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Summary  Drug resistance in   P   lasmodium falciparum  remains a challenge for the malaria eradication programmes around the world. With the emergence of artemisinin resistance, the efficacy of the partner drugs in the artemisinin combination therapies ( ACT ) that include quinoline‐based drugs is becoming critical. So far only few resistance markers have been identified from which only two transmembrane transporters namely  PfMDR 1 (an  ATP ‐binding cassette transporter) and  PfCRT  (a drug‐metabolite transporter) have been experimentally verified. Another   P   . falciparum  transporter, the  ATP ‐binding cassette containing multidrug resistance‐associated protein ( PfMRP2 ) represents an additional possible factor of drug resistance in   P   . falciparum . In this study, we identified a parasite clone that is derived from the  3D7  P   . falciparum  strain and shows increased resistance to chloroquine, mefloquine and quinine through the trophozoite and schizont stages. We demonstrate that the resistance phenotype is caused by a 4.1 kb deletion in the 5′ upstream region of the   pfmrp2   gene that leads to an alteration in the   pfmrp2   transcription and thus increased level of  PfMRP2  protein. These results also suggest the importance of putative promoter elements in regulation of gene expression during the   P   . falciparum  intra‐erythrocytic developmental cycle and the potential of genetic polymorphisms within these regions to underlie drug resistance.

Structural polymorphism in the promoter of pfmrp2 confers P lasmodium falciparum tolerance to quinoline drugs