Replication Initiation In Mammalian Cells: Changing Preferences

Debatisse, Michèlle; Toledo, Franck; Anglana, Mauro

doi:10.4161/cc.3.1.628

Cited by 29 publications

(25 citation statements)

References 21 publications

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“…Here, we show in a solid tumor that, indeed, the nucleoside analogue gemcitabine is capable to convey drug resistance to tumors by chromosomal instability. The role of nucleotide availability in DNA replication and chromosomal stability has recently been shown by Debatisse et al (18). Acquired drug resistance leading to chromosomal copy number was also observed in cell lines for other nucleoside analogues (19).…”

Section: Discussionmentioning

confidence: 82%

Expression Microarray Analysis and Oligo Array Comparative Genomic Hybridization of Acquired Gemcitabine Resistance in Mouse Colon Reveals Selection for Chromosomal Aberrations

et al. 2005

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Gemcitabine is a commonly used therapy for many solid tumors. Acquired resistance to this nucleoside analogue, however, diminishes the long-term effectiveness in a majority of patients. To better define the molecular background of gemcitabine resistance, a mouse colon tumor was selected during successive rounds of transplantation with continued treatment of gemcitabine. Expression microarray analysis was applied to determine which genes are consistently and highly overexpressed or underexpressed in the resistant versus the nonresistant tumor. For the statistical interpretation of the microarray data, a parametric model was implemented, which returns model-based differential gene expression (log-) ratios and their uncertainties. This defined a set of 13 genes, putatively responsible for the gemcitabine resistance in solid tumors. One of these, RRM1, was previously identified as an important marker for gemcitabine resistance in human cell lines. Five of the 13 genes, including RRM1, are located within a 3 Mb region at chromosome 7E1 of which four are highly overexpressed, suggesting a chromosomal amplification. Therefore, chromosomal copy number changes were measured, using oligo array comparative genomic hybridization. A narrow and high amplification area was identified on 7E1 that encompassed all five genes. In addition, reduced RNA expression of two other genes at 8E1 encoding COX4I1 and RPL13 could be explained by a decrease in chromosomal copy number on chromosome 8. In conclusion, the array comparative genomic hybridization biologically validates our statistical approach and shows that gemcitabine is capable to select for chromosomally aberrant tumor cells, where changed gene expression levels lead to drug resistance. (Cancer Res 2005; 65(22): 10208-13)

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Section: Discussionmentioning

confidence: 82%

Expression Microarray Analysis and Oligo Array Comparative Genomic Hybridization of Acquired Gemcitabine Resistance in Mouse Colon Reveals Selection for Chromosomal Aberrations

et al. 2005

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“…Nuclear genomes also appear to have inherent flexibility in their use of various replication origins. 2 Therefore, although a large amount of data supports the strand-displacement model of mammalian mtDNA replication, it is reasonable to consider that under some circumstances alternative modes of mtDNA replication may occur. Holt, Jacobs and coworkers proposed such an alternative model of mtDNA replication based on interpretation of 2-dimensional (2D) agarose gel electrophoresis patterns.…”

Section: Alternative Modes Of Mtdna Replicationmentioning

confidence: 99%

Genesis and Wanderings: Origins and Migrations in Asymmetrically Replicating Mitochondrial DNA

Brown¹,

Clayton²

2006

Cell Cycle

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Mammalian mitochondria maintain a small circular genome that encodes RNA and polypeptides that are essential for the generation of ATP through oxidative phosphorylation. The mechanism of replication of mammalian mitochondrial DNA (mtDNA) has recently been a topic of controversy. New evidence has led to a modified strand-displacement model that reconciles much of the current data. This revision stems from a new appreciation for alternative light-strand origins. We consider here some of the potential mechanisms for light-strand origin initiation. We also consider further the susceptibility of branch migration within replicating mtDNA molecules. The existence of alternative light-strand origins and a propensity for branch migration in replicating mtDNA molecules exposes a new array of possible configurations of mtDNA. The assortment and assignment of these forms is relevant to the interpretation of experimental data and may also yield insight into the molecular basis of replication errors.

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“…Fission yeast and Drosophila have ORCs that recognize AT-rich sequences (Austin et al, 1999;Chuang and Kelly, 1999), rather than specific motifs. Moreover, human ORCs, which are chosen as initiators of replication, have also been shown to require AT-rich sequences as well as various other features, including matrix attachment region sequences, dinucleotide repeats and asymmetrical purine-pyrimidine sequences (Altman and Fanning, 2004;Debatisse et al, 2004;Paixao et al, 2004;Schaarschmidt et al, 2004;Wang et al, 2004). Other factors that may affect the initiation of replication at certain ORs also include DNA topology, transcription factors, and elements of the pre-replicative complex (pre-RC) (reviewed in Masai et al, 2010).…”

Section: Replication Initiationmentioning

confidence: 99%

Replication Timing: Evolution, Nuclear Organization and Relevance for Human Disease

Wright¹,

Grützner²

2011

DNA Replication-Current Advances

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Replication Initiation In Mammalian Cells: Changing Preferences

Cited by 29 publications

References 21 publications

Expression Microarray Analysis and Oligo Array Comparative Genomic Hybridization of Acquired Gemcitabine Resistance in Mouse Colon Reveals Selection for Chromosomal Aberrations

Expression Microarray Analysis and Oligo Array Comparative Genomic Hybridization of Acquired Gemcitabine Resistance in Mouse Colon Reveals Selection for Chromosomal Aberrations

Genesis and Wanderings: Origins and Migrations in Asymmetrically Replicating Mitochondrial DNA

Replication Timing: Evolution, Nuclear Organization and Relevance for Human Disease

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