Eukaryotic Cell doi:10.1128/EC.00245-07
Copyright (c) 2007, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.
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,
and
Christian Doerig*
INSERM U609, Wellcome Centre for Molecular Parasitology, University of Glasgow, Glasgow G12 8TA, Scotland, UK; Division of Infection and Immunity, Institute of Biomedical and Life Sciences, University of Glasgow, Glasgow G12 8TA, Scotland, UK
* To whom correspondence should be addressed. Email:
cdoer001{at}udcf.gla.ac.uk.
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Abstract |
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PfPK7 is an orphan protein kinase of Plasmodium falciparum with maximal homology to MEK3/6 and to fungal PKAs 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 MAPK homologues, suggesting 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 the 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. Normal asexual growth rate and ability to produce oocysts are restored if a functional copy of the pfPK7 gene is re-introduced into the pfPK7- parasites. Hence, PfPK7 is involved in a pathway regulating parasite proliferation and development.
