Inhibition of Plasmodium falciparum spermidine synthase indicates unique perturbation-specific effects in the transcriptome and proteome

Abstract

Antiplasmodial drug discovery efforts are hampered by the lack of an extensive set of novel, validated drug targets. A requirement of these targets (or the pathways in which they function) is that they prove essential for parasite survival. The polyamine biosynthetic pathway, responsible for the metabolism of highly abundant amines crucial for parasite growth, proliferation and differentiation, is currently under investigation as an antimalarial target. In order to further evaluate polyamine depletion as possible antimalarial intervention, the consequences of inhibiting Plasmodium falciparum spermidine synthase was examined on a transcriptomic and proteomic level.