Epigenetic control of gene expression switching in malaria parasites
The malaria-causing parasite Plasmodium falciparum has developed clonally variant gene expression to control essential biological processes during its persistent blood-stage infection of the human host. Heritable epigenetic silencing ensures the limited expression of only a subset of the genes at any time. Switching the expression of individual clonally variant genes enables the parasite to rapidly adapt to changes in its environment, evade the immune system and switch to the development of mosquito-transmissible gametocyte stages. The EU-funded MALSWITCH project aims to combine the proprietary method of conditional expression switching of endogenous genes in the parasite with CRISPR/Cas-derived methodology and proximity-based labelling approaches to identify and characterise the molecular mechanisms controlling epigenetic gene expression switching.
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