Table 1.
P. falciparum gene names (abbreviation), ID numbers and primers used for amplification of CDKs and cyclins.
The seryl-tRNA synthetase gene was used as a positive control.
Fig 1.
Percentage of life cycle stages of P. falciparum lines of W2, D6 and S55 at different time points (0, 12, 24, 36, 48 and 60 h).
S, T and R represents schizont, trophozoite and ring-stages, respectively.
Fig 2.
Transcription levels of CDK and cyclins (shown in different colours) in untreated and DHA treated P. falciparum W2, D6 and S55 parasites.
Panel A: untreated parasites. Transcription levels of each gene at 12, 24, 36, 48 and 60 h are grouped from left to right and are expressed as fold ratio relative to time 0. Panel B: DHA treated parasites. Transcription levels of each gene between day 1 and day 10 are grouped from left to right and are expressed as fold ratio relative to pre-treatment (time 0 h of untreated parasites on Day 0). Error bars represent standard error.
Fig 3.
Dynamics of parasite density following DHA treatment of P. falciparum lines of W2, D6 and S55.
Parasitemia are determined by SYBR Green staining and FACS analysis. Dotted lines indicate boundaries between dormancy and recovery phase in each parasite line.
Fig 4.
Effect of the CDK inhibitors (WR636638, olomoucineon and roscovitine) on untreated and DHA-treated W2 parasites.
Parasites were treated with DHA alone for 6 h, or one of the CDK inhibitors alone for 48 h (at Day 0), or DHA (for 6 h) plus one of the CDK inhibitors (for 48 h). For DHA plus CDK inhibitors, one of the CDK inhibitors was added either together with DHA (Day 0) or after DHA treatment (Days 2, 4 and 6) for 48 h. Two panels (Exp 1 and Exp 2) represent results of 2 independent experiments, each in triplicate. Parasitemia (percentages of parasitized erythrocytes by morphologically normal parasites) was determined by microscopy.