Plasmodium falciparum ligand binding to erythrocytes induce alterations in deformability essential for invasion

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Sisquella, X; Nebr, T; Thompson, JK; Whitehead, L; Malpede, BM; Salinas, ND; Rogers, K; Tolia, NH; Fleig, A; O'Neill, J; ...Date
2017-02-22Source Title
eLifePublisher
ELIFE SCIENCES PUBLICATIONS LTDAffiliation
Medical Biology (W.E.H.I.)Metadata
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Sisquella, X., Nebr, T., Thompson, J. K., Whitehead, L., Malpede, B. M., Salinas, N. D., Rogers, K., Tolia, N. H., Fleig, A., O'Neill, J., Timm, W. -H., Horgen, F. D. & Cowman, A. F. (2017). Plasmodium falciparum ligand binding to erythrocytes induce alterations in deformability essential for invasion. ELIFE, 6, https://doi.org/10.7554/eLife.21083.Access Status
Open AccessAbstract
The most lethal form of malaria in humans is caused by Plasmodium falciparum. These parasites invade erythrocytes, a complex process involving multiple ligand-receptor interactions. The parasite makes initial contact with the erythrocyte followed by dramatic deformations linked to the function of the Erythrocyte binding antigen family and P. falciparum reticulocyte binding-like families. We show EBA-175 mediates substantial changes in the deformability of erythrocytes by binding to glycophorin A and activating a phosphorylation cascade that includes erythrocyte cytoskeletal proteins resulting in changes in the viscoelastic properties of the host cell. TRPM7 kinase inhibitors FTY720 and waixenicin A block the changes in the deformability of erythrocytes and inhibit merozoite invasion by directly inhibiting the phosphorylation cascade. Therefore, binding of P. falciparum parasites to the erythrocyte directly activate a signaling pathway through a phosphorylation cascade and this alters the viscoelastic properties of the host membrane conditioning it for successful invasion.
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