Home | Help | Feedback | Subscriptions | Archive | Search | Table of Contents

This Article Full Text Full Text (PDF, 1739K) PPT slides of all figures Supplemental Material Index Alert me when this article is cited Citation Map Services Email this article Similar articles in this journal Similar articles in PubMed Alert me to new content in the JCB Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Deckbar, D. Articles by Löbrich, M. Search for Related Content PubMed PubMed Citation Articles by Deckbar, D. Articles by Löbrich, M. Related Collections Related Article Social Bookmarking                            What's this?

Chromosome breakage after G2 checkpoint release

¹ Fachrichtung Biophysik, Universität des Saarlandes, 66421 Homburg/Saar, Germany
² Genome Damage and Stability Centre, University of Sussex, East Sussex BN1 9RQ, England, UK

Correspondence to Penny Jeggo: p.a.jeggo{at}sussex.ac.uk; or Markus Löbrich: markus.loebrich{at}uniklinik-saarland.de

DNA double-strand break (DSB) repair and checkpoint control represent distinct mechanisms to reduce chromosomal instability. Ataxia telangiectasia (A-T) cells have checkpoint arrest and DSB repair defects. We examine the efficiency and interplay of ATM's G2 checkpoint and repair functions. Artemis cells manifest a repair defect identical and epistatic to A-T but show proficient checkpoint responses. Only a few G2 cells enter mitosis within 4 h after irradiation with 1 Gy but manifest multiple chromosome breaks. Most checkpoint-proficient cells arrest at the G2/M checkpoint, with the length of arrest being dependent on the repair capacity. Strikingly, cells released from checkpoint arrest display one to two chromosome breaks. This represents a major contribution to chromosome breakage. The presence of chromosome breaks in cells released from checkpoint arrest suggests that release occurs before the completion of DSB repair. Strikingly, we show that checkpoint release occurs at a point when approximately three to four premature chromosome condensation breaks and 20 H2AX foci remain.

CiteULike    Complore    Connotea    Del.icio.us    Digg    Facebook    Reddit    Technorati    Twitter    What's this?

Related Article

A sloppy checkpoint

Mitch Leslie
J. Cell Biol. 2007 176: 731. [Full Text] [PDF]

This article has been cited by other articles:

• Dodson, H., Morrison, C. G. (2009). Increased sister chromatid cohesion and DNA damage response factor localization at an enzyme-induced DNA double-strand break in vertebrate cells. Nucleic Acids Res 37: 6054-6063 [Abstract] [Full Text]  
• Forand, A., Fouchet, P., Lahaye, J.-B., Chicheportiche, A., Habert, R., Bernardino-Sgherri, J. (2009). Similarities and Differences in the In Vivo Response of Mouse Neonatal Gonocytes and Spermatogonia to Genotoxic Stress. Biol. Reprod. 80: 860-873 [Abstract] [Full Text]  
• Kinner, A., Wu, W., Staudt, C., Iliakis, G. (2008). {gamma}-H2AX in recognition and signaling of DNA double-strand breaks in the context of chromatin. Nucleic Acids Res 36: 5678-5694 [Abstract] [Full Text]  
• Huang, H., Fletcher, L., Beeharry, N., Daniel, R., Kao, G., Yen, T. J., Muschel, R. J. (2008). Abnormal Cytokinesis after X-Irradiation in Tumor Cells that Override the G2 DNA Damage Checkpoint. Cancer Res. 68: 3724-3732 [Abstract] [Full Text]  
• Toden, S., Bird, A. R., Topping, D. L., Conlon, M. A. (2007). High red meat diets induce greater numbers of colonic DNA double-strand breaks than white meat in rats: attenuation by high-amylose maize starch. Carcinogenesis 28: 2355-2362 [Abstract] [Full Text]  

Home | Help | Feedback | Subscriptions | Archive | Search | Table of Contents