Epigenetic variation in malaria parasites II
Investigating new aspects of the mechanisms and biological functions of epigenetic variation in malaria parasites

- Duration
- 01/01/2017-31/12/2019
- Coordinator
- Alfred Cortés
- Funded by
- RETOS (MINECO, Spanish Government)
Many genes of the parasite responsible for the most severe forms of malaria, Plasmodium falciparum, are switched on in some individual parasites and switched off in others. The expression of these genes, termed clonally variant genes, is regulated at the epigenetic level. Importantly, clonally variant genes participate in key host-parasite interactions including antigenic variation, sexual conversion, nutrient acquisition or erythrocyte invasion.
In this project we explore the role of epigenetic variation and clonally variant gene expression in relevant P. falciparum biological pathways. We mainly focus on the clag gene family, involved in nutrient acquisition and resistance to toxic compounds, and pfap2-g, which is the master regulator of sexual conversion, a process necessary for malaria transmission. We also investigate how parasites adapt to heat-shock mimicking malaria cyclical fevers. We study both the chromatin-based mechanisms of epigenetic regulation and the function of these clonally variant genes. More generally, using these genes as models we gain insight into how parasites use epigenetic variation as an adaptive strategy to survive under different conditions of their human host.
Our Team
PI
-
Alfred Cortés Closas
ISGlobal Team
-
Sofia Mira Predoctoral fellow
-
Núria Rovira Scientific Support Assistant - Laboratory
-
Elisabet Tinto Font
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