Induction of DNA Replication by Transcription in the Region Upstream of the Human c-<i>myc</i> Gene in a Model Replication System

Ohba, Reiko; Matsumoto, Ken; Ishimi, Yukio

doi:10.1128/mcb.16.10.5754

Cited by 24 publications

(17 citation statements)

References 54 publications

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“…), suggests that the perinucleolar foci might contain chromosomal regions corresponding to E2F target genes. Physical association between late G 1 transcriptional regulatory proteins and the initiation of DNA synthesis would be consistent with the view of research on a number of organisms that transcriptional activation is linked to the initiation of DNA replication (DeVilliers et al 1984;Prives et al 1987;Guo et al 1989;Mul et al 1990;Cheng et al 1992;Ohba et al 1996;Murakami and Ito 1999). It may also provide a rationale for why origin selection could be different in distinct cell types; that is, the transcriptional profile of a cell in G 1 may influence which origins are ready for firing.…”

Section: Focal Sites Of Dna Replicationsupporting

confidence: 52%

Nuclear organization of DNA replication in primary mammalian cells

Kennedy¹,

Barbie²,

Classon³

et al. 2000

Genes Dev.

272

240

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Using methods that conserve nuclear architecture, we have reanalyzed the spatial organization of the initiation of mammalian DNA synthesis. Contrary to the commonly held view that replication begins at hundreds of dispersed nuclear sites, primary fibroblasts initiate synthesis in a limited number of foci that contain replication proteins, surround the nucleolus, and overlap with previously identified internal lamin A/C structures. These foci are established in early G 1 -phase and also contain members of the retinoblastoma protein family. Later, in S-phase, DNA replication sites distribute to regions located throughout the nucleus. As this progression occurs, association with the lamin structure and pRB family members is lost. A similar temporal progression is found in all the primary cells we have examined but not in most established cell lines, indicating that the immortalization process modifies spatial control of DNA replication. These findings indicate that in normal mammalian cells, the onset of DNA synthesis is coordinately regulated at a small number of previously unrecognized perinucleolar sites that are selected in early G 1 -phase.

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Section: Focal Sites Of Dna Replicationsupporting

confidence: 52%

Nuclear organization of DNA replication in primary mammalian cells

Kennedy¹,

Barbie²,

Classon³

et al. 2000

Genes Dev.

272

240

View full text Add to dashboard Cite

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“…These include the concentration and conformation of initiator proteins (6,7), as well as the specific DNA sequences acting as replication origins having differential affinities for the six subunits of the origin recognition complex (6)(7)(8). Transcription factors may also play important roles in the initiation and timing of replication for different cell types (9,10). Gene transcription, by way of transcriptional activation of certain gene loci in cells, has been linked to the initiation of DNA replication, which occurs earlier in S phase than in cells in which the same loci are not transcribed (11,12).…”

Section: Introductionmentioning

confidence: 99%

Differentially Active Origins of DNA Replication in Tumor versus Normal Cells

Paola

Price²,

Zannis‐Hadjopoulos

2006

Cancer Research

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Previously, a degenerate 36 bp human consensus sequence was identified as a determinant of autonomous replication in eukaryotic cells. Random mutagenesis analyses further identified an internal 20 bp of the 36 bp consensus sequence as sufficient for acting as a core origin element. Here, we have located six versions of the 20 bp consensus sequence (20mer) on human chromosome 19q13 over a region spanning f211 kb and tested them for ectopic and in situ replication activity by transient episomal replication assays and nascent DNA strand abundance analyses, respectively. The six versions of the 20mer alone were capable of supporting autonomous replication of their respective plasmids, unlike random genomic sequence of the same length. Furthermore, comparative analyses of the endogenous replication activity of these 20mers at their respective chromosomal sites, in five tumor/ transformed and two normal cell lines, done by in situ chromosomal DNA replication assays, involving preparation of nascent DNA by the L exonuclease method and quantification by real-time PCR, showed that these sites coincided with chromosomal origins of DNA replication in all cell lines. Moreover, a 2-to 3-fold higher origin activity in the tumor/ transformed cells by comparison to the normal cells was observed, suggesting a higher activation of these origins in tumor/transformed cell lines. (Cancer Res 2006; 66(10): 5094-103)

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“…A growing body of information indicates that all of these processes, mediated variously by DNA and RNA polymerases, recombinases, the multiple DNA repair systems, and the cell cycle machinery, are intimately linked. Transcription and replication, for example, are known to be closely coregulated (1,4,10,34,37,38). Other recent reports indicate a close mechanistic relationship between replication and recombination (23) and a negative relationship between cell division and transcription (47).…”

mentioning

confidence: 99%

Recruitment of the Putative Transcription-Repair Coupling Factor CSB/ERCC6 to RNA Polymerase II Elongation Complexes

Tantin¹,

Kansal

Carey

1997

Molecular and Cellular Biology

185

145

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Cockayne's syndrome (CS) is a disease characterized by developmental and growth defects, sunlight sensitivity, and a defect in transcription-coupled nucleotide excision repair. The two principle proteins involved in CS, CSA and CSB/ERCC6, have been hypothesized to bind RNA polymerase II (Pol II) and link transcription to DNA repair. We have tested CSA and CSB in assays designed to determine their role in transcriptioncoupled repair. Using a unique oligo(dC)-tailed DNA template, we provide biochemical evidence that CSB/ ERCC6 interacts with Pol II molecules engaged in ternary complexes containing DNA and nascent RNA. CSB is a DNA-activated ATPase, and hydrolysis of the ATP ␤-␥ phosphoanhydride bond is required for the formation of a stable Pol II-CSB-DNA-RNA complex. Unlike CSB, CSA does not directly bind Pol II.A cell's genetic information can be replicated, recombined with other DNA molecules, and expressed in the form of RNA. It must furthermore be defended against continuous attack from internal and external DNA-damaging agents. These nuclear events must also take place within the framework of the cell cycle and its control. A growing body of information indicates that all of these processes, mediated variously by DNA and RNA polymerases, recombinases, the multiple DNA repair systems, and the cell cycle machinery, are intimately linked. Transcription and replication, for example, are known to be closely coregulated (1,4,10,34,37,38). Other recent reports indicate a close mechanistic relationship between replication and recombination (23) and a negative relationship between cell division and transcription (47).Hanawalt and coworkers originally identified an interaction between transcription and DNA repair when they found that in cultured hamster and human cells, UV radiation-induced pyrimidine dimers were repaired in the actively transcribed dihydrofolate reductase gene at a higher rate than the photodimers in surrounding DNA (5, 31). This phenomenon, known as transcription-coupled repair (TCR), was largely restricted to the transcribed strand of the active gene in human cells, indirectly implicating RNA polymerases in the process (33). Experiments later extended TCR to Escherichia coli (32), and an activity dubbed transcription-repair coupling factor (TRCF) that facilitated TCR in vitro was isolated (48). TRCF, the product of the previously described mfd gene (50), was shown to displace stalled bacterial RNA polymerase and interact with the UvrA nucleotide excision repair (NER) protein, providing a mechanism of TCR in prokaryotic cells. TCR has also been described for the yeast RPB2 and GAL7 genes, where it has been shown to require an actively transcribing polymerase (27,51). Nothing is known, however, of the molecular mechanism of facilitated repair in eukaryotes.More recent evidence for the link between transcription and DNA repair came from studies of the eukaryotic RNA polymerase II (Pol II) general transcription factor IIH (TFIIH). The well-documented energetic requirements for Pol II transcription init...

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Induction of DNA Replication by Transcription in the Region Upstream of the Human c-myc Gene in a Model Replication System

Cited by 24 publications

References 54 publications

Nuclear organization of DNA replication in primary mammalian cells

Nuclear organization of DNA replication in primary mammalian cells

Differentially Active Origins of DNA Replication in Tumor versus Normal Cells

Recruitment of the Putative Transcription-Repair Coupling Factor CSB/ERCC6 to RNA Polymerase II Elongation Complexes

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