A5048423328- DNA Repair Mechanisms
- Genomics and Chromatin Dynamics
- Epigenetics and DNA Methylation
- CRISPR and Genetic Engineering
- PARP inhibition in cancer therapy
- RNA Research and Splicing
- RNA modifications and cancer
- Cancer Genomics and Diagnostics
- Cellular Mechanics and Interactions
- RNA Interference and Gene Delivery
- Cancer-related gene regulation
- Microtubule and mitosis dynamics
- Genetics, Bioinformatics, and Biomedical Research
- Glioma Diagnosis and Treatment
- Cancer-related Molecular Pathways
- Molecular Biology Techniques and Applications
- Cancer therapeutics and mechanisms
- Chromosomal and Genetic Variations
- Skin and Cellular Biology Research
- Plant Molecular Biology Research
- Cell Adhesion Molecules Research
- DNA and Nucleic Acid Chemistry
- Genetics and Neurodevelopmental Disorders
- Cancer Research and Treatments
- Plant Genetic and Mutation Studies
Epigénétique et Destin Cellulaire
2016-2025
Université Paris Cité
2016-2025
Centre National de la Recherche Scientifique
2016-2025
Sorbonne Paris Cité
2015-2018
Délégation Paris 7
2013-2014
Institut Curie
2004-2013
University of Cambridge
2009-2012
Dynamique du noyau
2004-2012
The Gurdon Institute
2007-2011
Wellcome Trust
2007-2010
Posttranslational modifications play key roles in regulating chromatin plasticity. Although various chromatin-remodeling enzymes have been described that respond to specific histone modifications, little is known about the role of poly[adenosine 5'-diphosphate (ADP)-ribose] remodeling. Here, we identify a enzyme, ALC1 (Amplified Liver Cancer 1, also as CHD1L), interacts with poly(ADP-ribose) and catalyzes PARP1-stimulated nucleosome sliding. Our results define DNA damage-response protein...
Chromosomal deletions and rearrangements in tumors are often associated with common fragile sites, which specific genomic loci prone to gaps breaks metaphase chromosomes. Common sites appear arise through incomplete DNA replication because they induced after partial inhibition by agents such as aphidicolin. Here, we show that G1 cells, large nuclear bodies contain p53 binding protein 1 (53BP1), phosphorylated H2AX (γH2AX), mediator of damage checkpoint (MDC1), well components previously...
Safeguarding cell function and identity following a genotoxic stress challenge entails tight coordination of DNA damage signaling repair with chromatin maintenance. How this is achieved what impact on integrity remains elusive. Here, we address these questions by investigating the mechanisms governing distribution in mammalian histone variant H2A.X, central player signaling. We reveal that H2A.X deposited de novo at sites repair-coupled manner, whereas H2A.Z evicted, thus reshaping landscape...
Abstract Pediatric high-grade gliomas (pHGG) are devastating and incurable brain tumors with recurrent mutations in histone H3.3. These promote oncogenesis by dysregulating gene expression through alterations of modifications. We identify aberrant DNA repair as an independent mechanism, which fosters genome instability H3.3 mutant pHGG, opens new therapeutic options. The two most frequent K27M G34R, drive replication-associated damage non-homologous end joining (NHEJ). Aberrant NHEJ is...
The faithful segregation of intact genetic material and the perpetuation chromatin states through mitotic cell divisions are pivotal for maintaining function identity across generations. However, most exogenous mutagens generate long-lasting DNA lesions that segregated during mitosis. How this is controlled unknown. Here, we uncover a chromatin-marking pathway governs UV-induced damage in human cells. Our mechanistic analyses reveal two layers control: histone ADP-ribosylation, incorporation...
Abstract Heterochromatin is a critical chromatin compartment, whose integrity governs genome stability and cell fate transitions. How heterochromatin features, including higher-order folding histone modifications associated with transcriptional silencing, are maintained following genotoxic stress challenge unknown. Here, we establish system for targeting UV damage to pericentric in mammalian cells tracking the response real time. We uncover profound compaction changes during repair,...
Abstract Histone synthesis and chromatin assembly are mainly associated with DNA replication thus intimately involved in cell cycle regulation. The expression of key components these events human cells was studied relation to cell-proliferative status. Among several factors, factor (CAF)-1 stood out as the most discriminating marker proliferative state. We show, using both immunofluorescence Western blot analysis, that CAF-1 large subunits, p150 p60, is massively down-regulated during...
Highlights•Parental H3 histones redistribute to the periphery of UVC-damaged regions•The redistribution involves histone mobilization on chromatin and opening•Parental recover massively during repair progression•Parental dynamics may help coordinate DNA with epigenome integritySummaryChromatin integrity is critical for cell function identity but challenged by damage. To understand how architecture information that it conveys are preserved or altered following genotoxic stress, we established...
Polo S E, Theocharis Grandin L, Gambotti Antoni G, Savignoni A, Asselain B, Patsouris E & Almouzni G (2010) Histopathology 57 , 716–724 Clinical significance and prognostic value of chromatin assembly factor‐1 overexpression in human solid tumours Aims: Chromatin (CAF‐1), whose function is critical for maintaining stability during DNA replication repair, has been identified as a proliferation marker breast cancer. The aim was to investigate CAF‐1 wide variety tumours, assess its...