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Published on: April 5, 2015
Gliding motility leads to active cellular invasion by Cryptosporidium parvum sporozoites
Dawn M Wetzel1, Joann Schmidt, Mark S Kuhlenschmidt
1Department of Molecular Microbiology, Campus Box 8230, Washington University School of Medicine, St. Louis, MO 63110, USA.
Abstract:
We examined gliding motility and cell invasion by an early-branching apicomplexan, Cryptosporidium parvum, which causes diarrheal disease in humans and animals. Real-time video microscopy demonstrated that C. parvum sporozoites undergo circular and helical gliding, two of the three stereotypical movements exhibited by Toxoplasma gondii tachyzoites. C. parvum sporozoites moved more rapidly than T. gondii sporozoites, which showed the same rates of motility as tachyzoites. Motility by C. parvum sporozoites was prevented by latrunculin B and cytochalasin D, drugs that depolymerize the parasite actin cytoskeleton, and by the myosin inhibitor 2,3-butanedione monoxime. Imaging of the initial events in cell entry by Cryptosporidium revealed that invasion occurs rapidly; however, the parasite does not enter deep into the cytosol but rather remains at the cell surface in a membrane-bound compartment. Invasion did not stimulate rearrangement of the host cell cytoskeleton and was inhibited by cytochalasin D, even in host cells that were resistant to the drug. Our studies demonstrate that C. parvum relies on a conserved actin-myosin motor for motility and active penetration of its host cell, thus establishing that this is a widely conserved feature of the Apicomplexa.
Insights
Cryptosporidium parvum uses actin-myosin motors for gliding and host cell invasion, similar to other apicomplexans. This parasite causes diarrheal disease and its motility is crucial for infection.
Area of Science:
- Parasitology
- Cell Biology
- Molecular Biology
Background:
- Cryptosporidium parvum is an early-branching apicomplexan parasite responsible for human and animal diarrheal diseases.
- Understanding the motility and invasion mechanisms of C. parvum is crucial for developing effective interventions.
Purpose of the Study:
- To investigate the gliding motility and cell invasion processes of Cryptosporidium parvum sporozoites.
- To determine the molecular mechanisms underlying C. parvum motility and host cell penetration.
Main Methods:
- Real-time video microscopy was employed to observe C. parvum sporozoite movement.
- The effects of actin cytoskeleton inhibitors (latrunculin B, cytochalasin D) and a myosin inhibitor (2,3-butanedione monoxime) on motility were assessed.
- Imaging techniques were used to analyze the initial events of host cell entry.
Main Results:
- C. parvum sporozoites exhibit circular and helical gliding motility, distinct from but related to Toxoplasma gondii tachyzoites.
- Motility was dependent on the actin cytoskeleton and myosin motor, as evidenced by drug inhibition studies.
- Parasite invasion was rapid but resulted in the parasite residing within a membrane-bound compartment, without significant host cell cytoskeleton rearrangement.
Conclusions:
- Cryptosporidium parvum utilizes a conserved actin-myosin motor system for motility and active host cell invasion.
- This finding establishes a widely conserved feature of motility and invasion across the phylum Apicomplexa.
- The study provides insights into the fundamental biology of C. parvum, relevant for disease control.
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