ArticlePLoS pathogens2011
Non-lytic, actin-based exit of intracellular parasites from C. elegans intestinal cells.
Article in PLoS pathogens, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
41 citing papers in PubMed, 77 citations in OpenAlex.
- Microsporidia: evolution, infection mechanisms and host impact.Nature reviews. Microbiology · 2026Review
- Article
- Glucose-fed microbiota alters C. elegans intestinal epithelium and increases susceptibility to multiple bacterial pathogens.Scientific reports · 2024Article
- Proteasome inhibition triggers tissue-specific immune responses against different pathogens in C. elegans.PLoS biology · 2024Article
- Collagen and actin network mediate antiviral immunity against Orsay virus in C. elegans intestinal cells.PLoS pathogens · 2024Article
- Article
- A pals-25 gain-of-function allele triggers systemic resistance against natural pathogens of C. elegans.PLoS genetics · 2022Article
- High-throughput small molecule screen identifies inhibitors of microsporidia invasion and proliferation in C. elegans.Nature communications · 2022Article
- Insights from C. elegans into Microsporidia Biology and Host-Pathogen Relationships.Experientia supplementum (2012) · 2022Review
- A parental transcriptional response to microsporidia infection induces inherited immunity in offspring.Science advances · 2021Article
- Host CDK-1 and formin mediate microvillar effacement induced by enterohemorrhagic Escherichia coli.Nature communications · 2021Article
- A cullin-RING ubiquitin ligase promotes thermotolerance as part of the intracellular pathogen response inProceedings of the National Academy of Sciences of the United States of America · 2020Article
- Transcriptional adaptation ineLife · 2020Article
- The Caenorhabditis elegans RIG-I Homolog DRH-1 Mediates the Intracellular Pathogen Response upon Viral Infection.Journal of virology · 2020Article
- Natural variation in the roles of C. elegans autophagy components during microsporidia infection.PloS one · 2019Article
- Orsay δ Protein Is Required for Nonlytic Viral Egress.Journal of virology · 2018Article
- Review
- A Model for Evolutionary Ecology of Disease: The Case forJournal of nematology · 2017Article
- Identification of microsporidia host-exposed proteins reveals a repertoire of rapidly evolving proteins.Nature communications · 2017Article
- Interplay of neuronal and non-neuronal genes regulates intestinal DAF-16-mediated immune response duringCell death discovery · 2017Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The intestine is a common site for invasion by intracellular pathogens, but little is known about how pathogens restructure and exit intestinal cells in vivo. The natural microsporidian parasite N. parisii invades intestinal cells of the nematode C. elegans, progresses through its life cycle, and then exits cells in a transmissible spore form. Here we show that N. parisii causes rearrangements of host actin inside intestinal cells as part of a novel parasite exit strategy. First, we show that N. parisii infection causes ectopic localization of the normally apical-restricted actin to the basolateral side of intestinal cells, where it often forms network-like structures. Soon after this actin relocalization, we find that gaps appear in the terminal web, a conserved cytoskeletal structure that could present a barrier to exit. Reducing actin expression creates terminal web gaps in the absence of infection, suggesting that infection-induced actin relocalization triggers gap formation. We show that terminal web gaps form at a distinct stage of infection, precisely timed to precede spore exit, and that all contagious animals exhibit gaps. Interestingly, we find that while perturbations in actin can create these gaps, actin is not required for infection progression or spore formation, but actin is required for spore exit. Finally, we show that despite large numbers of spores exiting intestinal cells, this exit does not cause cell lysis. These results provide insight into parasite manipulation of the host cytoskeleton and non-lytic escape from intestinal cells in vivo.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.