Unité
Dynamique du noyau (UMR3664)
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Unité
ANGELA TADDEI / NATHALIE DOSTATNI
Dynamique du noyau (UMR3664)
Les équipes de cette unité s’intéressent aux relations entre information génétique et épigénétique au cours du développement, lors de la mise en place des destins cellulaires propres à chaque lignée de l’organisme. Il s’agit aussi de comprendre comment ces informations sont altérées en contexte pathologique comme le cancer.
Les équipes
Chiffres-clés
18
nationalités pour 55 personnes
6
systèmes modèles
37200
milliards de noyaux dans le corps humain
Publications clés
Toutes les publications
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CENP-A overexpression promotes distinct fates in human cells, depending on p53 statusCommunications Biology
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3 minutes to precisely measure morphogen concentrationPLOS Genetics
Actualités
Toutes les actualités
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Manipuler les chromosomes dans une cellule vivante révèle qu’ils sont fluidesDes scientifiques du CNRS, de l’Institut Curie, et de Sorbonne Université ont pu, pour la première fois, physiquement manipuler des chromosomes de cellules vivantes. En soumettant les chromosomes à différentes forces, à l’aide d’aimants, ils ont découvert que les chromosomes sont en réalité très fluides, presque liquides en dehors des phases de division de la cellule. Cette étude est publiée dans Science, le 29 juillet 2022.29/07/2022
Événements scientifiques
Tous les événements scientifiques
13 déc
2022
Séminaire Nuclear dynamic series
09h-10h
Centre de recherche - Paris - Amphithéâtre Marie Curie
Clash of the titans: RNA viruses and interferons
The interferon (IFN) response is a critical arm of the innate immune response and a major host defense mechanism against viral infections. Numerous genes that contribute to this antiviral state remain to be identified and characterized. Using large-scale loss-of-function strategies, we screened siRNAs or gRNAs libraries targeting hundreds of IFN-stimulated genes (ISGs) in IFN-treated cells infecte
6 déc
2022
Séminaire Nuclear dynamic series
16h-17h
Centre de recherche - Paris - Amphithéâtre Hélène Martel-Massignac (BDD)
Machine Learning for Reverse Engineering in Biology, Embryology and Aging
In this seminar I will briefly review some success stories of Machine Learning in biology and speculate on what it will take to enable a much more substantial progress. I will specifically discuss connections between embryology and biology of aging - the field which remains perhaps the most promising and most fraudulent over thousands of years in history of the medical science. I will present my p
24 nov
2022
Séminaire Nuclear dynamic series
14h-15h
Centre de recherche - Paris - Amphithéâtre Marie Curie
Enhancer-promoter "interaction", dynamics and transcriptional control: lessons from Sox2
Enhancers mediate transcriptional activation from a distance, and 3C-based studies have given a textbook view that this is somehow mediated by chromatin looping events directly juxtaposing enhancers with their target gene promoters. Recent studies have placed this simple model into question, especially when looking at chromatin organization in individual cells. Using Sox2 as a model gene locus, we
15 nov
2022
Séminaire Nuclear dynamic series
09h-10h
Centre de recherche - Paris - Amphithéâtre Marie Curie
KU Paradox at Telomeres: Working Less - Working Better to Ensure End Protection
DNA-bound telomere factors (i.e. TRF2, Taz1, Rap1) strongly inhibit NHEJ to ensure that chromosome ends do not fuse. On the other hand, the NHEJ factor KU paradoxically binds telomere ends and protects them against resection activities without engaging NHEJ. How KU functions can be so tightly separated at telomeres is unclear. It is also unclear whether telomere factors and KU could co-exist or co
20 Sep
2022
Séminaire Nuclear dynamic series
09h-10h
Centre de recherche - Paris - Amphithéâtre Marie Curie
Clustering of CTCF binding is required for efficient loop extrusion blocking at TAD boundaries in normal and cancer cells
Vertebrate genomes are organized into Topologically Associating Domains (TADs) that constitute insulated domains where enhancer-promoter contacts are privileged. TADs are formed by Cohesin-mediated loop extrusion, followed by CTCF-mediated blocking of loop extrusion to create boundaries between TADs. Disruption of TAD boundaries can cause ectopic gene activation, which can lead to developmental de