Abstract
During the G1 phase of the cell cycle, replication origins are prepared to fire, a process that is referred to as origin licensing. It was often pondered what a cell's fate would be if not all of its replication origins were licensed and subsequently activated during S phase. One obvious prediction was that S phase would simply be prolonged. As it turns out, however, the consequences are much more complex. A short G1 phase enforced by premature entry into S phase, or other events that negatively affect origin licensing, will ultimately compromise the cell's ability to complete DNA replication before entering mitosis. As a result, the cell becomes genomically unstable when it attempts to repair unreplicated DNA during anaphase. Thus, the density of active replication origins in the chromosomes of eukaryotic cells determines S phase dynamics and chromosome stability during mitosis.
Publication types
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Animals
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Ataxia Telangiectasia Mutated Proteins
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Cell Cycle Proteins
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Cells, Cultured
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Chromosome Aberrations
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DNA Replication / physiology*
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DNA-Binding Proteins / metabolism*
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G1 Phase / physiology
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Intracellular Signaling Peptides and Proteins
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Mice
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Mitosis / physiology
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Myoblasts / metabolism
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Origin Recognition Complex
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Protein Serine-Threonine Kinases / metabolism
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Replication Origin / physiology*
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S Phase / physiology
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Saccharomyces cerevisiae Proteins / metabolism
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Schizosaccharomyces / genetics
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Schizosaccharomyces / metabolism
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Tumor Suppressor Proteins
Substances
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Cell Cycle Proteins
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DNA-Binding Proteins
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Intracellular Signaling Peptides and Proteins
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Origin Recognition Complex
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Saccharomyces cerevisiae Proteins
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Tumor Suppressor Proteins
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Ataxia Telangiectasia Mutated Proteins
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Atm protein, mouse
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MEC1 protein, S cerevisiae
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Protein Serine-Threonine Kinases