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EMBO reports 6, 5, 464–469 (2005)
doi:10.1038/sj.embor.7400404
Published online: 22 April 2005
A mitogen-activated protein kinase regulates male gametogenesis and transmission of the malaria parasite Plasmodium berghei
Radha Rangarajan1, Amy K Bei1, Deepa Jethwaney1, Priscilla Maldonado1, Dominique Dorin2, Ali A Sultan1 & Christian Doerig2
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1 Department of Immunology and Infectious Diseases, Harvard School of Public Health, 665 Huntington Avenue, Boston, Massachusetts 02115, USA
2 INSERM U609, Wellcome Centre for Molecular Parasitology, University of Glasgow, Glasgow G11 6NU, UK
To whom correspondence should be addressed
Ali A Sultan Tel: +1 617 432 1563; Fax: +1 617 739 8348; E-mail: asultan@hsph.harvard.edu
Christian Doerig Tel: +44 141 339 8855 x6201; Fax: +44 141 330 5422; E-mail: cdoer001@udcf.gla.ac.uk
Received 4 January 2005; Accepted 24 March 2005; Published online 22 April 2005.
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Abstract
Differentiation of malaria parasites into sexual forms (gametocytes) in the vertebrate host and their subsequent development into gametes in the mosquito vector are crucial steps in the completion of the parasite's life cycle and transmission of the disease. The molecular mechanisms that regulate the sexual cycle are poorly understood. Although several signal transduction pathways have been implicated, a clear understanding of the pathways involved has yet to emerge. Here, we show that a Plasmodium berghei homologue of Plasmodium falciparum mitogen-activated kinase-2 (Pfmap-2), a gametocyte-specific mitogen-activated protein kinase (MAPK), is required for male gamete formation. Parasites lacking Pbmap-2 are competent for gametocytogenesis, but exflagellation of male gametocytes, the process that leads to male gamete formation, is almost entirely abolished in mutant parasites. Consistent with this result, transmission of mutant parasites to mosquitoes is grossly impaired. This finding identifies a crucial role for a MAPK pathway in malaria transmission.
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