Conditional expression of apical membrane antigen 1 in Plasmodium falciparum shows it is required for erythrocyte invasion by merozoites
Article first published online: 27 MAR 2014
© 2014 The Authors. Cellular Microbiology published by John Wiley & Sons Ltd.
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Special Issue: Malaria
Volume 16, Issue 5, pages 642–656, May 2014
How to Cite
Yap, A., Azevedo, M. F., Gilson, P. R., Weiss, G. E., O'Neill, M. T., Wilson, D. W., Crabb, B. S. and Cowman, A. F. (2014), Conditional expression of apical membrane antigen 1 in Plasmodium falciparum shows it is required for erythrocyte invasion by merozoites. Cellular Microbiology, 16: 642–656. doi: 10.1111/cmi.12287
- Issue published online: 15 APR 2014
- Article first published online: 27 MAR 2014
- Accepted manuscript online: 27 FEB 2014 02:20AM EST
- Manuscript Accepted: 24 FEB 2014
- Manuscript Revised: 23 FEB 2014
- Manuscript Received: 23 DEC 2013
- National Health and Medical Research Council of Australia (NHMRC). Grant Number: 637406
- Victorian State Government Operational Infrastructure Support
- Walter and Eliza Hall Institute of Medical Research
- University of Melbourne (Australia)
Malaria is caused by obligate intracellular parasites, of which Plasmodium falciparum is the most lethal species. In humans, P. falciparum merozoites (invasive forms of the parasite) employ a host of parasite proteins to rapidly invade erythrocytes. One of these is the P. falciparum apical membrane antigen 1 (PfAMA1) which forms a complex with rhoptry neck proteins at the tight junction. Here, we have placed the Pfama1 gene under conditional control using dimerizable Cre recombinase (DiCre) in P. falciparum. DiCre-mediated excision of the loxP-flanked Pfama1 gene results in approximately 80% decreased expression of the protein within one intraerythrocytic growth cycle. This reduces growth by 40%, due to decreased invasion efficiency characterized by a post-invasion defect in sealing of the parasitophorous vacuole. These results show that PfAMA1 is an essential protein for merozoite invasion in P. falciparum and either directly or indirectly plays a role in resealing of the red blood cell at the posterior end of the invasion event.