Abstract
Common fragile sites (CFSs) are large chromosomal regions long identified by conventional cytogenetics as sequences prone to breakage in cells subjected to replication stress. The interest in CFSs came from their key role in the formation of DNA damage, resulting in chromosomal rearrangements. The instability of CFSs was notably correlated with the appearance of genome instability in precancerous lesions and during tumor progression. Identification of the molecular mechanisms responsible for their instability therefore represents a major challenge. A number of data show that breaks result from mitotic entry before replication completion but the mechanisms responsible for such delayed replication of CFSs and relaxed checkpoint surveillance are still debated. In addition, clues to the molecular events leading to breakage just start to emerge. We present here the results of recent reports addressing these questions.
Highlights
The replication process should be as reliable as possible in order to minimize mutations, but some regions of the genome, notably common fragile sites (CFSs), appear to raise specific problems
Common fragile sites (CFSs) are large chromosomal regions long identified by conventional cytogenetics as sequences prone to breakage in cells subjected to replication stress
To reconcile this whole set of results, we propose the following scenario: upon replication stress, forks traveling along the initiation-poor core of CFSs may further slow down or stall if they encounter impediments such as DNA secondary structures
Summary
Updating the mechanisms of common fragile site instability: how to reconcile the different views?. This article is published with open access at Springerlink.com
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