Once the parasite docks with the host cell it sends out proteins that bind tightly to host cell receptors and create an indented pocket in the surface of the cell. The parasite's myosin molecules then latch onto the newly formed protein-receptor complexes pulling the myosin along a skeleton of actin and into the cell.
"Myosin A is an extremely fast moving motor, comparable in speed to the myosin responsible for the contraction of muscle in humans. The motor propels the parasite at a speed of five micrometers per second, allowing it to penetrate host cells within 10 to 30 seconds.
"This rapid entry process is essential for Apicomplexan parasites to replicate safely, hidden from the immune system," says Dr Soldati.
Researchers established myosin A's function by knocking out the gene in Toxoplasma gondii and observing the effects on its motility. They used time-lapse microscopy to score the percentage of parasites able to glide and perform normal forms of movement on coated glass slides.
"In optimum conditions freshly released parasites exhibit circular gliding, upright twirling and helical gliding. But with only partial gene function the parasites performed a reduced number or incomplete circles and at a lower speed. With the gene completely shut down the parasites were totally unable to move."
"Toxoplasma remains an important threat to human health with the continual spread of AIDS, while the malaria parasite kills more than 1 million children each year.
"A detailed understanding of the mechanism of host cell invasion by the Apicomplexans is an important and acute goal since such studies will lead to the identification of novel therapeutic targets, which are urgently needed," says Dr Soldati.
The work was funded by the Deutsche Forschungsgemeinschaft.
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Contact: Judith H Moore
j.h.moore@ic.ac.uk
44-207-594-6702
Imperial College London
24-Oct-2002