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Published online before print April 2, 2003, 10.1101/gad.1065103
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Vol. 17, No. 8, pp. 965-970, April 15, 2003

RESEARCH COMMUNICATION
Genomic instability and endoreduplication triggered by RAD17 deletion

Xin Wang,1 Lee Zou,2,3 Huyong Zheng,1 Qingyi Wei,4 Stephen J. Elledge,2,3,5 and Lei Li1,6,7

1 Departments of Experimental Radiation Oncology, 4 Epidemiology, and 6 Molecular Genetics, University of Texas M.D. Anderson Cancer Center, Houston, Texas 77030; 2 Verna & Mars McLean Department of Biochemistry and Molecular Biology, 3 Howard Hughes Medical Institute, and 5 Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, Texas 77030, USA

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: RAD17; DNA damage; checkpoint; endoreduplication]

7 Corresponding author.

© 2003 by Cold Spring Harbor Laboratory Press  ISSN 0890-9369/03 $5.00
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