Fertilization Mechanisms of the Rodent Malarial Parasite Plasmodium berghei

Abstract

Malaria, caused by Plasmodium spp., is transmitted by anopheline mosquitoes. When male and female gametes are introduced into the mosquito midgut, they reproduce sexually and proliferate, at which time the mosquito becomes infectious to vertebrates. It has been proposed that fertilization is a critical target in the parasite life cycle for the reduction of malarial prevalence. Although understanding parasite fertilization is crucial for the control of malaria, the precise molecular mechanisms involved have long remained unknown. Generative cell-specifi c 1 (GCS1) has been reported to be a critical fertilization factor in angiosperms. It was subsequently shown that the function of GCS1 is conserved in both the rodent malaria parasite Plasmodium berghei and the green alga Chlamydomonas reinhardtii . Moreover, a GCS1 -like gene has been detected in the genomes of various organisms, suggesting that it plays a conserved role in gamete interaction. As GCS1 is thought to act as a membrane-anchoring protein in male gametes, a female counterpart is assumed to exist. To reveal the mechanisms involved in parasite fertilization, it is important to clarify the function of GCS1 and to identify GCS1 partners and other fertilization factors. In this review, I fi rst describe the life cycle of malaria parasites, focusing on gametogenesis and fertilization and the underlying mechanisms. I then discuss the functions of GCS1 at the time of gamete interaction. Finally, I consider whether parasite fertilization factors, including GCS1, might be utilized in the development of antimalarial vaccines.

The C-terminal region of the Plasmodium berghei gamete surface 184-kDa protein Pb184 contributes to fertilization and male gamete binding to the residual body

“…[8,14]. These results suggest the presence of male and female gamete conjugationinvolved membrane proteins [15]. Recently, female gamete-binding peptide (FG1), selected by phage display screening of P. berghei male gametes, conformed to heat shock protein 90 (HSP90) on the surface of female gametes and competitively inhibited fertilization [16].…”

The C-terminal region of the Plasmodium berghei gamete surface 184-kDa protein Pb184 contributes to fertilization and male gamete binding to the residual body

“…falciparum parasites have been reported to exhibit functions similar to those of P. berghei . [ 8 , 14 ], suggesting the presence of male and female gamete conjugation-involved membrane proteins [ 15 ]. Recently, female gamete-binding peptide (FG1), selected by phage display screening of P. berghei male gametes, was found to conform to heat shock protein 90 (HSP90) on the surface of female gametes and to competitively inhibit fertilization [ 16 ].…”