Editors' ChoiceReproduction

Gamete Interactions

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Sci. Signal.  29 Apr 2008:
Vol. 1, Issue 17, pp. ec153
DOI: 10.1126/stke.117ec153

Two articles this week reveal that sexual reproduction of the invasive aquatic organism Ciona intestinalis, which is hermaphroditic, and the malaria-causing parasite Plasmodium appears to involve processes similar to those used by flowering plants. Self-incompatibility is a mechanism by which hermaphroditic plants and animals prevent self-fertilization. Although insights have been made for self-incompatibility systems of plants, relatively little is known about animal mechanisms. Harada et al. show that self-sterility in the chordate C. intestinalis is controlled by two genetic loci. The self/nonself-discriminating gamete interaction takes place on the basis of allele-specific molecular interactions between fibrogen-like ligands on the egg coat and polycystin 1-like receptors on the sperm. Genes for the receptors and ligands are linked and are polymorphic, similar to self-sterility genes in plants. In a second example of similarity to flowering plant reproduction, Hirai et al. found that sexual reproduction of Plasmodium berghei, which infects rodents, involves a male-specific role for GENERATIVE CELL SPECIFIC 1 (PbGCS1), which is also important for male fertility in angiosperms and is conserved in the Plasmodium species that infect humans. Experiments with PbGCS1-deficient P. berghei indicated that gametogenesis occurred correctly but that male fertility was compromised. PbGCS1 was essential for the mosquito phases of the life cycle, and interference with gamete interactions may provide a new target for the prevention of malaria.

Y. Harada, Y. Takagaki, M. Sunagawa, T. Saito, L. Yamada, H. Taniguchi, E. Shoguchi, H. Sawada, Mechanism of self-sterility in a hermaphroditic chordate. Science 320, 548-550 (2008). [Abstract] [Full Text]

M. Hirai, M. Arai, T. Mori, S.-y. Miyagishima, S. Kawai, K. Kita, T. Kuroiwa, O. Terenius, H. Matsuoka, Male fertility of malaria parasites is determined by GCS1, a plant-type reproduction factor. Curr. Biol. 18, 607-613 (2008). [PubMed]