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Functional characterization of malaria parasites deficient in the K+ channel Kch2

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K+ channels are integral membrane proteins, which contribute to maintain vital parameters such as the cellular membrane potential and cell volume. Malaria parasites encode two K+ channel homologues, Kch1 and Kch2, which are well-conserved among members of the Plasmodium genus. In the rodent malaria parasite P. berghei, the functional significance of K+ channel homologue PbKch2 was studied using targeted gene knock-out. The knockout parasites were characterized in a mouse model in terms of growth-kinetics and infectivity in the mosquito vector. Furthermore, using a tracer-uptake technique with 86Rb+ as a K+ congener, the K+ transporting properties of the knockout parasites were assessed.

RESULTS: Genetic disruption of Kch2 did not grossly affect the phenotype in terms of asexual replication and pathogenicity in a mouse model. In contrast to Kch1-null parasites, Kch2-null parasites were fully capable of forming oocysts in female Anopheles stephensi mosquitoes. 86Rb+ uptake in Kch2-deficient blood-stage P. berghei parasites (Kch2-null) did not differ from that of wild-type (WT) parasites. About two-thirds of the 86Rb+ uptake in WT and in Kch2-null parasites could be inhibited by K+ channel blockers and could be inferred to the presence of functional Kch1 in Kch2 knockout parasites. Kch2 is therefore not required for transport of K+ in P. berghei and is not essential to mosquito-stage sporogonic development of the parasite.

Original languageEnglish
JournalBiochemical and Biophysical Research Communications
Volume493
Issue number1
Pages (from-to)690-696
Number of pages7
ISSN0006-291X
DOIs
Publication statusPublished - 4 Nov 2017

    Research areas

  • Animals, Anopheles, Female, Malaria, Male, Mice, Plasmodium berghei, Potassium Channels, Protozoan Proteins, Journal Article, Research Support, N.I.H., Extramural, Research Support, Non-U.S. Gov't

ID: 52633506