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Chemical Amputation and Regeneration of the Pharynx in the Planarian Schmidtea mediterranea
Published on: March 26, 2018
The planarian Schmidtea mediterranea is a new model to study host-pathogen interactions during fungal infections
Eli Isael Maciel1, Cen Jiang2, Paul G Barghouth1
1Department of Molecular & Cell Biology, University of California, Merced, USA; Quantitative and Systems Biology Graduate Program, University of California, Merced, USA.
Abstract:
Candida albicans is one of the most common fungal pathogens of humans. Currently, there are limitations in the evaluation of C. albicans infection in existing animal models, especially in terms of understanding the influence of specific infectious stages of the fungal pathogen on the host. We show that C. albicans infects, grows and invades tissues in the planarian flatworm Schmidtea mediterranea, and that the planarian responds to infection by activating components of the host innate immune system to clear and repair host tissues. We study different stages of C. albicans infection and demonstrate that planarian stem cells increase division in response to fungal infection, a process that is likely evolutionarily conserved in metazoans. Our results implicate MORN2 and TAK1/p38 signaling pathways as possible mediators of the host innate immune response to fungal infection. We propose the use of planarians as a model system to investigate host-pathogen interactions during fungal infections.
Insights
The planarian flatworm Schmidtea mediterranea serves as a novel model for studying Candida albicans fungal infections. This model reveals conserved stem cell responses and immune pathways during host-pathogen interactions.
Area of Science:
- Microbiology
- Immunology
- Developmental Biology
Background:
- Candida albicans is a prevalent human fungal pathogen.
- Existing animal models have limitations in studying C. albicans infection stages and host responses.
- Understanding host-pathogen interactions is crucial for managing fungal infections.
Purpose of the Study:
- To establish and validate the planarian flatworm Schmidtea mediterranea as a model organism for studying C. albicans infection.
- To investigate the host response to different stages of C. albicans infection in planarians.
- To identify conserved molecular pathways involved in the host innate immune response to fungal pathogens.
Main Methods:
- Infection of planarians (Schmidtea mediterranea) with Candida albicans.
- Observation of fungal growth, tissue invasion, and host immune responses.
- Analysis of planarian stem cell proliferation and activation of signaling pathways (MORN2, TAK1/p38).
Main Results:
- Candida albicans successfully infects, grows, and invades tissues in planarians.
- Planarians mount an innate immune response to clear the infection and repair tissues.
- Planarian stem cells exhibit increased division in response to fungal infection, suggesting conserved mechanisms.
- The MORN2 and TAK1/p38 signaling pathways are implicated in the planarian immune response.
Conclusions:
- The planarian Schmidtea mediterranea is a viable model for studying host-pathogen interactions in C. albicans infections.
- Planarian stem cell response to fungal infection highlights evolutionarily conserved mechanisms in metazoans.
- The study identifies potential molecular mediators of innate immunity against fungal pathogens.
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