Previous work has shown that an origin-deficient YAC (5ORIdeltaYAC) induces a novel checkpoint. This checkpoint is independent of DNA damage. It is also different from the HU-induced replication checkpoint because replication forks do not stall and Rad53 is not activated. Therefore, it was postulated that this novel checkpoint monitors ongoing DNA synthesis. Interestingly, Rad9 was found essential for maintaining this checkpoint, indicating a previously unknown role of Rad9 in monitoring S phase progression in a normal cell cycle. A genetic screen will be conducted to identify additional components of this novel checkpoint pathway. This work will contribute to our understanding of how checkpoint mechanisms operate during an unperturbed cell cycle. It will also further our understanding of how cancer cells escape cell cycle and checkpoint control, leading to genome instability.

Agency
National Institute of Health (NIH)
Institute
National Institute of General Medical Sciences (NIGMS)
Type
Postdoctoral Individual National Research Service Award (F32)
Project #
1F32GM069080-01
Application #
6691504
Study Section
Special Emphasis Panel (ZRG1-F05 (20))
Program Officer
Tompkins, Laurie
Project Start
2003-08-01
Project End
2006-07-31
Budget Start
2003-08-01
Budget End
2004-07-31
Support Year
1
Fiscal Year
2003
Total Cost
$41,608
Indirect Cost
Name
University of Washington
Department
Genetics
Type
Schools of Medicine
DUNS #
605799469
City
Seattle
State
WA
Country
United States
Zip Code
98195