Deubiquitination of FANCD2 Is Required for DNA Crosslink Repair

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Deubiquitination of FANCD2 Is Required for DNA Crosslink Repair. / Oestergaard, Vibe H.; Langevin, Frederic; Kuiken, Hendrik J.; Pace, Paul; Niedzwiedz, Wojciech; Simpson, Laura J.; Ohzeki, Mioko; Takata, Minoru; Sale, Julian E.; Patel, Ketan J.

In: Molecular Cell, Vol. 28, No. 5, 14.12.2007, p. 798-809.

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

Harvard

Oestergaard, VH, Langevin, F, Kuiken, HJ, Pace, P, Niedzwiedz, W, Simpson, LJ, Ohzeki, M, Takata, M, Sale, JE & Patel, KJ 2007, 'Deubiquitination of FANCD2 Is Required for DNA Crosslink Repair', Molecular Cell, vol. 28, no. 5, pp. 798-809. https://doi.org/10.1016/j.molcel.2007.09.020

APA

Oestergaard, V. H., Langevin, F., Kuiken, H. J., Pace, P., Niedzwiedz, W., Simpson, L. J., Ohzeki, M., Takata, M., Sale, J. E., & Patel, K. J. (2007). Deubiquitination of FANCD2 Is Required for DNA Crosslink Repair. Molecular Cell, 28(5), 798-809. https://doi.org/10.1016/j.molcel.2007.09.020

Vancouver

Oestergaard VH, Langevin F, Kuiken HJ, Pace P, Niedzwiedz W, Simpson LJ et al. Deubiquitination of FANCD2 Is Required for DNA Crosslink Repair. Molecular Cell. 2007 Dec 14;28(5):798-809. https://doi.org/10.1016/j.molcel.2007.09.020

Author

Oestergaard, Vibe H. ; Langevin, Frederic ; Kuiken, Hendrik J. ; Pace, Paul ; Niedzwiedz, Wojciech ; Simpson, Laura J. ; Ohzeki, Mioko ; Takata, Minoru ; Sale, Julian E. ; Patel, Ketan J. / Deubiquitination of FANCD2 Is Required for DNA Crosslink Repair. In: Molecular Cell. 2007 ; Vol. 28, No. 5. pp. 798-809.

Bibtex

@article{c99703e230a54b439b1cf20649e17bbb,
title = "Deubiquitination of FANCD2 Is Required for DNA Crosslink Repair",
abstract = "Monoubiquitination of FANCD2 and PCNA promotes DNA repair. It causes chromatin accumulation of FANCD2 and facilitates PCNA's recruitment of translesion polymerases to stalled replication. USP1, a protease that removes monoubiquitin from FANCD2 and PCNA, was thought to reverse the DNA damage response of these substrates. We disrupted USP1 in chicken cells to dissect its role in a stable genetic system. USP1 ablation increases FANCD2 and PCNA monoubiquitination but unexpectedly results in DNA crosslinker sensitivity. This defective DNA repair is associated with constitutively chromatin-bound, monoubiquitinated FANCD2. In contrast, persistent PCNA monoubiquitination has negligible impact on DNA repair or mutagenesis. USP1 was previously shown to autocleave after DNA damage. In DT40, USP1 autocleavage is not stimulated by DNA damage, and expressing a noncleavable mutant in the USP1 knockout strain partially rescues crosslinker sensitivity. We conclude that efficient DNA crosslink repair requires FANCD2 deubiquitination, whereas FANCD2 monoubiquitination is not dependent on USP1 autocleavage.",
keywords = "DNA, PROTEINS",
author = "Oestergaard, {Vibe H.} and Frederic Langevin and Kuiken, {Hendrik J.} and Paul Pace and Wojciech Niedzwiedz and Simpson, {Laura J.} and Mioko Ohzeki and Minoru Takata and Sale, {Julian E.} and Patel, {Ketan J.}",
year = "2007",
month = dec,
day = "14",
doi = "10.1016/j.molcel.2007.09.020",
language = "English",
volume = "28",
pages = "798--809",
journal = "Molecular Cell",
issn = "1097-2765",
publisher = "Cell Press",
number = "5",

}

RIS

TY - JOUR

T1 - Deubiquitination of FANCD2 Is Required for DNA Crosslink Repair

AU - Oestergaard, Vibe H.

AU - Langevin, Frederic

AU - Kuiken, Hendrik J.

AU - Pace, Paul

AU - Niedzwiedz, Wojciech

AU - Simpson, Laura J.

AU - Ohzeki, Mioko

AU - Takata, Minoru

AU - Sale, Julian E.

AU - Patel, Ketan J.

PY - 2007/12/14

Y1 - 2007/12/14

N2 - Monoubiquitination of FANCD2 and PCNA promotes DNA repair. It causes chromatin accumulation of FANCD2 and facilitates PCNA's recruitment of translesion polymerases to stalled replication. USP1, a protease that removes monoubiquitin from FANCD2 and PCNA, was thought to reverse the DNA damage response of these substrates. We disrupted USP1 in chicken cells to dissect its role in a stable genetic system. USP1 ablation increases FANCD2 and PCNA monoubiquitination but unexpectedly results in DNA crosslinker sensitivity. This defective DNA repair is associated with constitutively chromatin-bound, monoubiquitinated FANCD2. In contrast, persistent PCNA monoubiquitination has negligible impact on DNA repair or mutagenesis. USP1 was previously shown to autocleave after DNA damage. In DT40, USP1 autocleavage is not stimulated by DNA damage, and expressing a noncleavable mutant in the USP1 knockout strain partially rescues crosslinker sensitivity. We conclude that efficient DNA crosslink repair requires FANCD2 deubiquitination, whereas FANCD2 monoubiquitination is not dependent on USP1 autocleavage.

AB - Monoubiquitination of FANCD2 and PCNA promotes DNA repair. It causes chromatin accumulation of FANCD2 and facilitates PCNA's recruitment of translesion polymerases to stalled replication. USP1, a protease that removes monoubiquitin from FANCD2 and PCNA, was thought to reverse the DNA damage response of these substrates. We disrupted USP1 in chicken cells to dissect its role in a stable genetic system. USP1 ablation increases FANCD2 and PCNA monoubiquitination but unexpectedly results in DNA crosslinker sensitivity. This defective DNA repair is associated with constitutively chromatin-bound, monoubiquitinated FANCD2. In contrast, persistent PCNA monoubiquitination has negligible impact on DNA repair or mutagenesis. USP1 was previously shown to autocleave after DNA damage. In DT40, USP1 autocleavage is not stimulated by DNA damage, and expressing a noncleavable mutant in the USP1 knockout strain partially rescues crosslinker sensitivity. We conclude that efficient DNA crosslink repair requires FANCD2 deubiquitination, whereas FANCD2 monoubiquitination is not dependent on USP1 autocleavage.

KW - DNA

KW - PROTEINS

UR - http://www.scopus.com/inward/record.url?scp=36749100034&partnerID=8YFLogxK

U2 - 10.1016/j.molcel.2007.09.020

DO - 10.1016/j.molcel.2007.09.020

M3 - Journal article

C2 - 18082605

AN - SCOPUS:36749100034

VL - 28

SP - 798

EP - 809

JO - Molecular Cell

JF - Molecular Cell

SN - 1097-2765

IS - 5

ER -

ID: 238744045