Responsables
Gerard Mazón and Eric Le Cam
E-mail
gerard.mazon[at]gustaveroussy.fr
Pavillon de recherche 2, Niveau RDC
The team’s biological questions focus on understanding, at a mechanistic level, the key pathways involved in repairing DNA double-strand breaks and replication-stalling lesions, particularly the Homologous Recombination and Non-Homologous End Joining repair pathways. We combine strong molecular biology and genetics approaches to investigate the regulation of these repair pathways in cells. In parallel, we bring unique expertise and employ original methodological strategies, notably the use of Electron Microscopy (EM) and Atomic Force Microscopy (AFM) to study DNA repair factors during reconstituted biochemical reactions, as well as to visualize DNA intermediates enriched from cells. Additionally, we have developed Cryo-EM techniques to determine, at very high resolution, the structures of nucleoprotein complexes central to DNA repair, providing deep insights into the molecular mechanisms that maintain genome stability.
We are open to candidates for a M2 stage and we are also willing to host candidates applying for post-doctorla fellowships, please contact the lab.
Position as Engineer (1-2 years) in characterization of Homolgous Recombination molecular mechanisms (apply through https://emploi.cnrs.fr/Offres.aspx). Application closes 01/10/2025.
Responsables
Patricia Kannouche
E-mail
patricia.kannouche[at] gustaveroussy.fr
Pavillon de recherche 2, Niveau 4
Translesion synthesis (TLS) is a crucial DNA damage tolerance mechanism that allows specialized low-fidelity polymerases to replicate past DNA lesions that stall replicative polymerases and block replication forks. While this process is error-prone and introduces many point mutations, it prevents more severe genomic instability such as double-strand breaks and chromosomal rearrangements, which are closely linked to cancer development. Beyond damage bypass, TLS polymerases also play a key role in somatic hypermutation during the immune response, where the protein AID induces targeted mutations in immunoglobulin genes. AID converts cytosine to uracil, which is processed to abasic sites and single-stranded gaps, both filled by TLS polymerases REV1 and eta (polη), generating mutations that diversify antibodies. Our research also focuses on the impact of FANC proteins (Fanconi Anemia-associated gene products) from DNA damage responses to gene expression and protein synthesis.
Patricia Kannouche (DRCE CNRS, team leader)
Filippo Rosselli (DR1 CNRS, group leader)
Said Aoufouchi (CRHC Inserm, group leader)
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Group Kannouche
Group Rosselli
Group Aoufouchi
Open to applicants for M2 stage or fellowship applications for post-docs.
Responsables
Alexander Ischenko and Murat Saparbaev
E-mail
alexandre.ischenko[at]gustaveroussy.fr
Pavillon de recherche 2, Niveau 3 et 4
The research activities of the team aim to decipher the mechanisms involved in the repair of complex DNA lesions in order to better understand cancer development, particularly kidney cancer, and the mechanisms of chemoresistance in tumor cells, by leveraging the complementarity and expertise of the team members. The knowledge gained from mechanistic studies of alternative DNA repair pathways and post-replicative DNA modifications could lead to the development of new diagnostic and therapeutic targets, with the goal of designing DNA repair inhibitors to combat acquired resistance in cancers—particularly in renal carcinoma, which will be used as a model.
Alexander Ishenko (DR2 CNRS) – Team leader
Murat Saparbaev (DR1 CNRS)
Sophie Gad-Lapiteau (DE EPHE) – Group Leader
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Group Ishchenko
Group Rein
Open for candidates to PhD and post-doctoral fellowships.
Responsables
Béatrice Rondinelli
E-mail
beatrice.rondinelli[at]gustaveroussy.fr
Pavillon de recherche 2, Niveau 4
Our research team investigates how chromatin regulates the response to replication fork (RF) damage and how its disruption contributes to cancer. Many cancers, such as pediatric high-grade gliomas (pHGG), exhibit abnormal DNA repair, resistance to therapies, and mutations in chromatin-related genes, yet the underlying mechanisms remain poorly understood. Building on advanced tools to study RF damage and repair in mammalian cells, we focus on cancer-associated mutations in histone genes and novel chromatin factors involved in this process. Our goal is to uncover how these alterations affect genome integrity and promote tumor cell survival, ultimately advancing our understanding of chromatin’s role in cancer biology.
The team is looking actively for candidates for PhD and post-doctoral felloships.
Responsables
Nataliya Petryk
E-mail
nataliya.petryk[at]gustaveroussy.fr
Pavillon de recherche 2, Niveau 4
Our team studies how eukaryotic cells accurately replicate their chromosomes and preserve genome integrity during each cell division. Chromosome replication is a complex process that goes beyond copying DNA—it also involves assembling chromatin, maintaining epigenetic marks, and restoring full genomic function after replication. These steps are essential for preserving cellular identity and tissue health. Our research focuses on how replication forks manage these interconnected tasks across diverse chromatin environments and physiological conditions. Current projects investigate the role of the nuclear lamina in replication and genome stability, the link between DNA replication and DNA methylation maintenance, and how oxidative DNA damage affects chromatin and differentiation in BRAF-mutated thyroid cancers, with the goal of identifying new therapeutic strategies.
Open for applications.
Responsables
Olivier Gavet
E-mail
olivier.gavet[at]gustaveroussy.fr
Pavillon de recherche 2, Niveau 4
Our team studies how cells respond to persistent DNA damage during proliferation, focusing on checkpoint adaptation—a process where cells override DNA damage checkpoints to enter mitosis despite unresolved damage. This phenomenon contributes to genetic instability and resistance to treatments but remains poorly understood. Using advanced live-cell imaging and biosensors, we analyze checkpoint signaling dynamics in single cells to uncover mechanisms behind checkpoint adaptation and its role in genetic heterogeneity and disease.
Morwenna Le Guillou (IE, Univ. Paris-Saclay)
Open to candidates for fellowship applications.
Responsables
Gabriel De Matos Rodrigues
E-mail
gabrieleduardo.de-matos-rodrigues[at]gustaveroussy.fr
Pavillon de recherche 2, Niveau 4
The team studies the mechanisms controlling the (in)stability of repetitive genomic regions and the link between repeat instability, the formation of alternative DNA structures, and targeted cancer therapies. Additionally, the team seeks to understand how DSB repair is connected to DNA repeat instability and its relationship to tumorigenesis and aging.
Open to candidates for fellowship applications.