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Updated: May 22, 2026
The Nematode Caenorhabditis Elegans - A Versatile In Vivo Model to Study Host-microbe Interactions
Published on: October 18, 2017
The fungal virulence factor PefD activates sleep neurons of Caenorhabditis elegans
Anna-Lena Klemke1, Xiaodi Hu1, Pietrina Steudel1
1Karlsruhe Institute of Technology (KIT) - South Campus, Institute for Applied Biosciences, Department of Microbiology, Fritz-Haber-Weg 4, D-76131 Karlsruhe, Germany.
Abstract:
Nematode-trapping fungi such as Arthrobotrys flagrans employ sophisticated strategies to immobilize and digest their prey. A critical, yet poorly understood, step in this interaction is the induction of prey paralysis following capture. Here, we characterize putative effector D (PefD), a small secreted protein from A. flagrans. We demonstrate that pefD expression is specifically upregulated during the early and middle stages of infection of Caenorhabditis elegans (12-24 h post inoculation) and PefD localizes to the infection bulb within the nematode. Deletion of pefD significantly delayed the paralysis of C. elegans, whereas its overexpression accelerated the process. Through heterologous pan-neuronal expression in C. elegans, we show that PefD directly attenuates host locomotion and significantly enhances the activity of the sleep-promoting RIS interneuron. Unlike other effectors such as NipA or CyrA, PefD specifically modulates neuronal activity patterns without inducing general neurodegeneration. Our results identify PefD as a key virulence factor that hijacks the endogenous sleep induction circuitry of the host to facilitate rapid prey immobilization.
Insights
Nematode-trapping fungi use PefD, a secreted protein, to paralyze prey. PefD hijacks the host
Area of Science:
- Mycology and Nematology
- Molecular Biology and Biochemistry
Background:
- Nematode-trapping fungi (NTF) capture and digest nematodes using complex mechanisms.
- The precise molecular events leading to prey paralysis by NTF remain largely unknown.
- Small-secreted proteins (SSPs) are crucial virulence factors in fungal-nematode interactions.
Purpose of the Study:
- To characterize the role of PefD (Putative Effector D), a novel SSP from Arthrobotrys flagrans, in nematode paralysis.
- To elucidate the mechanism by which PefD contributes to prey immobilization.
Main Methods:
- Gene expression analysis of pefD during infection stages.
- Localization studies of PefD within the nematode.
- Functional analysis using gene deletion and overexpression in A. flagrans.
- Heterologous expression of PefD in Caenorhabditis elegans to assess neuronal effects.
Main Results:
- pefD expression is upregulated during early-to-middle infection stages (12-24 hpi) and PefD localizes to the infection bulb.
- Deletion of pefD significantly delayed C. elegans paralysis, while overexpression accelerated it.
- PefD directly attenuates host locomotion and enhances sleep-promoting RIS interneuron activity in C. elegans without causing neurodegeneration.
Conclusions:
- PefD is a key virulence factor in Arthrobotrys flagrans.
- PefD facilitates rapid prey immobilization by directly modulating host neuronal activity and inducing a sleep-like state.
- This study reveals a novel mechanism of prey manipulation by fungal pathogens.
