Epigenetic marks reduce erythrocyte uptake of antimalarials

Acquired antimalarial drug resistance produces treatment failures and has led to periods of global disease resurgence. In P. falciparum, resistance is known to arise through genome-level changes such as mutations and gene duplications. We now report an epigenetic resistance mechanism involving genes responsible for the plasmodial surface anion channel, a nutrient channel that also transports ions and antimalarial compounds at the host erythrocyte membrane. Two blasticidin S-resistant lines exhibited markedly reduced expression of clag Mutant FCB-br1 and wild-type FCB samples were hybridized to seven arrays (biological repeats) using forward (n=2) and reverse (n=5) fluoro.