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Decoding epistatic genome/RNome interactions in eukaryotic fitness gain using Leishmania parasites as a unique model system

Project description

Genomic instability in eukaryotic cells: a fitness driver?

Leishmania are protozoan parasites that are transmitted to humans and animals through the bite of infected sandflies, causing a range of diseases. Unlike most eukaryotic cells, Leishmania can increase the expression of specific genes by gene dosage changes through the amplification of entire chromosomes, chromosome regions or individual genes. Funded by the European Research Council, the DECOLeishRN project aims to investigate how Leishmania employ such genome instability to regulate their fitness. Researchers will focus on the molecular mechanisms that can filter toxic from beneficial gene dosage changes, including RNA modifications guided by non-coding RNAs. Given that genomic instability drives cancer development, project findings extend beyond Leishmania.

Objective

Darwinian evolution plays a central yet poorly understood role in human disease. Iterations between genetic mutation and environmental selection drive cancer development, microbial infection and therapeutic failure, thus increasing human mortality. The molecular mechanisms that harness the deleterious effects of genome instability to generate beneficial phenotypes in these pathogenic systems are unknown. Here we investigate this important unsolved question in the protozoan parasite Leishmania that causes devastating human infections. In the absence of transcriptional regulation, these early-branching eukaryotes exploit genome instability to regulate expression by gene dosage. Leishmania thus represents an ideal system to investigate how genome instability drives fitness gain in fast evolving, eukaryotic cells, such as observed during cancer development. Synergizing our expertise in genomics, evolution, systems and RNA biology, we have recently made several breakthrough discoveries that link parasite fitness gain to epistatic interactions between co-amplifying genes of small, non-coding RNAs, which program epitranscriptomic and translational regulation. We hypothesize that these genome/RNome interactions generate the phenotypic landscape underlying Leishmania fitness gain. Our proposal investigates this ground-breaking concept through two Specific Aims that (i) combine experimental parasite differentiation and evolution in vitro and in vivo to reveal molecular mechanisms underlying Leishmania predictive adaptation and fitness gain, and (ii) investigate how RNA modification and non-coding RNAs contribute to adaptation by regulating mRNA stability and translational control. Our findings will be highly relevant to other fast growing, eukaryotic systems that rely on genome instability, such as cancer or fungal pathogens.

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Topic(s)

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Funding Scheme

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HORIZON-ERC-SYG - HORIZON ERC Synergy Grants

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Call for proposal

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(opens in new window) ERC-2022-SYG

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Host institution

INSTITUT PASTEUR
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.

€ 3 134 594,00
Address
RUE DU DOCTEUR ROUX 25-28
75724 Paris
France

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Region
Ile-de-France Ile-de-France Hauts-de-Seine
Activity type
Research Organisations
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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.

€ 3 134 594,00

Beneficiaries (3)

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