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DNA replication is required for the checkpoint response to damaged DNA in Xenopus egg extracts.

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DNA replication is required for the checkpoint response to damaged DNA in Xenopus egg extracts. / Stokes, Matthew P.; Van Hatten, Ruth; Lindsay, Howard D.; Michael, W. Matthew.

In: Journal of Cell Biology, Vol. 158, No. 5, 09.2002, p. 863-872.

Research output: Contribution to journalJournal articlepeer-review

Harvard

Stokes, MP, Van Hatten, R, Lindsay, HD & Michael, WM 2002, 'DNA replication is required for the checkpoint response to damaged DNA in Xenopus egg extracts.', Journal of Cell Biology, vol. 158, no. 5, pp. 863-872. https://doi.org/10.1083/jcb.200204127

APA

Stokes, M. P., Van Hatten, R., Lindsay, H. D., & Michael, W. M. (2002). DNA replication is required for the checkpoint response to damaged DNA in Xenopus egg extracts. Journal of Cell Biology, 158(5), 863-872. https://doi.org/10.1083/jcb.200204127

Vancouver

Author

Stokes, Matthew P. ; Van Hatten, Ruth ; Lindsay, Howard D. ; Michael, W. Matthew. / DNA replication is required for the checkpoint response to damaged DNA in Xenopus egg extracts. In: Journal of Cell Biology. 2002 ; Vol. 158, No. 5. pp. 863-872.

Bibtex

@article{5fccc4cf556e4db58d66b136be267c46,
title = "DNA replication is required for the checkpoint response to damaged DNA in Xenopus egg extracts.",
abstract = "Alkylating agents, such as methyl methanesulfonate (MMS), damage DNA and activate the DNA damage checkpoint. Although many of the checkpoint proteins that transduce damage signals have been identified and characterized, the mechanism that senses the damage and activates the checkpoint is not yet understood. To address this issue for alkylation damage, we have reconstituted the checkpoint response to MMS in Xenopus egg extracts. Using four different indicators for checkpoint activation (delay on entrance into mitosis, slowing of DNA replication, phosphorylation of the Chk1 protein, and physical association of the Rad17 checkpoint protein with damaged DNA), we report that MMS-induced checkpoint activation is dependent upon entrance into S phase. Additionally, we show that the replication of damaged double-stranded DNA, and not replication of damaged single-stranded DNA, is the molecular event that activates the checkpoint. Therefore, these data provide direct evidence that replication forks are an obligate intermediate in the activation of the DNA damage checkpoint.",
keywords = "cell cycle, Rad17, DNA damage, DNA replication, S phase",
author = "Stokes, {Matthew P.} and {Van Hatten}, Ruth and Lindsay, {Howard D.} and Michael, {W. Matthew}",
note = "{\textcopyright} Rockefeller University Press",
year = "2002",
month = sep,
doi = "10.1083/jcb.200204127",
language = "English",
volume = "158",
pages = "863--872",
journal = "Journal of Cell Biology",
issn = "0021-9525",
publisher = "Rockefeller University Press",
number = "5",

}

RIS

TY - JOUR

T1 - DNA replication is required for the checkpoint response to damaged DNA in Xenopus egg extracts.

AU - Stokes, Matthew P.

AU - Van Hatten, Ruth

AU - Lindsay, Howard D.

AU - Michael, W. Matthew

N1 - © Rockefeller University Press

PY - 2002/9

Y1 - 2002/9

N2 - Alkylating agents, such as methyl methanesulfonate (MMS), damage DNA and activate the DNA damage checkpoint. Although many of the checkpoint proteins that transduce damage signals have been identified and characterized, the mechanism that senses the damage and activates the checkpoint is not yet understood. To address this issue for alkylation damage, we have reconstituted the checkpoint response to MMS in Xenopus egg extracts. Using four different indicators for checkpoint activation (delay on entrance into mitosis, slowing of DNA replication, phosphorylation of the Chk1 protein, and physical association of the Rad17 checkpoint protein with damaged DNA), we report that MMS-induced checkpoint activation is dependent upon entrance into S phase. Additionally, we show that the replication of damaged double-stranded DNA, and not replication of damaged single-stranded DNA, is the molecular event that activates the checkpoint. Therefore, these data provide direct evidence that replication forks are an obligate intermediate in the activation of the DNA damage checkpoint.

AB - Alkylating agents, such as methyl methanesulfonate (MMS), damage DNA and activate the DNA damage checkpoint. Although many of the checkpoint proteins that transduce damage signals have been identified and characterized, the mechanism that senses the damage and activates the checkpoint is not yet understood. To address this issue for alkylation damage, we have reconstituted the checkpoint response to MMS in Xenopus egg extracts. Using four different indicators for checkpoint activation (delay on entrance into mitosis, slowing of DNA replication, phosphorylation of the Chk1 protein, and physical association of the Rad17 checkpoint protein with damaged DNA), we report that MMS-induced checkpoint activation is dependent upon entrance into S phase. Additionally, we show that the replication of damaged double-stranded DNA, and not replication of damaged single-stranded DNA, is the molecular event that activates the checkpoint. Therefore, these data provide direct evidence that replication forks are an obligate intermediate in the activation of the DNA damage checkpoint.

KW - cell cycle

KW - Rad17

KW - DNA damage

KW - DNA replication

KW - S phase

U2 - 10.1083/jcb.200204127

DO - 10.1083/jcb.200204127

M3 - Journal article

VL - 158

SP - 863

EP - 872

JO - Journal of Cell Biology

JF - Journal of Cell Biology

SN - 0021-9525

IS - 5

ER -