Journal
MUTATION RESEARCH-FUNDAMENTAL AND MOLECULAR MECHANISMS OF MUTAGENESIS
Volume 616, Issue 1-2, Pages 11-23Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/j.mrfmmm.2006.11.017
Keywords
sister-chromatid exchange; single-strand break DNA repair; CHO EM9; XRCC1; bloom syndrome; homologous recombination; DNA replication forks
Funding
- NATIONAL INSTITUTE ON AGING [Z01AG000743] Funding Source: NIH RePORTER
- NCI NIH HHS [CA11256] Funding Source: Medline
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Sister-chromatid exchange (SCE) is the process whereby, during DNA replication, two sister chromatids break and rejoin with one another, physically exchanging regions of the parental strands in the duplicated chromosomes. This process is considered to be conservative and error-free, since no information is generally altered during reciprocal interchange by homologous recombination. Upon the advent of non-radiolabel detection methods for SCE, such events were used as genetic indicators for potential genotoxins/mutagens in laboratory toxicology tests, since, as we now know, most forms of DNA damage induce chromatid exchange upon replication fork collapse. Much of our present understanding of the mechanisms of SCE stems from studies involving nonhuman vertebrate cell lines that are defective in processes of DNA repair and/or recombination. In this article, we present a historical perspective of studies spearheaded by Dr. Anthony V. Carrano and colleagues focusing on SCE as a genetic outcome, and the role of the single-strand break DNA repair protein XRCC1 in suppressing SCE. A more general overview of the cellular processes and key protein effectors that regulate the manifestation of SCE is also presented. (c) 2006 Elsevier B.V All rights reserved.
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