Cell Cycle Control of DNA Replication by Phosphorylation and Dephosphorylation of Replication-Initiation Proteins in Budding Yeast

Zhai, Yuanliang; Yung, Philip Yuk Kwong; Liang, Chun

doi:10.5772/20597

Cited by 8 publications

(10 citation statements)

References 112 publications

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“…In addition to the previous reports of Noc3p's role in DNA replication initiation in budding yeast [3,5] and of hNOC3's role in human DNA replication [51][52][53], there were published experimental data indicating that Noc3 in fission yeast also plays a role in DNA replication, as depletion, which was inevitably incomplete in genetic experiments, of Noc3 in fission yeast significantly slowed down S-phase entry and progression, and finally led to a block in G 2 /M phase, most probably due to incomplete genome duplication, which is reminiscent of the phenotypes in ORC or MCM depleted cells (reviewed in [54]).…”

Section: Discussionmentioning

confidence: 99%

Human NOC3 is essential for DNA replication licensing in human cells

Cheung

Amin

et al. 2019

Cell Cycle

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Noc3p (Nucleolar Complex-associated protein) is an essential protein in budding yeast DNA replication licensing. Noc3p mediates the loading of Cdc6p and MCM proteins onto replication origins during the M-to-G 1 transition by interacting with ORC (Origin Recognition Complex) and MCM (Minichromosome Maintenance) proteins. FAD24 (Factor for Adipocyte Differentiation, clone number 24), the human homolog of Noc3p (hNOC3), was previously reported to play roles in the regulation of DNA replication and proliferation in human cells. However, the role of hNOC3 in replication licensing was unclear. Here we report that hNOC3 physically interacts with multiple human pre-replicative complex (pre-RC) proteins and associates with known replication origins throughout the cell cycle. Moreover, knockdown of hNOC3 in HeLa cells abrogates the chromatin association of other pre-RC proteins including hCDC6 and hMCM, leading to DNA replication defects and eventual apoptosis in an abortive S-phase. In comparison, specific inhibition of the ribosome biogenesis pathway by preventing pre-rRNA synthesis, does not lead to any cell cycle or DNA replication defect or apoptosis in the same timeframe as the hNOC3 knockdown experiments. Our findings strongly suggest that hNOC3 plays an essential role in pre-RC formation and the initiation of DNA replication independent of its potential role in ribosome biogenesis in human cells.

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Section: Discussionmentioning

confidence: 99%

Human NOC3 is essential for DNA replication licensing in human cells

Cheung

Amin

et al. 2019

Cell Cycle

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“…Eukaryotic DNA replication is a fundamental process by which the cell duplicates its genomic DNA for inheritance. Replication initiation is tightly regulated to ensure chromosomal DNA is replicated exactly once per cell cycle (Diffley, 2011;Zhai et al, 2011;Costa et al, 2013;Amin et al, 2019). The pre-replicative complex (pre-RC) is assembled at replication origins during the M-to-G 1 transition (Liang and Stillman, 1997;Zhai et al, 2010;Amin et al, 2019).…”

Section: Introductionmentioning

confidence: 99%

“…The ORC cycle in S. cerevisiae is somewhat different from other species. While ORC remains bound on chromatin throughout the cell cycle, phosphorylation of Orc2p and Orc6p after DNA replication prevents pre-RC formation (Nguyen et al, 2001;Zhai et al, 2010;Chen and Bell, 2011;Zhai et al, 2011). Therefore, perhaps in all eukaryotic cells, there exists some form of an ORC cycle, which promotes replication licensing and also restricts DNA replication to once per cell cycle.…”

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confidence: 99%

An Essential and Cell-Cycle-Dependent ORC Dimerization Cycle Regulates Eukaryotic Chromosomal DNA Replication

Amin

Cheung

et al. 2020

Cell Reports

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“…[8][9][10][11]. These and some other related replicationinitiation proteins are required for DNA replication, and their subsequent removal or inactivation before and/or during DNA replication helps to prevent re-replication within the same cell cycle.…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-26a/b Regulate DNA Replication Licensing, Tumorigenesis, and Prognosis by Targeting CDC6 in Lung Cancer

Zhang

Xiao

Wang

et al. 2014

Molecular Cancer Research

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Cancer is characterized by mutations, genome rearrangements, epigenetic changes, and altered gene expression that enhance cell proliferation, invasion, and metastasis. To accommodate deregulated cellular proliferation, many DNA replication-initiation proteins are overexpressed in human cancers. However, the mechanism that represses the expression of these proteins in normal cells and the cellular changes that result in their overexpression are largely unknown. One possible mechanism is through miRNA expression differences. Here, it is demonstrated that miR26a and miR26b inhibit replication licensing and the proliferation, migration, and invasion of lung cancer cells by targeting CDC6. Importantly, miR26a/b expression is significantly decreased in human lung cancer tissue specimens compared with the paired adjacent normal tissues, and miR26a/b downregulation and the consequential upregulation of CDC6 are associated with poorer prognosis of patients with lung cancer. These results indicate that miR26a/b repress replication licensing and tumorigenesis by targeting CDC6. Implications:The current study suggests that miR26a, miR26b, and CDC6 and factors regulating their expression represent potential cancer diagnostic and prognostic markers as well as anticancer targets.

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Cell Cycle Control of DNA Replication by Phosphorylation and Dephosphorylation of Replication-Initiation Proteins in Budding Yeast

Cited by 8 publications

References 112 publications

Human NOC3 is essential for DNA replication licensing in human cells

Human NOC3 is essential for DNA replication licensing in human cells

An Essential and Cell-Cycle-Dependent ORC Dimerization Cycle Regulates Eukaryotic Chromosomal DNA Replication

MicroRNA-26a/b Regulate DNA Replication Licensing, Tumorigenesis, and Prognosis by Targeting CDC6 in Lung Cancer

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