ArticleCellular microbiology2016
Small GTPases promote actin coat formation on microsporidian pathogens traversing the apical membrane of Caenorhabditis elegans intestinal cells.
Article in Cellular microbiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 26 citations in OpenAlex.
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- A conserved megaprotein-based molecular bridge critical for lipid trafficking and cold resilience.Nature communications · 2022Article
- Loss of heat shock factor initiates intracellular lipid surveillance by actin destabilization.Cell reports · 2022Article
- Imaging of Actin Cytoskeleton in the Nematode Caenorhabditis elegans.Methods in molecular biology (Clifton, N.J.) · 2022Article
- Insights from C. elegans into Microsporidia Biology and Host-Pathogen Relationships.Experientia supplementum (2012) · 2022Review
- Invasion of Host Cells by Microsporidia.Frontiers in microbiology · 2020Review
- Age-Onset Phosphorylation of a Minor Actin Variant Promotes Intestinal Barrier Dysfunction.Developmental cell · 2019Article
- Orsay δ Protein Is Required for Nonlytic Viral Egress.Journal of virology · 2018Article
- Developmental basis for intestinal barrier against the toxicity of graphene oxide.Particle and fibre toxicology · 2018Article
- A Model for Evolutionary Ecology of Disease: The Case forJournal of nematology · 2017Article
- The Natural Biotic Environment ofGenetics · 2017Review
- A Large Collection of Novel Nematode-Infecting Microsporidia and Their Diverse Interactions with Caenorhabditis elegans and Other Related Nematodes.PLoS pathogens · 2016Article
- Calcineurin Orchestrates Lateral Transfer of Aspergillus fumigatus during Macrophage Cell Death.American journal of respiratory and critical care medicine · 2016Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Many intracellular pathogens co-opt actin in host cells, but little is known about these interactions in vivo. We study the in vivo trafficking and exit of the microsporidian Nematocida parisii, which is an intracellular pathogen that infects intestinal cells of the nematode Caenorhabditis elegans. We recently demonstrated that N. parisii uses directional exocytosis to escape out of intestinal cells into the intestinal tract. Here, we show that an intestinal-specific isoform of C. elegans actin called ACT-5 forms coats around membrane compartments that contain single exocytosing spores, and that these coats appear to form after fusion with the apical membrane. We performed a genetic screen for host factors required for actin coat formation and identified small GTPases important for this process. Through analysis of animals defective in these factors, we found that actin coats are not required for pathogen exit although they may boost exocytic output. Later during infection, we find that ACT-5 also forms coats around membrane-bound vesicles that contain multiple spores. These vesicles are likely formed by clathrin-dependent compensatory endocytosis to retrieve membrane material that has been trafficked to the apical membrane as part of the exocytosis process. These findings provide insight into microsporidia interaction with host cells, and provide novel in vivo examples of the manner in which intracellular pathogens co-opt host actin during their life cycle.
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