Density Transfer as a Method to Analyze the Progression of DNA Replication Forks
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Replicon
Replication
Origin recognition complex
Replication factor C
Semiconservative replication
Licensing factor
Pre-replication complex
Origin recognition complex
Pre-replication complex
Replication factor C
Minichromosome maintenance
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SeqA protein domain
Autonomously replicating sequence
Ter protein
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Origin recognition complex
Pre-replication complex
Semiconservative replication
Minichromosome maintenance
Replication factor C
Licensing factor
S phase
Replication
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Pre-replication complex
Origin recognition complex
Replication factor C
Licensing factor
S phase
Minichromosome maintenance
DNA re-replication
Semiconservative replication
Ter protein
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S phase
Origin recognition complex
Replication factor C
Semiconservative replication
Pre-replication complex
Licensing factor
DNA re-replication
DNA polymerase II
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Preventing re-replication of DNA in a single cell cycle: evidence for a replication licensing factor
Xenopus egg extracts treated with the protein kinase inhibitor 6-dimethylaminopurine (6-DMAP) are unable to support the initiation of DNA replication. Nuclei assembled in 6-DMAP extracts behave as though they are in G2, and will not undergo another round of DNA replication until passage through mitosis. 6-DMAP extracts are functionally devoid of a replication factor that modifies chromatin in early G1 before nuclear envelope assembly, but which is itself incapable of crossing the nuclear envelope. This chromatin modification is capable of supporting only a single round of semiconservative replication. The behavior of this replication factor is sufficient to explain why eukaryotic DNA is replicated once and only once in each cell cycle, and conforms to the previous model of a Replication Licensing Factor. Cell cycle analysis shows that this putative Licensing Factor is inactive during metaphase, but becomes rapidly activated on exit from metaphase when it can modify chromatin before nuclear envelope assembly is complete.
Origin recognition complex
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Licensing factor
S phase
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Chromatin structure affects DNA replication patterns, but the role of specific chromatin modifiers in regulating the replication process is yet unclear. We report that phosphorylation of the human SIRT1 deacetylase on Threonine 530 (T530-pSIRT1) modulates DNA synthesis. T530-pSIRT1 associates with replication origins and inhibits replication from a group of 'dormant' potential replication origins, which initiate replication only when cells are subject to replication stress. Although both active and dormant origins bind T530-pSIRT1, active origins are distinguished from dormant origins by their unique association with an open chromatin mark, histone H3 methylated on lysine 4. SIRT1 phosphorylation also facilitates replication fork elongation. SIRT1 T530 phosphorylation is essential to prevent DNA breakage upon replication stress and cells harboring SIRT1 that cannot be phosphorylated exhibit a high prevalence of extrachromosomal elements, hallmarks of perturbed replication. These observations suggest that SIRT1 phosphorylation modulates the distribution of replication initiation events to insure genomic stability.Published by Oxford University Press on behalf of Nucleic Acids Research 2017. PMID: 28549174
Origin recognition complex
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Replication factor C
Semiconservative replication
Minichromosome maintenance
S phase
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Mechanisms for replicating DNA origins of DNA replication roles of transcription factors in DNA replication roles of nuclear structure in DNA replication mechanisms for priming DNA synthesis mechanisms for completing DNA replication fidelity of DNA replication DNA excision repair pathways chromatin structure and DNA replication - implications for transcriptional activity roles of phosphorylation in DNA replication control of S phase temporal order of DNA replication changes in DNA replication during animal development comparison of DNA replication in cells from prokarya and eukarya DNA replication in eukaryotic cells - 1998 to 1998.
Origin recognition complex
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The replication of DNA in the eukaryotic cell cycle is one of the most highly regulated events in cell growth and division. Biochemical studies on the replication of the genome of the small DNA virus simian virus 40 (SV40) have resulted in the identification of a number of DNA replication proteins from human cells. One of these, Replication Protein A (RPA), was phosphorylated in a cell cycle-dependent manner, beginning at the onset of DNA replication. RPA was phosphorylated in vitro by the cell cycle-regulated cdc2 protein kinase. This kinase also stimulated the unwinding of the SV40 origin of DNA replication during initiation of DNA replication in vitro, suggesting a mechanism by which cdc2 kinase may regulate DNA replication. Functional homologues of the DNA replication factors have been identified in extracts from the yeast Saccharomyces cerevisiae, enabling a genetic characterization of the role of these proteins in the replication of cellular DNA. A cellular origin binding protein had not been characterized. To identify proteins that function like T antigen at cellular origins of DNA replication, we examined the structure of a yeast origin of DNA replication in detail. This origin consists of four separate functional elements, one of which is essential. A multiprotein complex that binds to the essential element has been identified and purified. This protein complex binds to all known cellular origins from S. cerevisiae and may function as an origin recognition complex.
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Pre-replication complex
Replication factor C
Licensing factor
S phase
Replication protein A
Minichromosome maintenance
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One of the fundamental characteristics of life is the ability of an entity to reproduce itself, which stems from the ability of the DNA molecule to replicate itself. The initiation step of DNA replication, where control over the timing and frequency of replication is exerted, is poorly understood in eukaryotes in general, and in mammalian cells in particular. The cis-acting DNA element defining the position and providing control over initiation is the replication origin. The activation of replication origins seems to be dependent on the presence of both a particular sequence and of structural determinants. In the past few years, the development of new methods for identification and mapping of origins of DNA replication has allowed some understanding of the fundamental elements that control the replication process. This review summarizes some of the major findings of this century, regarding the mechanism of DNA replication, emphasizing what is known about the replication of mammalian DNA. J. Cell. Biochem. Suppls. 32/33:1-14, 1999.
Origin recognition complex
Pre-replication complex
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Replication factor C
Semiconservative replication
Minichromosome maintenance
Replication
DNA re-replication
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Minichromosome maintenance
Origin recognition complex
S phase
Replication factor C
Pre-replication complex
Licensing factor
Semiconservative replication
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