A combination of chloroplast transformation with nuclear transformation and large-scale metabolic screening of supertransformed plant lines has enabled an entire biochemical pathway to be transferred from a medicinal plant to a high-biomass crop.

The de novo selection of a mutation responsible for Plasmodium falciparum in vitro artemisinin resistance is confirmed in Guyana, making artemisinin combination therapies vulnerable to complete resistance in this region.

Plasmodium falciparum kelch13 mutations that cause artemisinin resistant malaria in Southeast Asia show markedly different patterns of evolutionary selection in Africa.

Plasmodium falciparum K13 mutations confer resistance to the antimalarial artemisinin in Asian and African parasites, with most gene-edited mutant K13 African parasite lines showing a fitness cost that may predict slow dissemination of artemisinin resistance in high-transmission settings.

Treatment of malaria parasites with the frontline antimalarial drug artemisinin can increase the proportion of parasites that convert into transmission forms.

Models of malaria and treatment dynamics were combined with emulator-based global sensitivity analysis to elucidate the interplay between drug, biology, and epidemiological factors on the evolution of resistance to malaria treatments, including artemisinin.

Insights into the basic metabolic architecture and adaptations of malaria parasites for growth within human erythrocytes exemplify how incisive knowledge of biochemical pathways and mechanisms may be leveraged to develop new therapies.

M1 alanyl aminopeptidase is chemically validated as an attractive antimalarial target by confirming the on-target activity of a novel selective inhibitor using chemoproteomics and metabolomics-based drug target deconvolution approaches.

Phosphatidylinositol 3-phosphate interacts with PfHsp70-1 and stabilizes the Plasmodium digestive vacuole under febrile temperatures.