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Curr Biol. 2004 Dec 14;14(23):2107-12.

Chromosome fragmentation after induction of a double-strand break is an active process prevented by the RMX repair complex.

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1
Laboratory of Molecular Genetics, National Institute of Environmental Health Sciences, National Institutes of Health, 101 Alexander Drive, Research Triangle Park, NC 27709 USA.

Abstract

Chromosome aberrations are common outcomes of exposure to DNA-damaging agents or altered replication events and are associated with various diseases and a variety of carcinomas, including leukemias, lymphomas, sarcomas, and epithelial tumors. The incidence of aberrations can be greatly increased as a result of defects in DNA repair pathways. Although there is considerable information about the molecular events associated with the induction and repair of a double-strand break (DSB), little is known about the events that ultimately lead to translocations or deletions through the formation of chromosome breaks or the dissociation of broken ends. We describe a system for visualizing DNA ends at the site of a DSB in living cells. After induction of the break, DNA ends flanking the DSB site in wild-type cells remained adjacent. Loss of a functional RMX complex (Rad50/Mre11/Xrs2) or a mutation in the Rad50 Zn-hook structure resulted in DNA ends being dispersed in approximately 10%-20% of cells. Thus, the RMX complex holds broken ends together and counteracts mitotic spindle forces that can be destructive to damaged chromosomes.

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PMID:
15589152
DOI:
10.1016/j.cub.2004.11.051
[Indexed for MEDLINE]
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