We have previously shown by targeted gene disruption that the clag9 gene of
Plasmodium falciparum is essential for cytoadherence to CD36. Here we repo
rt inhibition of the function of clag9 by the use of an antisense RNA vecto
r as an alternative to targeted gene disruption. We transfected an antisens
e construct of clag9 into the P. falciparum clone 3D7 and when the resultin
g line was cultured in the presence of pyrimethamine it showed 15-fold lowe
r cytoadherence to C32 melanoma cells than the control. Reversion to wildty
pe upon removal of the introduced plasmid provides direct evidence that the
event responsible for the phenotypic change is not at an unrelated site an
d this approach provides a valuable new tool in malaria transfection techno
logy. (C) 2000 Elsevier Science B.V. All rights reserved.