Mechanisms of signalling-memory governing progression through the eukaryotic cell cycle |
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| Affiliation: | 1. Department of Biochemistry, University of Oxford, Oxford, UK;2. Department of Biological Sciences (emeritus), Virginia Tech, Blacksburg, VA, USA;1. Institute of Technology, University of Tartu, Tartu 50411, Estonia;1. Department of Chemical and Systems Biology, Stanford University School of Medicine, Stanford, CA 94305-5174, USA;2. Department of Biochemistry, Stanford University School of Medicine, Stanford, CA 94305-5307, USA;1. Priority Organization for Innovation and Excellence, Kumamoto University, Kyoyoto-honjo 1, 2-2-1 Honjo, Chuo-ku, Kumamoto 860-0811, Japan;2. Institute for Medical Embryology and Genetics, Kumamoto University, Kyoyoto-honjo 1, 2-2-1 Honjo, Chuo-ku, Kumamoto 860-0811, Japan;3. International Research Center for Medical Science, Kumamoto University, Kyoyoto-honjo 1, 2-2-1 Honjo, Chuo-ku, Kumamoto 860-0811, Japan;4. Precursory Research for Embryonic Science and Technology (PRESTO) Program, Japan Science and Technology Agency, 4-1-8 Honcho, Kawaguchi, Saitama 332-0012, Japan;5. Department of Biochemistry, University of Oxford, South Parks Road, Oxford OX1 3QU, UK;6. The Institute of Scientific and Industrial Research, Osaka University, Mihogaoka 8-1, Ibaraki, Osaka 567-0047, Japan |
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| Abstract: | As cells pass through each replication–division cycle, they must be able to postpone further progression if they detect any threats to genome integrity, such as DNA damage or misaligned chromosomes. Once a ‘decision’ is made to proceed, the cell unequivocally enters into a qualitatively different biochemical state, which makes the transitions from one cell cycle phase to the next switch-like and irreversible. Each transition is governed by a unique signalling network; nonetheless, they share a common characteristic of bistable behaviour, a hallmark of molecular memory devices. Comparing the cell cycle signalling mechanisms acting at the restriction point, G1/S, G2/M and meta-to-anaphase transitions, we deduce a generic network motif of coupled positive and negative feedback loops underlying each transition. |
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| Keywords: | Cell cycle transition G2/M transition Meta/anaphase transition Restriction point G1/S transition Bistability Hysteresis Network motif Feedback loop Irreversible switch Checkpoint |
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