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Disruption of the PfPK7 Gene Impairs Schizogony and Sporogony in the Human Malaria Parasite Plasmodium falciparum

INSERM U609, Wellcome Centre for Molecular Parasitology, University of Glasgow, Glasgow G12 8TA, Scotland, United Kingdom,¹ Division of Infection and Immunity, Institute of Biomedical and Life Sciences, University of Glasgow, Glasgow G12 8TA, Scotland, United Kingdom²

Received 6 July 2007/ Accepted 14 November 2007

PfPK7 is an orphan protein kinase of Plasmodium falciparum with maximal homology to MEK3/6 and to fungal protein kinase A proteins in its C-terminal and N-terminal regions, respectively. We showed previously that recombinant PfPK7 is active on various substrates but is unable to phosphorylate the Plasmodium falciparum mitogen-activated protein kinase homologues, suggesting that it is not a MEK functional homologue. Using a reverse genetics approach to investigate the function of this enzyme in live parasites, we now show that PfPK7^– parasite clones display phenotypes at two stages of their life cycle: first, a decrease in the rate of asexual growth in erythrocytes associated with a lower number of daughter merozoites generated per schizont, and second, a dramatic reduction in the ability to produce oocysts in the mosquito vector. A normal asexual growth rate and the ability to produce oocysts are restored if a functional copy of the PfPK7 gene is reintroduced into the PfPK7^– parasites. Hence, PfPK7 is involved in a pathway that regulates parasite proliferation and development.

Published ahead of print on 14 December 2007.