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Updated: Jul 8, 2026
Selective Cleaning of Wild Caenorhabditis Nematodes to Enrich for Intestinal Microbiome Bacteria
Published on: August 13, 2021
Caenorhabditis elegans immune responses to microsporidia and viruses
Rubén González1, Marie-Anne Félix1
1Institut de Biologie de l'École Normale Supérieure, CNRS, INSERM, 75005, Paris, France.
Abstract:
The model organism Caenorhabditis elegans is susceptible to infection by obligate intracellular pathogens, specifically microsporidia and viruses. These intracellular pathogens infect intestinal cells, or, for some microsporidia, epidermal cells. Strikingly, intestinal cell infections by viruses or microsporidia trigger a common transcriptional response, activated in part by the ZIP-1 transcription factor. Among the strongest activated genes in this response are ubiquitin-pathway members and members of the pals family, an intriguing gene family with cross-regulations of different members of genomic clusters. Some of the induced genes participate in host defense against the pathogens, for example through ubiquitin-mediated inhibition. Other mechanisms defend the host specifically against viral infections, including antiviral RNA interference and uridylation. These various immune responses are altered by environmental factors and by intraspecific genetic variation of the host. These pathogens were first isolated 15 years ago and much remains to be discovered using C. elegans genetics; also, other intracellular pathogens of C. elegans may yet to be discovered.
Insights
Caenorhabditis elegans mounts a common immune response to microsporidia and viruses, involving the ZIP-1 transcription factor and host defense genes. This response is influenced by host genetics and environmental factors.
Area of Science:
- * Infectious disease and host-pathogen interactions.
- * Genetics and molecular biology of model organisms.
Background:
- * The model organism Caenorhabditis elegans is susceptible to intracellular pathogens like microsporidia and viruses.
- * These pathogens infect intestinal or epidermal cells, posing a significant threat to host health.
Purpose of the Study:
- * To investigate the common transcriptional response of C. elegans to microsporidia and viral infections.
- * To identify key molecular players, such as transcription factors and gene families, involved in this host defense.
Main Methods:
- * Transcriptional profiling to identify genes upregulated during pathogen infection.
- * Utilizing C. elegans genetics to study the role of specific genes, like ZIP-1, in the immune response.
- * Investigating host defense mechanisms including ubiquitin-mediated inhibition, RNA interference, and uridylation.
Main Results:
- * Intestinal infections by viruses or microsporidia induce a shared transcriptional response, partly mediated by the ZIP-1 transcription factor.
- * Key upregulated genes include ubiquitin-pathway members and the pals gene family, crucial for host defense.
- * Specific antiviral mechanisms like RNA interference and uridylation are also activated.
Conclusions:
- * C. elegans exhibits a conserved transcriptional defense against distinct intracellular pathogens.
- * The ZIP-1 transcription factor and specific gene families play critical roles in this immune response.
- * Environmental factors and host genetic variation modulate immune responses, highlighting the complexity of host-pathogen interactions.
