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Updated: Oct 7, 2025
Studying Inherited Immunity in a Caenorhabditis elegans Model of Microsporidia Infection
Published on: April 6, 2022
An intestinally secreted host factor promotes microsporidia invasion of C. elegans
Hala Tamim El Jarkass1, Calvin Mok1, Michael R Schertzberg2
1Department of Molecular Genetics, University of Toronto, Toronto, Canada.
Abstract:
Microsporidia are ubiquitous obligate intracellular pathogens of animals. These parasites often infect hosts through an oral route, but little is known about the function of host intestinal proteins that facilitate microsporidia invasion. To identify such factors necessary for infection by Nematocida parisii, a natural microsporidian pathogen of Caenorhabditis elegans, we performed a forward genetic screen to identify mutant animals that have a Fitness Advantage with Nematocida (Fawn). We isolated four fawn mutants that are resistant to Nematocida infection and contain mutations in T14E8.4, which we renamed aaim-1 (Antibacterial and Aids invasion by Microsporidia). Expression of AAIM-1 in the intestine of aaim-1 animals restores N. parisii infectivity and this rescue of infectivity is dependent upon AAIM-1 secretion. N. parisii spores in aaim-1 animals are improperly oriented in the intestinal lumen, leading to reduced levels of parasite invasion. Conversely, aaim-1 mutants display both increased colonization and susceptibility to the bacterial pathogen Pseudomonas aeruginosa and overexpression ofaaim-1 reduces P. aeruginosa colonization. Competitive fitness assays show that aaim-1 mutants are favored in the presence of N. parisii but disadvantaged on P. aeruginosa compared to wild-type animals. Together, this work demonstrates how microsporidia exploits a secreted protein to promote host invasion. Our results also suggest evolutionary trade-offs may exist to optimizing host defense against multiple classes of pathogens.
Insights
Researchers identified a secreted protein, AAIM-1 (Antibacterial and Aids invasion by Microsporidia), crucial for microsporidia parasite invasion in the host intestine. This discovery sheds light on host-pathogen interactions and potential evolutionary trade-offs in immunity.
Area of Science:
- Molecular parasitology
- Host-pathogen interactions
- Genetics and genomics
Background:
- Microsporidia are widespread intracellular animal pathogens, often entering hosts orally.
- The host intestinal proteins facilitating microsporidia invasion remain largely uncharacterized.
- Understanding these factors is key to deciphering host susceptibility to microsporidian infections.
Purpose of the Study:
- To identify host intestinal factors essential for microsporidian parasite invasion.
- To characterize the role of identified factors in host-pathogen dynamics.
- To explore potential evolutionary trade-offs in host defense mechanisms.
Main Methods:
- Forward genetic screen in *Caenorhabditis elegans* to identify mutants resistant to *Nematocida parisii* infection (Fawn mutants).
- Genetic mapping and sequencing to identify causative mutations.
- Functional assays including gene expression, protein secretion, and competitive fitness assays.
Main Results:
- Four *fawn* mutants resistant to *N. parisii* were identified, with mutations in *T14E8.4*, renamed *aaim-1*.
- AAIM-1 (Antibacterial and Aids invasion by Microsporidia) is a secreted protein required for *N. parisii* invasion; its absence leads to improper spore orientation.
- *aaim-1* mutants exhibit increased susceptibility to *Pseudomonas aeruginosa*, suggesting a trade-off in host defense.
Conclusions:
- Microsporidia exploit the secreted host protein AAIM-1 to facilitate invasion.
- AAIM-1 plays a dual role in host defense, impacting susceptibility to both microsporidia and bacteria.
- These findings suggest potential evolutionary constraints in optimizing host immunity against diverse pathogens.
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