Document Type
Article
Publication Date
5-8-2009
Publication Title
Science
Volume
324
Issue
5928
First Page
794
Last Page
797
Abstract
Apicomplexan parasites, including Plasmodium falciparum and Toxoplasma gondii (the causative agents of malaria and toxoplasmosis, respectively), are responsible for considerable morbidity and mortality worldwide. These pathogenic protozoa replicate within an intracellular vacuole inside of infected host cells, from which they must escape to initiate a new lytic cycle. By integrating cell biological, pharmacological, and genetic approaches, we provide evidence that both Plasmodium and Toxoplasma hijack host cell calpain proteases to facilitate parasite egress. Immunodepletion or inhibition of calpain-1 in hypotonically lysed and resealed erythrocytes prevented the escape of P. falciparum parasites, which was restored by adding purified calpain-1. Similarly, efficient egress of T. gondii from mammalian fibroblasts was blocked by either small interfering RNA– mediated suppression or genetic deletion of calpain activity and could be restored by genetic complementation.
Recommended Citation
Chandramohanadas, Rajesh; Davis, Paul H.; Beiting, Daniel P.; Harbut, Michael B.; Darling, Claire; Velmourougane, Geetha; Lee, Ming Yeh; Greer, Peter A.; Roos, David S.; and Greenbaum, Doron C., "Apicomplexan Parasites Co-Opt Host Calpains to Facilitate Their Escape from Infected Cells" (2009). Biology Faculty Publications. 117.
https://digitalcommons.unomaha.edu/biofacpub/117
Comments
Published in final edited form as: Science. 2009 May 8; 324(5928): 794–797. doi:10.1126/science.1171085.