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Eukaryotic Cell, January 2008, p. 131-140, Vol. 7, No. 1
1535-9778/08/$08.00+0 doi:10.1128/EC.00301-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Department of Microbiology, Molecular Biology, and Biochemistry, University of Idaho, Moscow, Idaho 83843
Received 15 August 2007/ Accepted 26 October 2007
The process by which the intracellular parasite Toxoplasma gondii exits its host cell is central to its propagation and pathogenesis. Experimental induction of motility in intracellular parasites results in parasite egress, leading to the hypothesis that egress depends on the parasite's actin-dependent motility. Using a novel assay to monitor egress without experimental induction, we have established that inhibiting parasite motility does not block this process, although treatment with actin-disrupting drugs does delay egress. However, using an irreversible actin inhibitor, we show that this delay is due to the disruption of host cell actin alone, apparently resulting from the consequent loss of membrane tension. Accordingly, by manipulating osmotic pressure, we show that parasite egress is delayed by releasing membrane tension and promoted by increasing it. Therefore, without artificial induction, egress does not depend on parasite motility and can proceed by mechanical rupture of the host membrane.
Published ahead of print on 9 November 2007.
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