Uncovering the essential genes of the human malaria parasite <i>Plasmodium falciparum</i> by saturation mutagenesis

Min Zhang(University of South Florida), Chengqi Wang(University of South Florida), Thomas D. Otto(Wellcome Sanger Institute), Jenna Oberstaller(University of South Florida), Xiangyun Liao(University of South Florida), Swamy R. Adapa(University of South Florida), Kenneth Udenze(University of South Florida), Iraad F. Bronner(Wellcome Sanger Institute), Deborah Casandra(University of South Florida), Matthew Mayho(Wellcome Sanger Institute), Jacqueline Brown(Wellcome Sanger Institute), Suzanne Li(University of South Florida), Justin Swanson(University of South Florida), Julian C. Rayner(Wellcome Sanger Institute), Rays H. Y. Jiang(University of South Florida), John H. Adams(University of South Florida)
Science
May 3, 2018
10.1126/science.aap7847
Cited by 996Open Access
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Abstract

Saturating malaria mutagenesis Malaria is caused by eukaryotic Plasmodium spp. parasites that classically infect red blood cells. These are difficult organisms to investigate genetically because of their AT-rich genomes. Zhang et al. have exploited this peculiarity by using piggyBac transposon insertion sites to achieve saturation-level mutagenesis for identifying and ranking essential genes and drug targets (see the Perspective by White and Rathod). Genes that are current candidates for drug targets were identified as essential, in contrast to many vaccine target genes. Notably, the proteasome degradation pathway was confirmed as a target for developing therapeutic interventions because of the several essential genes involved and the link to the mechanism of action of the current frontline drug, artemisinin. Science , this issue p. eaap7847 ; see also p. 490

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