Histone H4K20 methylation mediated chromatin compaction threshold ensures genome integrity by limiting DNA replication licensing

Research output: Contribution to journal › Journal article › Research › peer-review

Standard

Histone H4K20 methylation mediated chromatin compaction threshold ensures genome integrity by limiting DNA replication licensing. / Shoaib, Muhammad; Walter, David; Gillespie, Peter J.; Izard, Fanny; Fahrenkrog, Birthe; Lleres, David; Lerdrup, Mads; Johansen, Jens Vilstrup; Hansen, Klaus; Julien, Eric; Blow, J. Julian; Sørensen, Claus S.

In: Nature Communications, Vol. 9, No. 1, 3704, 2018, p. 1-11.

Research output: Contribution to journal › Journal article › Research › peer-review

Harvard

Shoaib, M, Walter, D, Gillespie, PJ, Izard, F, Fahrenkrog, B, Lleres, D, Lerdrup, M, Johansen, JV, Hansen, K, Julien, E, Blow, JJ & Sørensen, CS 2018, 'Histone H4K20 methylation mediated chromatin compaction threshold ensures genome integrity by limiting DNA replication licensing', Nature Communications, vol. 9, no. 1, 3704, pp. 1-11. https://doi.org/10.1038/s41467-018-06066-8

APA

Shoaib, M., Walter, D., Gillespie, P. J., Izard, F., Fahrenkrog, B., Lleres, D., Lerdrup, M., Johansen, J. V., Hansen, K., Julien, E., Blow, J. J., & Sørensen, C. S. (2018). Histone H4K20 methylation mediated chromatin compaction threshold ensures genome integrity by limiting DNA replication licensing. Nature Communications, 9(1), 1-11. [3704]. https://doi.org/10.1038/s41467-018-06066-8

Vancouver

Shoaib M, Walter D, Gillespie PJ, Izard F, Fahrenkrog B, Lleres D et al. Histone H4K20 methylation mediated chromatin compaction threshold ensures genome integrity by limiting DNA replication licensing. Nature Communications. 2018;9(1):1-11. 3704. https://doi.org/10.1038/s41467-018-06066-8

Author

Shoaib, Muhammad ; Walter, David ; Gillespie, Peter J. ; Izard, Fanny ; Fahrenkrog, Birthe ; Lleres, David ; Lerdrup, Mads ; Johansen, Jens Vilstrup ; Hansen, Klaus ; Julien, Eric ; Blow, J. Julian ; Sørensen, Claus S. / Histone H4K20 methylation mediated chromatin compaction threshold ensures genome integrity by limiting DNA replication licensing. In: Nature Communications. 2018 ; Vol. 9, No. 1. pp. 1-11.

Bibtex

@article{671b7d8f49b54bbab226e6cff445e93f,
title = "Histone H4K20 methylation mediated chromatin compaction threshold ensures genome integrity by limiting DNA replication licensing",
abstract = "The decompaction and re-establishment of chromatin organization immediately after mitosis is essential for genome regulation. Mechanisms underlying chromatin structure control in daughter cells are not fully understood. Here we show that a chromatin compaction threshold in cells exiting mitosis ensures genome integrity by limiting replication licensing in G1 phase. Upon mitotic exit, chromatin relaxation is controlled by SET8-dependent methylation of histone H4 on lysine 20. In the absence of either SET8 or H4K20 residue, substantial genome-wide chromatin decompaction occurs allowing excessive loading of the origin recognition complex (ORC) in the daughter cells. ORC overloading stimulates aberrant recruitment of the MCM2-7 complex that promotes single-stranded DNA formation and DNA damage. Restoring chromatin compaction restrains excess replication licensing and loss of genome integrity. Our findings identify a cell cycle-specific mechanism whereby fine-tuned chromatin relaxation suppresses excessive detrimental replication licensing and maintains genome integrity at the cellular transition from mitosis to G1 phase.",
author = "Muhammad Shoaib and David Walter and Gillespie, {Peter J.} and Fanny Izard and Birthe Fahrenkrog and David Lleres and Mads Lerdrup and Johansen, {Jens Vilstrup} and Klaus Hansen and Eric Julien and Blow, {J. Julian} and S{\o}rensen, {Claus S.}",
year = "2018",
doi = "10.1038/s41467-018-06066-8",
language = "English",
volume = "9",
pages = "1--11",
journal = "Nature Communications",
issn = "2041-1723",
publisher = "nature publishing group",
number = "1",

}

RIS

TY - JOUR

T1 - Histone H4K20 methylation mediated chromatin compaction threshold ensures genome integrity by limiting DNA replication licensing

AU - Shoaib, Muhammad

AU - Walter, David

AU - Gillespie, Peter J.

AU - Izard, Fanny

AU - Fahrenkrog, Birthe

AU - Lleres, David

AU - Lerdrup, Mads

AU - Johansen, Jens Vilstrup

AU - Hansen, Klaus

AU - Julien, Eric

AU - Blow, J. Julian

AU - Sørensen, Claus S.

PY - 2018

Y1 - 2018

N2 - The decompaction and re-establishment of chromatin organization immediately after mitosis is essential for genome regulation. Mechanisms underlying chromatin structure control in daughter cells are not fully understood. Here we show that a chromatin compaction threshold in cells exiting mitosis ensures genome integrity by limiting replication licensing in G1 phase. Upon mitotic exit, chromatin relaxation is controlled by SET8-dependent methylation of histone H4 on lysine 20. In the absence of either SET8 or H4K20 residue, substantial genome-wide chromatin decompaction occurs allowing excessive loading of the origin recognition complex (ORC) in the daughter cells. ORC overloading stimulates aberrant recruitment of the MCM2-7 complex that promotes single-stranded DNA formation and DNA damage. Restoring chromatin compaction restrains excess replication licensing and loss of genome integrity. Our findings identify a cell cycle-specific mechanism whereby fine-tuned chromatin relaxation suppresses excessive detrimental replication licensing and maintains genome integrity at the cellular transition from mitosis to G1 phase.

AB - The decompaction and re-establishment of chromatin organization immediately after mitosis is essential for genome regulation. Mechanisms underlying chromatin structure control in daughter cells are not fully understood. Here we show that a chromatin compaction threshold in cells exiting mitosis ensures genome integrity by limiting replication licensing in G1 phase. Upon mitotic exit, chromatin relaxation is controlled by SET8-dependent methylation of histone H4 on lysine 20. In the absence of either SET8 or H4K20 residue, substantial genome-wide chromatin decompaction occurs allowing excessive loading of the origin recognition complex (ORC) in the daughter cells. ORC overloading stimulates aberrant recruitment of the MCM2-7 complex that promotes single-stranded DNA formation and DNA damage. Restoring chromatin compaction restrains excess replication licensing and loss of genome integrity. Our findings identify a cell cycle-specific mechanism whereby fine-tuned chromatin relaxation suppresses excessive detrimental replication licensing and maintains genome integrity at the cellular transition from mitosis to G1 phase.

U2 - 10.1038/s41467-018-06066-8

DO - 10.1038/s41467-018-06066-8

M3 - Journal article

C2 - 30209253

AN - SCOPUS:85053243728

VL - 9

SP - 1

EP - 11

JO - Nature Communications

JF - Nature Communications

SN - 2041-1723

IS - 1

M1 - 3704

ER -

ID: 203592453