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Dissecting host-transposon interactions during germline development and their impact on genome integrity

Project description

How germ cells protect the genome from transposable elements

Transposable elements (TEs) are a natural part of mammalian genomes, but when activated, they can disrupt the stability of the genome. During foetal development, DNA methylation, which usually keeps TEs silent, is lost. This leads to the potential reactivation of TEs, which could cause genetic damage. It is still unclear how foetalmale germ cells, known as prospermatogonia, handle this challenge. Supported by the Marie Skłodowska-Curie Actions programme, the TE-Time will answer this question. Specifically, it will study gene activity patterns and the 3D organisation of the genome, researchers hope to uncover new insights into TE regulation, with potential applications for infertility, cancer, and other diseases.

Objective

Mammalian genomes are filled with transposable elements (TEs), whose activity is usually silenced by DNA methylation. However, during the fetal phase of germline development, DNA methylation is naturally lost as part of the epigenetic reprogramming of the future gametes. This leads to the transcriptional activation of transposition-competent TEs, which normally represents a threat to genomic integrity and species fitness. How fetal male germ cells (a.k.a. prospermatogonia) mechanistically cope with TE reactivation and protect the integrity of the genetic material?

Preliminary data from the lab indicates that TEs acquire both permissive H3K4me3 and repressive H3K9me3 marks in mouse prospermatogonia, and may be subject to early transcription termination. I will investigate whether these regulatory patterns may allow prospermatogonia to tolerate active TEs and even integrate them into their own developmental program. Focusing on this unique cellular model provided by prospermatogonia, I will 1) assess the dynamics of H3K4me3-K9me3 marks using single cell multimodal chromatin profiling in relation to prospermatogonia development, 2) analyze TE transcriptional features, 3) study the 3D coordination of TE regulation within the nucleus and 4) investigate whether TEs participate to the prospermatogonia gene expression program by providing regulatory sequences. I believe this project will identify novel principles in TE regulation with immediate relevance for the field of reproductive biology. Knowledge will be gained regarding the origin of infertilities, but also for other pathological contexts such as cancer and neurodegenerative diseases, whereby DNA methylation loss and TE reactivation are commonly observed.

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HORIZON-TMA-MSCA-PF-EF - HORIZON TMA MSCA Postdoctoral Fellowships - European Fellowships

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(opens in new window) HORIZON-MSCA-2023-PF-01

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INSTITUT CURIE
Net EU contribution

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€ 195 914,88
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RUE D ULM 26
75231 Paris
France

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Ile-de-France Ile-de-France Paris
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