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  4. Understanding replication fork progression, stability, and chromosome fragility by exploiting the Suppressor of Underreplication protein

Understanding replication fork progression, stability, and chromosome fragility by exploiting the Suppressor of Underreplication protein

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Author(s)
Nordman, Jared T.
•
Orr-Weaver, Terry
Date Issued
July 2015
Journal
BioEssays
Publisher
Wiley Blackwell
Citation
Nordman, Jared T., and Terry L. Orr-Weaver. “Understanding Replication Fork Progression, Stability, and Chromosome Fragility by Exploiting the Suppressor of Underreplication Protein.” BioEssays 37.8 (2015): 856–861.
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Author's final manuscript
Abstract
There are many layers of regulation governing DNA replication to ensure that genetic information is accurately transmitted from mother cell to daughter cell. While much of the control occurs at the level of origin selection and firing, less is known about how replication fork progression is controlled throughout the genome. In Drosophila polytene cells, specific regions of the genome become repressed for DNA replication, resulting in underreplication and decreased copy number. Importantly, underreplicated domains share properties with common fragile sites. The Suppressor of Underreplication protein SUUR is essential for this repression. Recent work established that SUUR functions by directly inhibiting replication fork progression, raising several interesting questions as to how replication fork progression and stability can be modulated within targeted regions of the genome. Here we discuss potential mechanisms by which replication fork inhibition can be achieved and the consequences this has on genome stability and copy number control.
MIT Department
Massachusetts Institute of Technology. Department of Biology
Whitehead Institute for Biomedical Research
Terms of Use
Creative Commons Attribution-Noncommercial-Share Alike
http://creativecommons.org/licenses/by-nc-sa/4.0/
Persistent DSpace Link
http://hdl.handle.net/1721.1/106515
DOI of Published Version
https://doi.org/10.1002/bies.201500021
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