Skip Navigation

This Article
Right arrow Full Text Freely available
Right arrow Print PDF (1210K) Freely available
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Search for citing articles in:
ISI Web of Science (8)
Right arrowRequest Permissions
Right arrow Commercial Re-use Guidelines
for Open Access NAR Content
Google Scholar
Right arrow Articles by Al-Moghrabi, N. M.
Right arrow Articles by Aboussekhra, A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Al-Moghrabi, N. M.
Right arrow Articles by Aboussekhra, A.
Social Bookmarking
 Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Nucleic Acids Research, 2001, Vol. 29, No. 10 2020-2025
© 2001 Oxford University Press

The Saccharomyces cerevisiae RAD9 cell cycle checkpoint gene is required for optimal repair of UV-induced pyrimidine dimers in both G1 and G2/M phases of the cell cycle

Nisreen M. Al-Moghrabi, Ibtehaj S. Al-Sharif and Abdelilah Aboussekhra*

King Faisal Specialist Hospital and Research Center, Department of Biological and Medical Research, MBC-03, PO Box 3354, Riyadh 11211, Kingdom of Saudi Arabia

Cells respond to DNA damage by activating both cellular growth arrest and DNA repair processes. In Saccharomyces cerevesiae the RAD9 gene controls DNA damage-mediated cell cycle arrest that is known to allow efficient repair. To ascertain whether RAD9 plays a role in DNA repair per se, the removal of UV-induced photolesions was assessed in synchronized isogenic normal and rad9{Delta} cells using the high resolution primer extension technique. The results show that RAD9 is indeed involved in the removal of photolesions from both the transcribed and the non-transcribed strands of the reporter GAL10 gene, in G1- as well as G2/M-arrested cells. Interestingly, these data also reveal that in both normal and rad9 mutant, the repair strand bias towards the transcribed stand is more pronounced in G2/M- than in G1-arrested cells. These data indicate that RAD9 coordinate the cellular response to DNA damage by activating both cell cycle checkpoint and excision repair.

* To whom correspondence should be addressed. Tel: +966 1 464 7272; Fax: +966 1 442 7858; Email: aboussekhra{at}kfshrc.edu.sa


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
CarcinogenesisHome page
M. A. Hannan, A. Hellani, F. M. Al-Khodairy, M. Kunhi, Y. Siddiqui, N. Al-Yussef, N. Pangue-Cruz, M. Siewertsen, M. N. Al-Ahdal, and A. Aboussekhra
Deficiency in the repair of UV-induced DNA damage in human skin fibroblasts compromised for the ATM gene
Carcinogenesis, October 1, 2002; 23(10): 1617 - 1624.
[Abstract] [Full Text] [PDF]



Disclaimer:
Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.