Abstract: Artemisinins are a key component of the combination therapy used to treat malaria. Plasmodium falciparum, the causative agent of the most deadly from of malaria is evolving resistance to artemisinins. The decreased effectiveness of artemisinins increases the probability of resistance to the partner drugs as well; risking total treatment failure which would result in thousands more deaths a year. The gene shown to have the largest affect in modulating resistance is K13. Here we present an RNA-seq study on an isogenic mutant with a dysregulated K13 gene that provides evidence that K13 is involved in regulating DNA replication and repair.Summary: Plasmodium falciparum is evolving resistance to Artemisinin Combination Therapy. The gene with the strongest association with resistance is K13. K13 is an ortholog of the well characterized transcriptional regulator Keap1. In this work we transcriptionally characterized a mutant with a transposon inserted in the K13 promoter region which results in dysregulation of K13 at 2 points of the intraerythrocytic cycle of the life-cycle to identify the processes regulated by K13.
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