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Updated: Jun 24, 2026
12:15
In Vitro Polymerization of F-actin on Early Endosomes
Published on: August 28, 2017
Host cell entry by apicomplexa parasites requires actin polymerization in the host cell
Virginie Gonzalez1, Audrey Combe, Violaine David
1Institut Cochin, Université Paris Descartes, CNRS (UMR 8104), Paris, France.
Cell Host & Microbe
|March 17, 2009
Summary
Host cell invasion by Apicomplexa parasites, like Toxoplasma gondii and Plasmodium, actively involves host actin. This study reveals a crucial role for host actin polymerization in parasite entry.
Area of Science:
- Parasitology
- Cell Biology
- Molecular Biology
Background:
- Apicomplexa are obligate intracellular parasites.
- Parasite invasion relies on a motor complex and a moving junction.
- Host actin's role in invasion was previously considered minimal.
Purpose of the Study:
- To investigate the role of host actin in Apicomplexa invasion.
- To elucidate the molecular mechanisms of host cell entry by Apicomplexa.
Main Methods:
- Utilized Toxoplasma gondii tachyzoites and Plasmodium berghei sporozoites.
- Observed host cell invasion dynamics using microscopy.
- Analyzed the involvement of actin and the Arp2/3 complex.
Main Results:
- Demonstrated host actin's active participation in parasite entry.
- Identified a stable, ring-shaped F-actin structure at the parasite-host junction.
- Showed recruitment of the Arp2/3 complex to the actin ring, essential for invasion.
Conclusions:
- Apicomplexa invasion requires both the parasite's motor and host actin polymerization.
- Host actin anchors the moving junction, facilitating parasite penetration.
- This finding challenges previous models of Apicomplexa invasion.
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