| Literature DB >> 27374406 |
Jennifer C Volz1, Alan Yap2, Xavier Sisquella1, Jenn K Thompson1, Nicholas T Y Lim1, Lachlan W Whitehead1, Lin Chen1, Marko Lampe3, Wai-Hong Tham2, Danny Wilson1, Thomas Nebl1, Danushka Marapana2, Tony Triglia1, Wilson Wong1, Kelly L Rogers1, Alan F Cowman4.
Abstract
Plasmodium falciparum parasites in the merozoite stage invade human erythrocytes and cause malaria. Invasion requires multiple interactions between merozoite ligands and erythrocyte receptors. P. falciparum reticulocyte binding homolog 5 (PfRh5) forms a complex with the PfRh5-interacting protein (PfRipr) and Cysteine-rich protective antigen (CyRPA) and binds erythrocytes via the host receptor basigin. However, the specific role that PfRipr and CyRPA play during invasion is unclear. Using P. falciparum lines conditionally expressing PfRipr and CyRPA, we show that loss of PfRipr or CyRPA function blocks growth due to the inability of merozoites to invade erythrocytes. Super-resolution microscopy revealed that PfRipr, CyRPA, and PfRh5 colocalize at the junction between merozoites and erythrocytes during invasion. PfRipr, CyRPA, and PfRipr/CyRPA/PfRh5-basigin complex is required for triggering the Ca(2+) release and establishing the tight junction. Together, these results establish that the PfRh5/PfRipr/CyRPA complex is essential in the sequential molecular events leading to parasite invasion of human erythrocytes.Entities:
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Year: 2016 PMID： 27374406 DOI： 10.1016/j.chom.2016.06.004
Source DB: PubMed Journal: Cell Host Microbe ISSN： 1931-3128 Impact factor: 21.023