© Guttery, D.S. et al./Cell Host & Microbe
Nearly half the world’s population is at risk from malaria, a disease that kills more than 600,000 people globally each year. Research into an ‘on/off switch’ within the genes of the parasite that causes malaria has revealed enzymes that control how cells develop and differentiate. Identifying these enzymes could pinpoint targets for future treatments of the deadly disease.
Malaria is caused by infection from mosquito borne parasitic protozoans of the Plasmodium type. This single-celled microorganism progresses through several distinct life cycle stages, with each stage affected by a suite of enzymes that modify phosphate tags on other proteins to switch them ‘on’ or ‘off’.
During the development stages of Plasmodium, a lot of research has scrutinized the role of enzymes that chemically add the phosphate groups. However, there has been little research into the role of enzymes that remove the phosphate tags, known as protein phosphatases.
Using a range of molecular and biochemical techniques, Rita Tewari and colleagues at the University of Nottingham, in collaboration with researchers from KAUST, Oxford and London, studied the genes coding each phosphatase enzyme in Plasmodium berghei, the mouse-infective relative of the human malaria parasite Plasmodium falciparum.
The research team focused on how the phosphatases affect the parasite’s life cycle in infected mice.
“Our comprehensive analysis revealed the unique and essential roles of individual protein phosphatases in malaria parasite development,” says Stefan Arold, associate professor in the Biological and Environmental Science and Engineering Division at KAUST.
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