期刊
CELLULAR MICROBIOLOGY
卷 15, 期 6, 页码 910-921出版社
WILEY
DOI: 10.1111/cmi.12086
关键词
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资金
- Department of Biotechnology (DBT) Govt. of India
- DBT
- European Commission
- Innovative Young Biotechnologist Award
- TATA Innovation Fellowship from DBT
- IYBA grant
- IYBA JRF
Egress of Plasmodium falciparum merozoites from host erythrocytes is a critical step in multiplication of blood-stage parasites. A cascade of proteolytic events plays a major role in degradation of membranes leading to egress of merozoites. However, the signals that regulate the temporal activation and/or secretion of proteases upon maturation of merozoites in intra-erythrocytic schizonts remain unclear. Here, we have tested the role of intracellular Ca2+ in regulation of egress of P.falciparum merozoites from schizonts. A sharp rise in intracellular Ca2+ just before egress, observed by time-lapse video microscopy, suggested a role for intracellular Ca2+ in this process. Chelation of intracellular Ca2+ with chelators such as BAPTA-AM or inhibition of Ca2+ release from intracellular stores with a phospholipase C (PLC) inhibitor blocks merozoite egress. Interestingly, chelation of intracellular Ca2+ in schizonts was also found to block the discharge of a key protease PfSUB1 (subtilisin-like protease 1) from exonemes of P.falciparum merozoites to parasitophorous vacuole (PV). This leads to inhibition of processing of PfSERA5 (serine repeat antigen 5) and a block in parasitophorous vacuolar membrane (PVM) rupture and merozoite egress. A complete understanding of the steps regulating egress of P.falciparum merozoites may provide novel targets for development of drugs that block egress and limit parasite growth.
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