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172 results on '"Brison, Olivier"'

4. Cell--type--specific replication initiation programs set fragility of the FRA3B fragile site

Author

Letessier, Anne, Millot, Gael A., Koundrioukoff, Stephane, Lachages, Anne-Marie, Vogt, Nicolas, Hansen, R. Scott, Malfoy, Bernard, Brison, Olivier, and Debatisse, Michelle

Subjects
DNA replication -- Health aspects -- Research -- Genetic aspects, Lymphocytes -- Genetic aspects -- Abnormalities -- Research -- Health aspects, Cancer -- Genetic aspects, Environmental issues, Science and technology, Zoology and wildlife conservation
Abstract

Common fragile sites have long been identified by cytogeneticists as chromosomal regions prone to breakage upon replication stress (1). They are increasingly recognized to be preferential targets for oncogene-induced DNA damage in pre-neoplastic lesions (2) and hotspots for chromosomal rearrangements in various cancers (3). Common fragile site instability was attributed to the fact that they contain sequences prone to form secondary structures that may impair replication fork movement, possibly leading to fork collapse resulting in DNA breaks (4). Here we show, in contrast to this view, that the fragility of FRA3B--the most active common fragile site in human lymphocytes--does not rely on fork slowing or stalling but on a paucity of initiation events. Indeed, in lymphoblastoid cells, but not in fibroblasts, initiation events are excluded from a FRA3B core extending approximately 700 kilobases, which forces forks coming from flanking regions to cover long distances in order to complete replication. We also show that origins of the flanking regions fire in mid-S phase, leaving the site incompletely replicated upon fork slowing. Notably, FRA3B instability is specific to cells showing this particular initiation pattern. The fact that both origin setting (5,6) and replication timing are highly plastic (7,8) in mammalian cells explains the tissue specificity of common fragile site instability we observed. Thus, we propose that common fragile sites correspond to the latest initiation-poor regions to complete replication in a given cell type. For historical reasons, common fragile sites have been essentially mapped in lymphocytes (1). Therefore, common fragile site contribution to chromosomal rearrangements in tumours should be reassessed after mapping fragile sites in the cell type from which each tumour originates., Replication forks commonly face sequences intrinsically difficult to replicate such as natural pause sites (9,10). Various observations have indicated that the sequence of common fragile sites may also constitute a [...]

Published
2011
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5. Replication fork movement sets chromatin loop size and origin choice in mammalian cells

Author

Courbet, Sylvain, Gay, Sophie, Arnoult, Nausica, Wronka, Gerd, Anglana, Mauro, Brison, Olivier, and Debatisse, Michelle

Subjects
Nucleotide sequencing -- Research, Primers (Molecular genetics) -- Research, DNA replication -- Research, DNA sequencing -- Research, Environmental issues, Science and technology, Zoology and wildlife conservation, Research
Abstract

Genome stability requires one, and only one, DNA duplication at each S phase. The mechanisms preventing origin firing on newly replicated DNA are well documented (1), but much less is [...]

Published
2008

18. Transcription-mediated organization of the replication initiation program across large genes sets up common fragile sites genome-wide

Author

Brison, Olivier, primary, EL-Hilali, Sami, additional, Azar, Dana, additional, Koundrioukoff, Stéphane, additional, Schmidt, Mélanie, additional, Naehse-Kumpf, Viola, additional, Jaszczyszyn, Yan, additional, Lachages, Anne-Marie, additional, Dutrillaux, Bernard, additional, Thermes, Claude, additional, Debatisse, Michelle, additional, and Chen, Chun-Long, additional

Published
2019
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34. Updating the mechanisms of common fragile site instability: how to reconcile the different views?

Author

Tallec, Benoît, Koundrioukoff, Stéphane, Wilhelm, Therese, Letessier, Anne, Brison, Olivier, and Debatisse, Michelle

Subjects
CHROMOSOME abnormalities, CYTOGENETICS, DNA replication, DNA damage, CANCER invasiveness, PRECANCEROUS conditions, CELL cycle
Abstract

Common fragile sites (CFSs) are large chromosomal regions long identified by conventional cytogenetics as sequences prone to breakage in cells subjected to replication stress. The interest in CFSs came from their key role in the formation of DNA damage, resulting in chromosomal rearrangements. The instability of CFSs was notably correlated with the appearance of genome instability in precancerous lesions and during tumor progression. Identification of the molecular mechanisms responsible for their instability therefore represents a major challenge. A number of data show that breaks result from mitotic entry before replication completion but the mechanisms responsible for such delayed replication of CFSs and relaxed checkpoint surveillance are still debated. In addition, clues to the molecular events leading to breakage just start to emerge. We present here the results of recent reports addressing these questions. [ABSTRACT FROM AUTHOR]

Published
2014
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36. Use of adenoviral E1A protein to analyze K18 promoter deregulation in colon carcinoma cells discloses a role for CtBP1 and BRCA1

Author

Laithier Madeleine, Prochasson Philippe, Delouis Cécile, and Brison Olivier

Subjects
lcsh:QH426-470, Keratin-18, lcsh:Cytology, Blotting, Western, Genes, BRCA1, Gene Expression, macromolecular substances, Phosphoproteins, Protein Structure, Tertiary, DNA-Binding Proteins, Gene Expression Regulation, Neoplastic, lcsh:Genetics, Alcohol Oxidoreductases, Cell Line, Tumor, Humans, Keratins, Adenovirus E1A Proteins, lcsh:QH573-671, Promoter Regions, Genetic, Research Article, Plasmids, Sequence Deletion
Abstract

Background The promoter of the keratin 18 (K18) gene is 5- to 10-fold more active in tumorigenic (T-type) cell clones derived from the SW613-S human colon carcinoma cell line than in non-tumorigenic (NT-type) clones. We have reported previously that the mechanism responsible for this differential activity is acting on the minimal K18 promoter (TATA box and initiation site). This mechanism does not require the binding of a factor to a specific site on the DNA but involves the acetylation of a non-histone substrate. To get further insight into this mechanism, we investigated the effect of the adenovirus E1A protein on the activity of the K18 promoter, both in T and NT cells. Results Wild type adenovirus E1A protein and C-terminal deletion mutants inhibit the K18 promoter, specifically in T-type cells. The domain responsible for this inhibitory effect is located in the 12–25 region of the viral protein. E1A mutants that have lost this region but retain the PLDLS motif (the C-terminal binding site for CtBP1) stimulate the K18 promoter, specifically in NT cells. The inhibitory or stimulatory effects of the different E1A mutants are not dependent on a particular sequence of the promoter. An E1A N-terminal deletion mutant carrying point mutations in the PLDLS motif cannot stimulate the K18 promoter. CtBP1 interacts with CtIP, which is a known partner of BRCA1, itself a component of the RNA polymerase II holoenzyme. The stimulatory effect of two BRCA1 mutants, specifically in NT cells, implicates a tripartite BRCA1-CtIP-CtBP1 complex in the regulation of the K18 promoter. Conclusion Since we have shown previously that the K18 promoter is stimulated by deacetylase inhibitors, specifically in NT cells, we conclude that the activity of the promoter is repressed in NT cells by a mechanism involving the recruitment, by a BRCA1/CtIP complex, of CtBP1 and associated deacetylases to the preinitiation complex. We propose a model depicting the mechanism responsible for the differential activity of the K18 promoter between T and NT cells of the SW613-S cell line.

Published
2005

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