Toxoplasma parasites replicate by dividing into two new parasites. Each new parasite requires a new apicoplast that must divide in synchrony with the parasite. What the team showed is that a protein called DrpA is crucial to the division of the apicoplast.
DrpA belongs to a family of proteins called dynamins, which are involved in a range of cellular processes that require constriction or pinching. Tracking the evolution of dynamins, the current work suggests that cells have the ability to retool these proteins to perform novel tasks, in this case to divide the symbiotic alga that was the ancestor of the apicoplast.
The group generated a mutant cell line to disrupt DrpA function in T. gondii. Using modern genetic and microscopy techniques, they showed that when the DrpA protein is no longer functional, the apicoplast can't pinch in two, preventing new parasites from acquiring this essential organelle. It results in the death of the parasite.
"Understanding that DrpA is necessary for apicoplast fission gives researchers a new working model to understand how the causative agents of several parasitic diseases flourish in human and animal hosts," said van Dooren.
Indeed, the team's search for similar dynamin-related proteins led them to examine, in addition to T. gondii, the genomes of four other parasitic organisms.
"In each, including Plasmodium, the cause of malaria, we found the DrpA protein, suggesting a common mechanism for apicoplast division in these parasites," said Striepen.
The new system now allows researchers to study what happens when organisms lose their apicoplast organelles.
Read the full story at http://www.prweb.com/releases/Toxoplasmosis/Cellular_Biology/prweb2041024.htm.
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