Journal
JOURNAL OF NUCLEIC ACIDS
Volume 2010, Issue -, Pages -Publisher
HINDAWI LTD
DOI: 10.4061/2010/319142
Keywords
-
Categories
Funding
- Association for International Cancer Research [AICR 05-005]
- Dutch Cancer Society [EMCR 2005-3412]
- Ramon y Cajal Program (Ministerio de Ciencia e Innovacion)
- European Commission [512113]
- Netherlands Genomics Initiative/Netherlands Organization for Scientific Research (NWO)
Ask authors/readers for more resources
The ATR-Chk1 checkpoint pathway is activated by UV-induced DNA lesions and replication stress. Little was known about the spatio and temporal behaviour of the proteins involved, and we, therefore, examined the behaviour of the ATRIP-ATR and Rad9-Rad1-Hus1 putative DNA damage sensor complexes and the downstream effector kinase Chk1. We developed assays for the generation and validation of stable cell lines expressing GFP-fusion proteins. Photobleaching experiments in living cells expressing these fusions indicated that after UV-induced DNA damage, ATRIP associates more transiently with damaged chromatin than members of the Rad9-Rad1-Hus1 complex. Interestingly, ATRIP directly associated with locally induced UV damage, whereas Rad9 bound in a cooperative manner, which can be explained by the Rad17-dependent loading of Rad9 onto damaged chromatin. Although Chk1 dissociates from the chromatin upon UV damage, no change in the mobility of GFP-Chk1 was observed, supporting the notion that Chk1 is a highly dynamic protein.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available