Quick Search:

uzh logo
Browse by:


Zurich Open Repository and Archive

Permanent URL to this publication: http://dx.doi.org/10.5167/uzh-31254

Sogo, J M; Lopes, M; Foiani, M (2002). Fork reversal and ssDNA accumulation at stalled replication forks owing to checkpoint defects. Science, 297(5581):599-602.

[img] PDF - Registered users only
View at publisher


Checkpoint-mediated control of replicating chromosomes is essential for preventing cancer. In yeast, Rad53 kinase protects stalled replication forks from pathological rearrangements. To characterize the mechanisms controlling fork integrity, we analyzed replication intermediates formed in response to replication blocks using electron microscopy. At the forks, wild-type cells accumulate short single-stranded regions, which likely causes checkpoint activation, whereas rad53 mutants exhibit extensive single-stranded gaps and hemi-replicated intermediates, consistent with a lagging-strand synthesis defect. Further, rad53 cells accumulate Holliday junctions through fork reversal. We speculate that, in checkpoint mutants, abnormal replication intermediates begin to form because of uncoordinated replication and are further processed by unscheduled recombination pathways, causing genome instability.


470 citations in Web of Science®
480 citations in Scopus®
Google Scholar™



0 downloads since deposited on 09 Jul 2010
0 downloads since 12 months

Additional indexing

Item Type:Journal Article, refereed, original work
Communities & Collections:04 Faculty of Medicine > Institute of Molecular Cancer Research
07 Faculty of Science > Institute of Molecular Cancer Research
Dewey Decimal Classification:570 Life sciences; biology
Deposited On:09 Jul 2010 09:10
Last Modified:02 Dec 2013 08:50
Publisher:American Association for the Advancement of Science (AAAS)
Publisher DOI:10.1126/science.1074023
PubMed ID:12142537

Users (please log in): suggest update or correction for this item

Repository Staff Only: item control page