Join the Cell-ID (Cell Identities and Destinies) Research Program – MD-PhD/PhD Positions Starting 2026

Are you an outstanding, creative, and motivated young researcher? Join Cell-ID, a multidisciplinary program uniting 29 French laboratories in a collaborative effort to understand how cells shape normal development, how these processes are disrupted in pediatric brain cancers, and how this knowledge can pave the way toward a cell-based interceptive medicine.

Timeline

Computational Systems Biology of Polycomb regulation in pediatric brain cancers

Giacomo Cavalli and Daniel Jost

The Polycomb machinery is essential in regulating gene silencing during embryogenesis and development, through the coordinated action of transcription factors, histone modifying enzymes and architectural proteins. The initiation of several pediatric brain cancers has been associated with perturbations in such a machinery, which have important system-scale consequences on gene regulation. While the molecules whose functions may be impaired have been identified, how such an impairment affects mechanistically gene expression locally and at the systems scale remains elusive.

Identifying the determinants of SMARCB1-mediated cell transformation

Franck Bourdeault and Raphaël Margueron

The leading genetic cause for Atypical Teratoid/Rhabdoid Tumors is the mutation of Smarcb1. Yet, inactivation of this gene in many cell lines impairs cell proliferation and is strongly counter selected (Depmap essential in 971/1186 cell lines). Moreover, we have shown that a specific developmental context is required for SMARCB1 to promote cell proliferation.  This raises the question of what control the cellular outcome of SMARCB1 inactivation.

Investigate the metabolomic dependencies in medulloblastoma

Alexandre Baffet and Olivier Ayrault

Deregulations in biological networks are key events in pathogenesis of cancer, whose knowledge should open the road to novel therapeutic strategies. In medulloblastoma (MB), the most common malignant pediatric brain tumor arising from the cerebellum, these network deregulations are not fully understood, and therapeutic success is still limited. MB is a heterogeneous disease; current genetically-defined subgroups include Wingless (WNT)-activated, Sonic Hedgehog (SHH)-activated and non-WNT/non-SHH. This last category corresponds to the established molecular subgroups “group 3” and “group 4” and accounts for the majority of MB cases. Studies have also provided genomic, epigenetic and transcriptomic landscape of human MB samples, nevertheless they have not yet attained the global comprehension of MB complex dynamic networks.

Long-Read Single-Cell and Spatial Transcriptomics of the Developing Human Hindbrain

Pascal Barbry and Alain Chédotal

This proposal aims to characterize human hindbrain (Cerebellum and brainstem) development using an integrated pipeline combining long-read nanopore sequencing (ScNaUmi-seq and SiT) with spatial transcriptomics, to better understand the cellular origins of medulloblastoma. We will shift from gene-centric to transcript-centric paradigms by capturing full-length sequence heterogeneity and splicing diversity lost in standard workflows. Our experimental approach combines single-nuclei/single-cell RNA sequencing with dual spatial methods: SiT for global isoform mapping and Xenium for precise cell-cell interaction analysis on adjacent tissue sections. Targeted in situ sequencing will generate spatial maps enabling probabilistic cell mapping and 3D reconstruction from optically cleared specimens or tissue section processed with multiplex immunostaining. We will develop AI-driven computational frameworks for multi-omics integration and annotation, incorporating Human Cell Atlas resources.

4D investigation of cellular interaction in a Drosophila model of ATRT brain tumours

Pauline Spéder and Christophe Zimmer

Atypical Teratoid Rhabdoid Tumours (ATRT) are highly aggressive pediatric brain tumours primarily driven by the loss of the chromatin remodeling factor SMARCB1. However, the role of the surrounding microenvironment in tumour progression remains poorly understood. To address this, we take advantage of a Drosophila model in which inactivation of snr1 —the fly homolog of SMARCB1— during development induces ATRT-like tumours. This model offers distinct advantages, including well-defined cells of origin, characterized developmental programs, and advanced genetic engineering.

Our research will focus on deciphering the interactions between tumour cells and the host tissue, including neurons, glial cells, and the blood-brain barrier. We will examine host cell responses at multiple levels —structural organisation, cellular processes, gene expression, epigenetic modifications and metabolic changes— to uncover how these factors influence tumour progression.

Imaging transcriptome evolution in live cells

Edouard Bertrand and Florian Muller

Single cell sequencing has revealed that cells differentiate along well-defined trajectories in the transcriptomic space. However, how the transcriptome evolves in real-time is poorly understood. The goal of the PhD will be to develop imaging-based methods to better apprehend the dynamic regulation of the transcriptome. To this end, transcription will be imaged using a combination of live and fixed cell methods during the differentiation of stem cells. Transcription will be visualized at both the global and gene-specific levels and the data will then be used to reconstruct the trajectories of single cells in real time.