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  • 1
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    Replication fork movement sets chromatin loop size and origin choice in mammalian cells (2008)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2008-08-22
    Description: 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, but much less is known about the mechanisms controlling the spacing of initiation events(2,3), namely the completion of DNA replication. Here we show that origin use in Chinese hamster cells depends on both the movement of the replication forks and the organization of chromatin loops. We found that slowing the replication speed triggers the recruitment of latent origins within minutes, allowing the completion of S phase in a timely fashion. When slowly replicating cells are shifted to conditions of fast fork progression, although the decrease in the overall number of active origins occurs within 2 h, the cells still have to go through a complete cell cycle before the efficiency specific to each origin is restored. We observed a strict correlation between replication speed during a given S phase and the size of chromatin loops in the next G1 phase. Furthermore, we found that origins located at or near sites of anchorage of chromatin loops in G1 are activated preferentially in the following S phase. These data suggest a mechanism of origin programming in which replication speed determines the spacing of anchorage regions of chromatin loops, that, in turn, controls the choice of initiation sites.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Courbet, Sylvain -- Gay, Sophie -- Arnoult, Nausica -- Wronka, Gerd -- Anglana, Mauro -- Brison, Olivier -- Debatisse, Michelle -- England -- Nature. 2008 Sep 25;455(7212):557-60. doi: 10.1038/nature07233. Epub 2008 Aug 17.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institut Curie, 26 rue d'Ulm, 75248 Paris, France; UPMC Univ. Paris 06, F-75005 Paris, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18716622" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Chromatin/genetics/*metabolism ; Cricetinae ; Cricetulus ; DNA/biosynthesis/genetics ; DNA Replication/*physiology ; G1 Phase ; *Movement ; Nuclear Matrix/metabolism ; Replication Origin/*genetics ; S Phase ; Time Factors
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 2
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    Cell-type-specific replication initiation programs set fragility of the FRA3B fragile site (2011)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2011-01-25
    Description: Common fragile sites have long been identified by cytogeneticists as chromosomal regions prone to breakage upon replication stress. They are increasingly recognized to be preferential targets for oncogene-induced DNA damage in pre-neoplastic lesions and hotspots for chromosomal rearrangements in various cancers. 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. 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 and replication timing are highly plastic 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. 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.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Letessier, Anne -- Millot, Gael A -- Koundrioukoff, Stephane -- Lachages, Anne-Marie -- Vogt, Nicolas -- Hansen, R Scott -- Malfoy, Bernard -- Brison, Olivier -- Debatisse, Michelle -- England -- Nature. 2011 Feb 3;470(7332):120-3. doi: 10.1038/nature09745. Epub 2011 Jan 23.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institut Curie, Centre de Recherche, 26 rue d'Ulm, 75248 Paris, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21258320" target="_blank"〉PubMed〈/a〉
    Keywords: Acid Anhydride Hydrolases/*genetics ; Cell Line ; Chromosome Breakage ; Chromosome Fragile Sites/*genetics ; Chromosome Fragility/genetics/*physiology ; DNA Replication/genetics/*physiology ; Fibroblasts ; Genes, Tumor Suppressor ; Genetic Loci/genetics ; Humans ; Lymphocytes/metabolism ; Models, Biological ; Neoplasm Proteins/*genetics ; Organ Specificity ; Replication Origin/*genetics
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 3
    Electronic Resource
    Electronic Resource
    The Highly Conserved Chinese Hamster GNAI3 Gene Maps Less Than 60 kb from the AMPD2 Gene and Lacks the Intronic U6 snRNA Present in Its Human Counterpart
    Amsterdam : Elsevier
    Genomics 24 (1994), S. 288-294 
    Details
    ISSN: 0888-7543
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1006/geno.1994.1618
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  • 4
    Electronic Resource
    Electronic Resource
    Increased inhibition of HGPRT by IMP and GMP and higher levels of PRPP in an 8-azaguanine - HAT resistant mutant of Chinese hamster cells
    Amsterdam : Elsevier
    Cell Biology International Reports 7 (1983), S. 121-128 
    Details
    ISSN: 0309-1651
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1016/0309-1651(83)90024-3
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  • 5
    Electronic Resource
    Electronic Resource
    GNAI3, GNAT2, AMPD2, GSTM are clustered in 120 kb of Chinese hamster Chromosome 1q (1996)
    Springer
    Mammalian genome 7 (1996), S. 429-432 
    Details
    ISSN: 1432-1777
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract. We studied a polygenic region located on Chromosome (Chr) 1q in Chinese hamster cells that is coamplified along with the AMPD2 gene. Previous sequence analysis identified both members of the GSTM family and the GNAI3 gene within a cloned 120-kb region surrounding the AMPD2 locus. We show here that the GNAT2 gene, which is inactive in the fibroblastic cells, lies within the 20 kb separating the transcriptionally active GNAI3 and AMPD2 genes. We map most gene ends by sequence comparison with human homologs; one is inferred from the presence of an unmethylated CpG island. This Chinese hamster locus corresponds to a region of conserved linkage between human Chr 1 (locus 1p13) and mouse Chr 3 (position 52.5 cM), where Gnai-3 and Gnat-2 have been mapped. The AMPD2 gene is presently unlocalized in human genome; its proposed position on mouse Chr 3 is at 53.4 cM. Our results, obtained by physical mapping, strongly suggest that the order and possibly the tight linkage of these genes are conserved on all three genomes.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s003359900127
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  • 6
    Electronic Resource
    Electronic Resource
    Chinese hamster transducin gene (GNAT2): genomic organization and peptide conservation (1996)
    Springer
    Mammalian genome 7 (1996), S. 922 -923 
    Details
    ISSN: 1432-1777
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s003359900274
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  • 7
    Electronic Resource
    Electronic Resource
    Adenosine-resistant chinese hamster fibroblast variants with hyperactive adenosine-deaminase: An analysis of the protection against exogenous adenosine afforded by increased activity of the deamination pathway (1984)
    New York, NY [u.a.] : Wiley-Blackwell
    Journal of Cellular Physiology 120 (1984), S. 321-328 
    Details
    ISSN: 0021-9541
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: The activity of purine salvage and interconversion enzymes was examined in two sublines of Chinese hamster cells-RA11 and RA41-isolated on the basis of their resistance to adenosine concentrations toxic to wild-type CCL39 cells. Adenosine deaminase (ADA) activity was found to be two times higher in RA11 and three times higher in RA41 than in CCL39. Inhibition of ADA activity by coformycin reduced the level of adenosine resistance but did not restore wild-type sensitivity, indicating that a second defect contributes to the adenosine-resistant phenotype of these variants; evidence was indeed obtained for the presence in both lines of additional alterations protecting them against the lethal depletion of phosphoribosylpyrophosphate (Ishii and Green, 1973) imposed by adenosine to wild-type cells. To gain better insight into the influence of ADA hyperactivity on adenosine resistance, a procedure was developed for the specific isolation of variants with increased levels of ADA activity. Cell lines with 3-5 times and then 100-500 times the wild-type ADA activity were stepwise recovered. These investigations confirmed that amplification of ADA can efficiently contribute in protecting cells against high concentrations of exogenous adenosine. The variants isolated by this procedure again manifested, in addition to amplification of ADA activity, another alteration decreasing their sensitivity to adenosine. A possible mechanism accounting for the frequent isolation of variants that coexpress ADA hyper-activity and a second defect contributing protection against adenosine toxicity are considered.
    Additional Material: 6 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcp.1041200310
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  • 8
    Electronic Resource
    Electronic Resource
    The potentiation of adenine toxicity to Chinese hamster cells by coformycin: Suppression in mutants with altered regulation of purine biosynthesis or increased adenylate-deaminase activity (1981)
    New York, NY [u.a.] : Wiley-Blackwell
    Journal of Cellular Physiology 106 (1981), S. 1-11 
    Details
    ISSN: 0021-9541
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: When added to medium containing coformycin (2 μM or above), adenine is lethal to Chinese hamster fibroblasts at the concentration inhibiting de novo purine biosynthesis (Debatisse and Buttin, '77b). Rescue by hypoxanthine suggested that cells die of IMP starvation when the analog can turn off deamination of both adenosine and adenylate. As predicted from this hypothesis, two classes of variants resistant to the mixture of coformycin + adenine have been isolated: Class 1 variants have altered control of de novo IMP biosynthesis; they fall into two subclasses on the basis of their resistance to adenosine. Class 2 variants have a 6-10-fold increased level of AMP-deaminase (E.C.: 3.5.4.6); their growth in the selective medium is temperature-dependent, a property accounted for by the observation that cell growth in the presence of coformycin imposes a gradual thermodependent decay of specific AMP-deaminase activity in both wild-type and variant lines. This control by coformycin of AMP-deaminase activity isunaltered in mutants deficient in the four activities of adenosine-kinase, APRT, HGPRT and deoxycytidine-kinase. Most of the resistant variants are unstable and exhibit either increased or reduced resistance, depending on prolonged growth in selective or normal medium.
    Additional Material: 5 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcp.1041060102
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  • 9
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    Spontaneous slow replication fork progression elicits mitosis alterations in homologous recombination-deficient mammalian cells (2013)
    National Academy of Sciences
    Details
    Publication Date: 2013-12-17
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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  • 10
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    Characterization at nucleotide resolution of the homogeneously staining region sites of insertion in two cancer cell lines (2013)
    Oxford University Press
    Details
    Publication Date: 2013-09-26
    Description: The mechanisms of formation of intrachromosomal amplifications in tumours are still poorly understood. By using quantitative polymerase chain reaction, DNA sequencing, chromosome walking, in situ hybridization on metaphase chromosomes and whole-genome analysis, we studied two cancer cell lines containing an MYC oncogene amplification with acquired copies ectopically inserted in rearranged chromosomes 17. These intrachromosomal amplifications result from the integration of extrachromosomal DNA molecules. Replication stress could explain the formation of the double-strand breaks involved in their insertion and in the rearrangements of the targeted chromosomes. The sequences of the junctions indicate that homologous recombination was not involved in their formation and support a non-homologous end-joining process. The replication stress-inducible common fragile sites present in the amplicons may have driven the intrachromosomal amplifications. Mechanisms associating break-fusion-bridge cycles and/or chromosome fragmentation may have led to the formation of the uncovered complex structures. To our knowledge, this is the first characterization of an intrachromosomal amplification site at nucleotide resolution.
    Print ISSN: 0305-1048
    Electronic ISSN: 1362-4962
    Topics: Biology
    Published by Oxford University Press
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