Present address: Harvard School of Public Health, 665 Huntington Avenue, Boston, MA 02115, USA.
Stage-specific depletion of myosin A supports an essential role in motility of malarial ookinetes
Article first published online: 28 SEP 2011
© 2011 Blackwell Publishing Ltd
Volume 13, Issue 12, pages 1996–2006, December 2011
How to Cite
Siden-Kiamos, I., Ganter, M., Kunze, A., Hliscs, M., Steinbüchel, M., Mendoza, J., Sinden, R. E., Louis, C. and Matuschewski, K. (2011), Stage-specific depletion of myosin A supports an essential role in motility of malarial ookinetes. Cellular Microbiology, 13: 1996–2006. doi: 10.1111/j.1462-5822.2011.01686.x
- Issue published online: 15 NOV 2011
- Article first published online: 28 SEP 2011
- Accepted manuscript online: 7 SEP 2011 11:35PM EST
- Received 16 May, 2011; revised 9 August, 2011; accepted 13 August, 2011.
Functional analysis of Plasmodium genes by classical reverse genetics is currently limited to mutants that are viable during erythrocytic schizogony, the pathogenic phase of the malaria parasite where transfection is performed. Here, we describe a conceptually simple experimental approach to study the function of genes essential to the asexual blood stages in a subsequent life cycle stage by a promoter-swap approach. As a proof of concept we targeted the unconventional class XIV myosin MyoA, which is known to be required for Toxoplasma gondii tachyzoite locomotion and host cell invasion. By placing the corresponding Plasmodium berghei gene, PbMyoA, under the control of the apical membrane antigen 1 (AMA1) promoter, expression in blood stages is maintained but switched off during transmission to the insect vector, i.e. ookinetes. In those mutant ookinetes gliding motility is entirely abolished resulting in a complete block of life cycle progression in Anopheles mosquitoes. Similar approaches should permit the analysis of gene function in the mosquito forms that are shared with the erythrocytic stages of the malaria parasite.