Abstract
Entomopathogenic nematodes (EPNs) are unique parasites due to their symbiosis with entomopathogenic bacteria and their ability to kill insect hosts quickly after infection. It is widely believed that EPNs rely on their bacterial partners for killing hosts. Here we disproved this theory by demonstrating that the in vitro activated infective juveniles (IJs) of Steinernema carpocapsae (a well-studied EPN species) release venom proteins that are lethal to several insects including Drosophila melanogaster. We confirmed that the in vitro activation is a good approximation of the in vivo process by comparing the transcriptomes of individual in vitro and in vivo activated IJs. We further analyzed the transcriptomes of non-activated and activated IJs and revealed a dramatic shift in gene expression during IJ activation. We also analyzed the venom proteome using mass spectrometry. Among the 472 venom proteins, proteases and protease inhibitors are especially abundant, and toxin-related proteins such as Shk domain-containing proteins and fatty acid- and retinol-binding proteins are also detected, which are potential candidates for suppressing the host immune system. Many of the venom proteins have conserved orthologs in vertebrate-parasitic nematodes and are differentially expressed during IJ activation, suggesting conserved functions in nematode parasitism. In summary, our findings strongly support a new model that S. carpocapsae and likely other Steinernema EPNs have a more active role in contributing to the pathogenicity of the nematode-bacterium complex than simply relying on their symbiotic bacteria. Furthermore, we propose that EPNs are a good model system for investigating vertebrate- and human-parasitic nematodes, especially regarding the function of excretory/secretory products.
Highlights
Hundreds of millions of people are infected with parasitic nematodes worldwide [1, 2]
Similar to some animalparasitic nematodes, when Entomopathogenic nematodes (EPNs) infective juveniles (IJs) enter a host, as yet undefined signals induce recovery from the developmentally arrested IJ stage. This transition from free-living IJ to an active parasitic life style has been called many things; reactivation [39], resumption of feeding [36], resumption of development or initiation of development [35, 39], recovery [43], and activation [36, 41]. Because this transition from free-living IJ to an active parasitic life style requires dramatic morphological and physiological changes, we refer to the process as IJ activation rather than recovery, as the process is called in C. elegans dauers [44]
In order to study the contribution of the nematode to parasitism and host pathology, we wanted to be able to quantify IJ activation
Summary
Hundreds of millions of people are infected with parasitic nematodes worldwide [1, 2]. ES products are complex mixtures and often include small molecules, proteins, and nucleic acids. The complexity of these products and technical limitations in obtaining sufficient quantities for separation studies have resulted in current efforts often being focused on the most abundant components [Reviewed in 4]. There are hundreds of identified ES products and few of them have been studied in any mechanistic detail. One major hindrance for mechanistic studies is the difficulty and cost in working with some vertebrate-parasitic nematodes and their hosts. Entomopathogenic nematodes (EPNs) are closely related to important species of human-parasitic nematodes [8] and could serve as model systems for studying parasitic nematode biology [9, 10]
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