Disruption of the PfPK7 gene impairs schizogony and sporogony in the human malaria parasite Plasmodium falciparum

Dominique Dorin-Semblat, Audrey Sicard, Caroline Doerig, Lisa Ranford-Cartwright, Christian Doerig

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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.

Original languageEnglish
Pages (from-to)279-285
Number of pages7
JournalEukaryotic Cell
Issue number2
Publication statusPublished - 1 Feb 2008
Externally publishedYes

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