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Uncovering the Mechanisms Behind Adaptive Gene Expression Switching in Malaria Parasites

Project description

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.

Objective

The malaria-causing parasite Plasmodium falciparum has evolved a strategy of clonally variant gene expression to control essential biological processes like antigenic variation and sexual commitment during its persistent blood-stage infection of the human host. Heritable epigenetic silencing of the underlying specialized gene families ensures the limited expression of only a subset of these 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 its cell cycle to the development of mosquito-transmissible gametocyte stages. Expression switching of these clonally variant genes therefore represents a key strategy for parasite survival and underlies the evolutionary success of this deadly pathogen. Despite decades of research, the molecular mechanisms coordinating this adaptive gene expression switching are not understood. In my recent research, I developed a unique experimental tool, which for the first time allows the conditional expression switching of endogenous genes in the parasite. I will combine this system with novel CRISPR/Cas derived methodology and proximity-based labelling approaches to deliver the first systematic identification and characterization of the molecular mechanisms controlling epigenetic gene expression switching. The experiments outlined in the proposal will reveal the core of the molecular machinery underlying this fundamental process and elucidate regulatory mechanisms that allow the parasite to translate environmental signals into adaptive switching of clonally variant genes. This will transform our understanding of the molecular mechanisms driving adaptation of this deadly parasite and in the long run might contribute to the design of intervention strategies that P. falciparum is unable to adapt to.

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Topic(s)

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ERC-STG - Starting Grant

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Call for proposal

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(opens in new window) ERC-2020-STG

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Host institution

EBERHARD KARLS UNIVERSITAET TUEBINGEN
Net EU contribution

Net EU financial contribution. The sum of money that the participant receives, deducted by the EU contribution to its linked third party. It considers the distribution of the EU financial contribution between direct beneficiaries of the project and other types of participants, like third-party participants.

€ 1 434 330,00
Address
GESCHWISTER-SCHOLL-PLATZ
72074 Tuebingen
Germany

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Region
Baden-Württemberg Tübingen Tübingen, Landkreis
Activity type
Higher or Secondary Education Establishments
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Total cost

The total costs incurred by this organisation to participate in the project, including direct and indirect costs. This amount is a subset of the overall project budget.

€ 1 434 330,00

Beneficiaries (2)

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