A core set of venom proteins is released by entomopathogenic nematodes in the genus Steinernema

Abstract

Parasitic helminths release molecular effectors into their hosts and these effectors can directly damage host tissue and modulate host immunity. Excreted/secreted proteins (ESPs) are one category of parasite molecular effectors that are critical to their success within the host. However, most studies of nematode ESPs rely on in vitro stimulation or culture conditions to collect the ESPs, operating under the assumption that in vitro conditions mimic actual in vivo infection. This assumption is rarely if ever validated. Entomopathogenic nematodes (EPNs) are lethal parasites of insects that produce and release toxins into their insect hosts and are a powerful model parasite system. We compared transcriptional profiles of individual Steinernema feltiae nematodes at different time points of activation under in vitro and in vivo conditions and found that some but not all time points during in vitro parasite activation have similar transcriptional profiles with nematodes from in vivo infections. These findings highlight the importance of experimental validation of ESP collection conditions. Additionally, we found that a suite of genes in the neuropeptide pathway were downregulated as nematodes activated and infection progressed in vivo , suggesting that these genes are involved in host-seeking behavior and are less important during active infection. We then characterized the ESPs of activated S . feltiae infective juveniles (IJs) using mass spectrometry and identified 266 proteins that are released by these nematodes. In comparing these ESPs with those previously identified in activated S . carpocapsae IJs, we identified a core set of 52 proteins that are conserved and present in the ESPs of activated IJs of both species. These core venom proteins include both tissue-damaging and immune-modulating proteins, suggesting that the ESPs of these parasites include both a core set of effectors as well as a specialized set, more adapted to the particular hosts they infect.

A putative UDP-glycosyltransferase from Heterorhabditis bacteriophora suppresses antimicrobial peptide gene expression and factors related to ecdysone signaling

“…An important avenue of future research would be to examine a potential role for UGTs in H. bacteriophora development and uncover the modes of regulation that make this possible. www.nature.com/scientificreports/ Another important characteristic of a virulence factor is that it is secreted to the exterior of the nematode so that it can interact with the host environment, as documented in other species 23 . To this end, we tested H. bacteriophora ES products for glycosyltransferase activity using UDP-glucose as a sugar donor and 20E as the acceptor molecule, as these are the prevalent substrates for glycosyltransferases of invertebrates and plants 24,25 .…”

Morphological adjustment in free-living Steinernema feltiae infective juveniles to increasing concentration of Nemafric-BL phytonematicide

“…The simultaneous relaxation and contraction of longitudinal somatic muscles in opposite symmetries, results in nematode bodies bending towards the symmetry with relaxed muscles. In S. feltiae IJ, nictation in during host searching [19] is the result of simultaneous relaxation and contraction of longitudinal somatic muscles towards the anterior end of the nematode. In contrast, simultaneous contraction of latero-dorsal and latero-ventral longitudinal somatic muscles in a particular region of the nematode body, results in that part of the body being straightened [28].…”

“…During host searching, S. feltiae IJ use an intermediate foraging strategy, which comprises a combination of ambush and cruiser type [18], that could last for at least a month [18], thereby having the potential to expose themselves to cucurbitacins in soil solution. Post-entry into the host, IJ undergo activation process which entails recovery from dauer-like, comprising fundamental changes that encompass gene expression for promoting transition from a freeliving form to active parasitic larval stages [19]. During activation process, parasitic larval stages release Xenorhabdus species from their intestines into the hemocoel of hosts, with the bacteria multiplying in hemolymph of hosts, resulting in hosts dying within 24-48 h [7].…”

Host Immunosuppression Induced by Steinernema feltiae, an Entomopathogenic Nematode, through Inhibition of Eicosanoid Biosynthesis

“…This supports the role of the nematode in insecticidal activity without the presence of symbiotic bacteria. Metabolite analysis of S. feltiae IJs using mass spectrometry identified 266 proteins, among which 52 proteins were conserved among nematode metabolites known to be associated with tissue-damaging and immune-modulating proteins [49]. In addition, the nematode cuticle plays a crucial role in avoiding insect immune surveillance by disguising nematode surface [50].…”