A genetic locus on Plasmodium falciparum chromosome 12 linked to a defect in mosquito-infectivity and male gametogenesis.
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 x 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 x Dd2. Comparison with a restriction fragment length polymorphism map of the HB3 x 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.
Vaidya
A B
AB
Laboratory of Malaria Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA.
Muratova
O
O
Guinet
F
F
Keister
D
D
Wellems
T E
TE
Kaslow
D C
DC
D000818:Animals; D000852:Anopheles / Q000469:parasitology; D005260:Female; D017125:Genes, Protozoan; D008040:Genetic Linkage; D008297:Male; D009154:Mutation; D010963:Plasmodium falciparum / Q000235:genetics* / Q000254:growth & development*; D012150:Polymorphism, Restriction Fragment Length; D013091:Spermatogenesis