formation with further binding of lamellocytes [4,5,6]. Parasitoid wasps are used for the biological control of some lepidopteran pests; the mechanisms by which wasp offspring suppress the encapsulation response in lepidopteran pest are largely unknown

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Conclusion