Roles of the RON3 C-terminal fragment in erythrocyte invasion and blood-stage parasite proliferation in Plasmodium falciparum

• DOI: 10.3389/fcimb.2023.1197126
• Publication Date: 2023-06-29T17:37:05Z
• Authors: Daisuke Ito; Yoko Kondo; Eizo Takashima; Hideyuki Iriko; Amporn Thongkukia...; Motomi Torii; Hitoshi Otsuki
• Keywords: Rhoptry; Plasmodium (life cycle); Organelle

Plasmodium species cause malaria, and in the instance of falciparum is responsible for a societal burden over 600,000 deaths annually. The symptoms pathology malaria are due to intraerythocytic parasites. Erythrocyte invasion mediated by parasite merozoite stage, accompanied formation parasitophorous vacuolar membrane (PVM), within which develops. apical rhoptry organelle contains various proteins that contribute erythrocyte attachment invasion. RON3, bulb protein, undergoes protein processing discharged into PVM during RON3-deficient parasites fail develop beyond intraerythrocytic ring export erythrocytes translocon exported (PTEX) apparatus abrogated, as well glucose uptake It known truncated N- C-terminal RON3 fragments present rhoptries, but it unclear PTEX through PVM. To investigate distinguish roles fragment at distinct developmental stages, we used C-terminus tag conditional post-translational control. We demonstrated essential blood-stage survival, knockdown expression from early schizont stage induces defect subsequent development Protein full-length was partially inhibited abolished ring-stage compared N-terminal fragment. were abrogated specifically late stage. Plasmodial surface anion channel (PSAC) activity retained, facilitating small molecule traffic across membrane. after did not alter growth. These data suggest participates serves an role progression growth establishment nutrient-permeable PVM, accompanying transport plasma