Epigenetic control of DNA replication dynamics in mammals

Casas-Delucchi, Corella S.; Cardoso, M. Cristina

doi:10.4161/nucl.2.5.17861

Cited by 20 publications

(12 citation statements)

References 247 publications

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“…Current proposals suggest that this “replication wave” may propagate through changes in chromatin structure, i.e. replication causes a local chromatin destabilization, so neighboring regions become more accessible for initiation [226]. In our DNA CTC hypothesis, key replication components (e.g.…”

Section: Hypothesis For Communication Between Fe-s Cluster Enzymementioning

confidence: 92%

Emerging critical roles of Fe–S clusters in DNA replication and repair

Fuss

Tsai

Ishida

et al. 2015

Biochimica et Biophysica Acta (BBA) - Molecular Cell Research

210

191

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Fe-S clusters are partners in the origin of life that predate cells, acetyl-CoA metabolism, DNA, and the RNA world. The double helix solved the mystery of DNA replication by base pairing for accurate copying. Yet, for genome stability necessary to life, the double helix has equally important implications for damage repair. Here we examine striking advances that uncover Fe-S cluster roles both in copying the genetic sequence by DNA polymerases and in crucial repair processes for genome maintenance, as mutational defects cause cancer and degenerative disease. Moreover, we examine an exciting, controversial role for Fe-S clusters in a third element required for life – the long-range coordination and regulation of replication and repair events. By their ability to delocalize electrons over both Fe and S centers, Fe-S clusters have unbeatable features for protein conformational control and charge transfer via double-stranded DNA that may fundamentally transform our understanding of life, replication, and repair.

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Section: Hypothesis For Communication Between Fe-s Cluster Enzymementioning

confidence: 92%

Emerging critical roles of Fe–S clusters in DNA replication and repair

Fuss

Tsai

Ishida

et al. 2015

Biochimica et Biophysica Acta (BBA) - Molecular Cell Research

210

191

View full text Add to dashboard Cite

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“…Although not yet well understood, animal DNA replication timing and its regulation through epigenetic mechanisms, ranging from DNA methylation to histone modifications and higher order chromatin structure, have been studied more deeply in the last years (reviewed by Casas-Delucchi and Cardoso, 2011). In plants, 130 epigenetic regulators have been described so far, revealing enormous diversity and contributing to the understanding of plant plasticity (Pikaard and Mittelsten Scheid, 2014).…”

Section: Epigenetic Mechanisms In Pre-rc Functionmentioning

confidence: 99%

The plant cell cycle: Pre-Replication complex formation and controls

et al. 2017

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The multiplication of cells in all living organisms requires a tight regulation of DNA replication. Several mechanisms take place to ensure that the DNA is replicated faithfully and just once per cell cycle in order to originate through mitoses two new daughter cells that contain exactly the same information from the previous one. A key control mechanism that occurs before cells enter S phase is the formation of a pre-replication complex (pre-RC) that is assembled at replication origins by the sequential association of the origin recognition complex, followed by Cdt1, Cdc6 and finally MCMs, licensing DNA to start replication. The identification of pre-RC members in all animal and plant species shows that this complex is conserved in eukaryotes and, more importantly, the differences between kingdoms might reflect their divergence in strategies on cell cycle regulation, as it must be integrated and adapted to the niche, ecosystem, and the organism peculiarities. Here, we provide an overview of the knowledge generated so far on the formation and the developmental controls of the pre-RC mechanism in plants, analyzing some particular aspects in comparison to other eukaryotes.

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“…As we observed a prolonged inhibition of the origin firing, we thought that UVA-induced ROS may destabilize or modify components of the DNA replication machinery. This process involves many players [ 60 ] that act in the formation of the pre-replication complex (pre-RC) at the end of mitosis, in its conversion into a pre-initiation complex (pre-IC) at the G1/S transition, and in the origin firing throughout S-phase[ 15 , 61 ]. As the sustained inhibition of DNA replication is observed when MRC5Vi cells are irradiated in S-phase but not when they are irradiated in G1 phase (see Fig 2B ), we reasoned that components of the pre-IC might directly or indirectly be altered by UVA-induced ROS.…”

Section: Resultsmentioning

confidence: 99%

“…These steps lead to the formation of a pre-replicative complex (pre-RC), commonly known as origin licensing, which is converted into a pre-initiation complex (pre-IC) by the activation of the CDKs (Cyclin-dependent kinases) and DDK (Dbf4-dependent kinase Cdc7) at the G1/S transition [ 12 , 13 ]. Activation of the CDKs and DDK allows the recruitment of additional factors including the GINS complex, Mcm10, RPA, DNA polymerase α, which initiate the origin firing (for reviews, see [ 15 – 18 ]). Recent works indicate that the time at which an origin fires is related to its ability to recruit replication initiation factors, such as Cdc45 and Sld3 (yeast ortholog of human Treslin/ticrr), which are limiting within the cells (see [ 19 ] and references therein).…”

Section: Introductionmentioning

confidence: 99%

Singlet Oxygen-Mediated Oxidation during UVA Radiation Alters the Dynamic of Genomic DNA Replication

et al. 2015

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UVA radiation (320–400 nm) is a major environmental agent that can exert its deleterious action on living organisms through absorption of the UVA photons by endogenous or exogenous photosensitizers. This leads to the production of reactive oxygen species (ROS), such as singlet oxygen (1O2) and hydrogen peroxide (H2O2), which in turn can modify reversibly or irreversibly biomolecules, such as lipids, proteins and nucleic acids. We have previously reported that UVA-induced ROS strongly inhibit DNA replication in a dose-dependent manner, but independently of the cell cycle checkpoints activation. Here, we report that the production of 1O2 by UVA radiation leads to a transient inhibition of replication fork velocity, a transient decrease in the dNTP pool, a quickly reversible GSH-dependent oxidation of the RRM1 subunit of ribonucleotide reductase and sustained inhibition of origin firing. The time of recovery post irradiation for each of these events can last from few minutes (reduction of oxidized RRM1) to several hours (replication fork velocity and origin firing). The quenching of 1O2 by sodium azide prevents the delay of DNA replication, the decrease in the dNTP pool and the oxidation of RRM1, while inhibition of Chk1 does not prevent the inhibition of origin firing. Although the molecular mechanism remains elusive, our data demonstrate that the dynamic of replication is altered by UVA photosensitization of vitamins via the production of singlet oxygen.

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Epigenetic control of DNA replication dynamics in mammals

Cited by 20 publications

References 247 publications

Emerging critical roles of Fe–S clusters in DNA replication and repair

Emerging critical roles of Fe–S clusters in DNA replication and repair

The plant cell cycle: Pre-Replication complex formation and controls

Singlet Oxygen-Mediated Oxidation during UVA Radiation Alters the Dynamic of Genomic DNA Replication

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