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Dissecting host-transposon interactions during germline development and their im...

Dissecting host-transposon interactions during germline development and their impact on genome integrity 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 epigen... see more

31/08/2027

INSTITUT CURIE FON...

196K€

Project Budget: 196K€

Project leader

INSTITUT CURIE No se ha especificado una descripción o un objeto social para esta compañía.

TRL 4-5

PARTICIPATION DEPralty Sin fecha límite de participación.

Financing granted El organismo HORIZON EUROPE notifico la concesión del proyecto The day 2024-04-15

HORIZON-MSCA-2023-PF-01-01: MSCA Postdoctoral Fellowships 2023 Expected Outcome:Project results are expected to contribute to the following outcomes:

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Este proyecto no cuenta con búsquedas de partenariado abiertas en este momento.

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1 Participantes

INSTITUT CURIE FONDATION

195.91K€ | Leader

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Project duration: 40 months Date Start: 2024-04-15
End date: 2027-08-31

Project leader

INSTITUT CURIE No se ha especificado una descripción o un objeto social para esta compañía.

TRL 4-5

Project Budget 196K€

participation deadline Sin fecha límite de participación.

Project description 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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