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ATM/Wip1 activities at chromatin control Plk1 re-activation to determine G2 checkpoint duration

H. Jaiswal, J. Benada, E. Müllers, K. Akopyan, K. Burdova, T. Koolmeister, T. Helleday, RH. Medema, L. Macurek, A. Lindqvist,

. 2017 ; 36 (14) : 2161-2176. [pub] 20170612

Jazyk angličtina Země Anglie, Velká Británie

Typ dokumentu časopisecké články

Perzistentní odkaz   https://www.medvik.cz/link/bmc17030755

After DNA damage, the cell cycle is arrested to avoid propagation of mutations. Arrest in G2 phase is initiated by ATM-/ATR-dependent signaling that inhibits mitosis-promoting kinases such as Plk1. At the same time, Plk1 can counteract ATR-dependent signaling and is required for eventual resumption of the cell cycle. However, what determines when Plk1 activity can resume remains unclear. Here, we use FRET-based reporters to show that a global spread of ATM activity on chromatin and phosphorylation of ATM targets including KAP1 control Plk1 re-activation. These phosphorylations are rapidly counteracted by the chromatin-bound phosphatase Wip1, allowing cell cycle restart despite persistent ATM activity present at DNA lesions. Combining experimental data and mathematical modeling, we propose a model for how the minimal duration of cell cycle arrest is controlled. Our model shows how cell cycle restart can occur before completion of DNA repair and suggests a mechanism for checkpoint adaptation in human cells.

Citace poskytuje Crossref.org

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$a After DNA damage, the cell cycle is arrested to avoid propagation of mutations. Arrest in G2 phase is initiated by ATM-/ATR-dependent signaling that inhibits mitosis-promoting kinases such as Plk1. At the same time, Plk1 can counteract ATR-dependent signaling and is required for eventual resumption of the cell cycle. However, what determines when Plk1 activity can resume remains unclear. Here, we use FRET-based reporters to show that a global spread of ATM activity on chromatin and phosphorylation of ATM targets including KAP1 control Plk1 re-activation. These phosphorylations are rapidly counteracted by the chromatin-bound phosphatase Wip1, allowing cell cycle restart despite persistent ATM activity present at DNA lesions. Combining experimental data and mathematical modeling, we propose a model for how the minimal duration of cell cycle arrest is controlled. Our model shows how cell cycle restart can occur before completion of DNA repair and suggests a mechanism for checkpoint adaptation in human cells.
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$a Benada, Jan $u Laboratory of Cancer Cell Biology, Institute of Molecular Genetics, Academy of Sciences of the Czech Republic, Prague, Czech Republic. Faculty of Science, Charles University in Prague, Prague, Czech Republic.
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$a Müllers, Erik $u Department of Cell and Molecular Biology, Karolinska Institutet, Stockholm, Sweden.
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$a Burdova, Kamila $u Laboratory of Cancer Cell Biology, Institute of Molecular Genetics, Academy of Sciences of the Czech Republic, Prague, Czech Republic.
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$a Koolmeister, Tobias $u Department of Medical Biochemistry and Biophysics, and Science for Life Laboratory, Karolinska Institutet, Stockholm, Sweden.
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$a Helleday, Thomas $u Department of Medical Biochemistry and Biophysics, and Science for Life Laboratory, Karolinska Institutet, Stockholm, Sweden.
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$a Medema, René H $u Division of Cell Biology, Netherlands Cancer Institute, Amsterdam, The Netherlands.
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$a Macurek, Libor $u Laboratory of Cancer Cell Biology, Institute of Molecular Genetics, Academy of Sciences of the Czech Republic, Prague, Czech Republic libor.macurek@img.cas.cz arne.lindqvist@ki.se.
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