Genomic instability and endoreduplication triggered by RAD17 deletion

被引：58

作者：

Wang, X

Zou, L

Zheng, HY

Wei, QY

Elledge, SJ

Li, L

机构：

[1] Univ Texas, MD Anderson Canc Ctr, Dept Expt Radiat Oncol, Houston, TX 77030 USA

[2] Univ Texas, MD Anderson Canc Ctr, Dept Epidemiol, Houston, TX 77030 USA

[3] Univ Texas, MD Anderson Canc Ctr, Dept Mol Genet, Houston, TX 77030 USA

[4] Baylor Coll Med, Verna & Marrs Mclean Dept Biochem & Mol Biol, Houston, TX 77030 USA

[5] Baylor Coll Med, Howard Hughes Med Inst, Houston, TX 77030 USA

[6] Baylor Coll Med, Dept Mol & Human Genet, Houston, TX 77030 USA

来源：

GENES & DEVELOPMENT | 2003年 / 17卷 / 08期

关键词：

RAD17; DNA damage; checkpoint; endoreduplication;

D O I：

10.1101/gad.1065103

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

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.

引用

页码：965 / 970

页数：6

共 29 条

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