Transmission of the malaria parasite requires ferlin for gamete egress from the red blood cell.

Transmission of the malaria parasite requires ferlin for gamete egress from the red blood cell.

Cell Microbiol. 2018 Dec 29;:e12999

Authors: Obrova K, Cyrklaff M, Frank R, Mair GR, Mueller AK

Abstract
Ferlins mediate calcium-dependent vesicular fusion. Although conserved throughout eukaryotic evolution, their function in unicellular organisms including apicomplexan parasites is largely unknown. Here, we define a crucial role for a ferlin-like protein (FLP) in host-to-vector transmission of the rodent malaria parasite Plasmodium berghei. Infection of the mosquito vectors requires the formation of free gametes and their fertilization in the mosquito midgut. Mature gametes will only emerge upon secretion of factors that stimulate the disruption of the red blood cell membrane and the parasitophorous vacuole membrane. Genetic depletion of FLP in sexual stages leads to a complete life cycle arrest in the mosquito. Although mature gametes form normally, mutants lacking FLP remain trapped in the red blood cell. The egress defect is rescued by detergent-mediated membrane lysis. In agreement with ferlin vesicular localization, HA-tagged FLP labels intracellular speckles, which relocalize to the cell periphery during gamete maturation. Our data define FLP as a novel critical factor for Plasmodium fertilization and transmission and suggest an evolutionarily conserved example of ferlin-mediated exocytosis.

PMID: 30597708 [PubMed - as supplied by publisher]

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