Resistance to malaria in ankyrin and spectrin deficient mice.
Inbred mice carrying mutations in ankyrin and/or spectrin synthesis and assembly were studied for their ability to support the growth of the rodent malarias, Plasmodium chabaudi adami and P. berghei, in vivo. Mice carrying the nb/nb (normoblastosis) mutation which do not synthesize ankyrin and therefore also have a deficiency in membrane-bound spectrin, were refractory to P. chabaudi adami, which invades mature erythrocytes and to P. berghei, which invades reticulocytes. Similarly, sph/sph mice which do not synthesize the alpha chain of spectrin but do synthesize ankyrin, were also resistant to both parasites. The heterozygote for the nb defect (nb/+) exhibited a diminution of parasitaemia. We conclude that the host cell spectrin may be necessary for the invasion and/or growth of rodent malarial parasites.
Shear
H L
HL
Department of Medical and Molecular Parasitology, New York University School of Medicine, N.Y.
Roth
E F
EF
Ng
C
C
Nagel
R L
RL
D000740:Anemia / Q000150:complications; D000818:Animals; D017487:Ankyrins; D001798:Blood Proteins / Q000172:deficiency*; D004912:Erythrocytes / Q000648:ultrastructure; D005260:Female; D008288:Malaria / Q000097:blood* / Q000150:complications; D008297:Male; D008565:Membrane Proteins / Q000172:deficiency*; D051379:Mice; D008810:Mice, Inbred C57BL; D008815:Mice, Inbred Strains; D008855:Microscopy, Electron, Scanning; D010961:Plasmodium / Q000254:growth & development*; D010962:Plasmodium berghei / Q000254:growth & development; D013049:Spectrin / Q000172:deficiency*
D017487:Ankyrins; D001798:Blood Proteins; D008565:Membrane Proteins; D013049:Spectrin