Abstract

The causative agent of malaria is the unicellular protozoan Plasmodium. The parasite has a complex life cycle, involving asexual replication in human red blood cells (RBCs) as well as sexual replication, forming egg-like cells called oocysts in the mosquito vector. In endemic areas it is estimated that 250 million people get infected with malaria annually, resulting in 500.000-1.000.000 deaths. Increasing resistance towards known antimalarial drugs poses a significant problem in the fight against malaria. Therefore, the development of novel drugs that target vital proteins encoded by the parasite has attracted major attention. Plasmodium falciparum, the species responsible for the majority of malaria- associated fatalities, encodes two putative K+ channels, PfKch1 and PfKch2, which have been cloned in our laboratories. Although viable in all intraerythrocytic stages, Kch1-null P. berghei parasites exhibit a total inhibition of oocyst development in the mosquito midgut. Thus, Kch1 might serve as a potential target in novel parasite transmission-blocking strategies. However, earlier published immunofluorescence microscopy images have suggested that Kch1 is located in the infected human red blood cell membrane. In the present study, polyclonal antibodies were raised against the PfKch1 channel and our results demonstrate that Kch1 is located in the parasites plasma membrane in all blood stages of malaria. This finding is in accordance with functional data previously published from our lab. Thus, Kch1 may be a major K+ transporter in the parasite plasma membrane and play an important role for regulation of the membrane potential of the Plasmodium parasite.

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