A genetic locus on Plasmodium falciparum chromosome 12 linked to a defect in mosquito-infectivity and male gametogenesis

Abstract

Infection of mosquitoes by Plasmodium spp. requires sexual differentiation of the malarial parasite in the vertebrate host and mating of the heterogametes in the vector midgut. A Plasmodium falciparum clone, Dd2, differentiates into normal-appearing gametocytes, yet poorly infects mosquitoes. The Dd2 clone, however, effectively cross-fertilized HB3, a Central American P. falciparum clone, and yielded several independent recombinant progeny. We have examined 11 HB3 × Dd2 progeny for their ability to infect mosquitoes and to differentiate into male gametes. Our analyses indicate that the poor mosquito-infectivity of the Dd2 clone results from a defect in male gametogenesis. This defect was inherited as a single locus in the independent recombinant progeny of HB3 × Dd2. Comparison with a restriction fragment length polymorphism map of the HB3 × Dd2 cross indicates that the defective phenotype of Dd2 maps to a locus on P. falciparum chromosome 12. This genetic locus may contain determinants that play a crucial role in male gametogenesis by P. falciparum. © 1995.