Differential regulation of the cellular response to DNA double-strand breaks in G1.

Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › fagfællebedømt

Standard

Differential regulation of the cellular response to DNA double-strand breaks in G1. / Barlow, Jacqueline H; Lisby, Michael; Rothstein, Rodney.

I: Molecular Cell, Bind 30, Nr. 1, 2008, s. 73-85.

Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › fagfællebedømt

Harvard

Barlow, JH, Lisby, M & Rothstein, R 2008, 'Differential regulation of the cellular response to DNA double-strand breaks in G1.', Molecular Cell, bind 30, nr. 1, s. 73-85. https://doi.org/10.1016/j.molcel.2008.01.016

APA

Barlow, J. H., Lisby, M., & Rothstein, R. (2008). Differential regulation of the cellular response to DNA double-strand breaks in G1. Molecular Cell, 30(1), 73-85. https://doi.org/10.1016/j.molcel.2008.01.016

Vancouver

Barlow JH, Lisby M, Rothstein R. Differential regulation of the cellular response to DNA double-strand breaks in G1. Molecular Cell. 2008;30(1):73-85. https://doi.org/10.1016/j.molcel.2008.01.016

Author

Barlow, Jacqueline H ; Lisby, Michael ; Rothstein, Rodney. / Differential regulation of the cellular response to DNA double-strand breaks in G1. I: Molecular Cell. 2008 ; Bind 30, Nr. 1. s. 73-85.

Bibtex

@article{6ef51580124211ddbee902004c4f4f50,

title = "Differential regulation of the cellular response to DNA double-strand breaks in G1.",

abstract = "Double-strand breaks (DSBs) are potentially lethal DNA lesions that can be repaired by either homologous recombination (HR) or nonhomologous end-joining (NHEJ). We show that DSBs induced by ionizing radiation (IR) are efficiently processed for HR and bound by Rfa1 during G1, while endonuclease-induced breaks are recognized by Rfa1 only after the cell enters S phase. This difference is dependent on the DNA end-binding Yku70/Yku80 complex. Cell-cycle regulation is also observed in the DNA damage checkpoint response. Specifically, the 9-1-1 complex is required in G1 cells to recruit the Ddc2 checkpoint protein to damaged DNA, while, upon entry into S phase, the cyclin-dependent kinase Cdc28 and the 9-1-1 complex both serve to recruit Ddc2 to foci. Together, these results demonstrate that the DNA repair machinery distinguishes between different types of damage in G1, which translates into different modes of checkpoint activation in G1 and S/G2 cells. Udgivelsesdato: 2008-Apr-11",

author = "Barlow, {Jacqueline H} and Michael Lisby and Rodney Rothstein",

note = "Author Keywords: DNA; SIGNALING; CELLCYCLE",

year = "2008",

doi = "10.1016/j.molcel.2008.01.016",

language = "English",

volume = "30",

pages = "73--85",

journal = "Molecular Cell",

issn = "1097-2765",

publisher = "Cell Press",

number = "1",

}

RIS

TY - JOUR

T1 - Differential regulation of the cellular response to DNA double-strand breaks in G1.

AU - Barlow, Jacqueline H

AU - Lisby, Michael

AU - Rothstein, Rodney

N1 - Author Keywords: DNA; SIGNALING; CELLCYCLE

PY - 2008

Y1 - 2008

N2 - Double-strand breaks (DSBs) are potentially lethal DNA lesions that can be repaired by either homologous recombination (HR) or nonhomologous end-joining (NHEJ). We show that DSBs induced by ionizing radiation (IR) are efficiently processed for HR and bound by Rfa1 during G1, while endonuclease-induced breaks are recognized by Rfa1 only after the cell enters S phase. This difference is dependent on the DNA end-binding Yku70/Yku80 complex. Cell-cycle regulation is also observed in the DNA damage checkpoint response. Specifically, the 9-1-1 complex is required in G1 cells to recruit the Ddc2 checkpoint protein to damaged DNA, while, upon entry into S phase, the cyclin-dependent kinase Cdc28 and the 9-1-1 complex both serve to recruit Ddc2 to foci. Together, these results demonstrate that the DNA repair machinery distinguishes between different types of damage in G1, which translates into different modes of checkpoint activation in G1 and S/G2 cells. Udgivelsesdato: 2008-Apr-11

AB - Double-strand breaks (DSBs) are potentially lethal DNA lesions that can be repaired by either homologous recombination (HR) or nonhomologous end-joining (NHEJ). We show that DSBs induced by ionizing radiation (IR) are efficiently processed for HR and bound by Rfa1 during G1, while endonuclease-induced breaks are recognized by Rfa1 only after the cell enters S phase. This difference is dependent on the DNA end-binding Yku70/Yku80 complex. Cell-cycle regulation is also observed in the DNA damage checkpoint response. Specifically, the 9-1-1 complex is required in G1 cells to recruit the Ddc2 checkpoint protein to damaged DNA, while, upon entry into S phase, the cyclin-dependent kinase Cdc28 and the 9-1-1 complex both serve to recruit Ddc2 to foci. Together, these results demonstrate that the DNA repair machinery distinguishes between different types of damage in G1, which translates into different modes of checkpoint activation in G1 and S/G2 cells. Udgivelsesdato: 2008-Apr-11

U2 - 10.1016/j.molcel.2008.01.016

DO - 10.1016/j.molcel.2008.01.016

M3 - Journal article

C2 - 18406328

VL - 30

SP - 73

EP - 85

JO - Molecular Cell

JF - Molecular Cell

SN - 1097-2765

IS - 1

ER -

ID: 3802259