Genomic instability and endoreduplication triggered by RAD17 deletion

Xin Wang; Lee Zou; Huyong Zheng; Qingyi Wei; Stephen J. Elledge; Lei Li

doi:10.1101/gad.1065103

Genomic instability and endoreduplication triggered by RAD17 deletion

Xin Wang, Lee Zou, Huyong Zheng, Qingyi Wei, Stephen J. Elledge, Lei Li

Research output: Contribution to journal › Article › peer-review

63 Scopus citations

Abstract

Cell cycle checkpoints are critical for genomic stability. Rad17, a component of the checkpoint clamp loader complex (Rad17/Rfc2-5), is required for the response to DNA damage and replication stress. To explore the role of Rad17 in the maintenance of genomic integrity, we established somatic conditional alleles of RAD17 in human cells. We find that RAD17 is not only important for the Atr-mediated checkpoint but is also essential for cell viability. Cells lacking RAD17 exhibited acute chromosomal aberrations and underwent endoreduplication at a high rate. Therefore, RAD17 links the checkpoint to ploidy control and is essential for the maintenance of chromosomal stability.

Original language	English (US)
Pages (from-to)	965-970
Number of pages	6
Journal	Genes and Development
Volume	17
Issue number	8
DOIs	https://doi.org/10.1101/gad.1065103
State	Published - Apr 15 2003

Keywords

Checkpoint
DNA damage
Endoreduplication
RAD17

ASJC Scopus subject areas

Genetics
Developmental Biology

Access to Document

10.1101/gad.1065103

Cite this

@article{0cfd8b5c48cd4e6a89958e5eabb1e6da,

title = "Genomic instability and endoreduplication triggered by RAD17 deletion",

abstract = "Cell cycle checkpoints are critical for genomic stability. Rad17, a component of the checkpoint clamp loader complex (Rad17/Rfc2-5), is required for the response to DNA damage and replication stress. To explore the role of Rad17 in the maintenance of genomic integrity, we established somatic conditional alleles of RAD17 in human cells. We find that RAD17 is not only important for the Atr-mediated checkpoint but is also essential for cell viability. Cells lacking RAD17 exhibited acute chromosomal aberrations and underwent endoreduplication at a high rate. Therefore, RAD17 links the checkpoint to ploidy control and is essential for the maintenance of chromosomal stability.",

keywords = "Checkpoint, DNA damage, Endoreduplication, RAD17",

author = "Xin Wang and Lee Zou and Huyong Zheng and Qingyi Wei and Elledge, {Stephen J.} and Lei Li",

year = "2003",

month = apr,

day = "15",

doi = "10.1101/gad.1065103",

language = "English (US)",

volume = "17",

pages = "965--970",

journal = "Genes and Development",

issn = "0890-9369",

publisher = "Cold Spring Harbor Laboratory Press",

number = "8",

}

TY - JOUR

T1 - Genomic instability and endoreduplication triggered by RAD17 deletion

AU - Wang, Xin

AU - Zou, Lee

AU - Zheng, Huyong

AU - Wei, Qingyi

AU - Elledge, Stephen J.

AU - Li, Lei

PY - 2003/4/15

Y1 - 2003/4/15

N2 - Cell cycle checkpoints are critical for genomic stability. Rad17, a component of the checkpoint clamp loader complex (Rad17/Rfc2-5), is required for the response to DNA damage and replication stress. To explore the role of Rad17 in the maintenance of genomic integrity, we established somatic conditional alleles of RAD17 in human cells. We find that RAD17 is not only important for the Atr-mediated checkpoint but is also essential for cell viability. Cells lacking RAD17 exhibited acute chromosomal aberrations and underwent endoreduplication at a high rate. Therefore, RAD17 links the checkpoint to ploidy control and is essential for the maintenance of chromosomal stability.

AB - Cell cycle checkpoints are critical for genomic stability. Rad17, a component of the checkpoint clamp loader complex (Rad17/Rfc2-5), is required for the response to DNA damage and replication stress. To explore the role of Rad17 in the maintenance of genomic integrity, we established somatic conditional alleles of RAD17 in human cells. We find that RAD17 is not only important for the Atr-mediated checkpoint but is also essential for cell viability. Cells lacking RAD17 exhibited acute chromosomal aberrations and underwent endoreduplication at a high rate. Therefore, RAD17 links the checkpoint to ploidy control and is essential for the maintenance of chromosomal stability.

KW - Checkpoint

KW - DNA damage

KW - Endoreduplication

KW - RAD17

UR - http://www.scopus.com/inward/record.url?scp=0344209296&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0344209296&partnerID=8YFLogxK

U2 - 10.1101/gad.1065103

DO - 10.1101/gad.1065103

M3 - Article

C2 - 12672690

AN - SCOPUS:0344209296

SN - 0890-9369

VL - 17

SP - 965

EP - 970

JO - Genes and Development

JF - Genes and Development

IS - 8

ER -

Genomic instability and endoreduplication triggered by RAD17 deletion

Abstract

Keywords

ASJC Scopus subject areas

Access to Document

Other files and links

Fingerprint

Cite this