Telomere maintenance: All's well that ends well

Sir William Dunn School of Pathology, University of Oxford, Oxford, UK.
Archives of Toxicology (Impact Factor: 5.98). 05/2009; 83(5):407-16. DOI: 10.1007/s00204-009-0423-1
Source: PubMed


The nucleoprotein structures termed telomeres serve to prevent the mis-identification of eukaryotic chromosome ends as sites of DNA damage, but are also among the genomic regions that pose the most problems during DNA replication. Here, we summarize some of the apparent difficulties encountered by the DNA replication machinery when it approaches the chromosome ends. Eukaryotic cells have evolved diverse mechanisms to overcome these problems, underlining the importance of telomere maintenance for a number of aspects of chromosome function. Of particular interest in this respect are the ways in which telomere-binding proteins and components of the DNA damage response machinery may facilitate replication fork progression through telomeres.

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    • "Genetic instability (Florl and Schulz 2008; Hengstler and Bolt 2007, 2008; Stoiber et al. 2008; Beyersmann and Hartwig 2008) and DNA damage induction (Bolt 2008; Periyakaruppan et al. 2007; Borza et al. 2008; Bolt and Hengstler 2008; Zhang et al. 2008; Wong et al. 2008; Glahn et al. 2008; Krishnamurthi et al. 2008; Ullmann et al. 2008; Wozniak et al. 2007; Schmid et al. 2007; Nishimura et al. 2008; Schug et al. 2008) are examples of cutting-edge topics reported in our journal. Therefore, the editors are delighted by the contribution of Dr. Li Phing Liew and Dr. Chris J. Norbury from Oxford University to the current issue of Archives of Toxicology on telomere maintenance (Liew and Norbury 2009, this issue). In addition to providing a comprehensive review about the mechanisms and relevance of telomere maintenance , the authors also focus on the question how the double-stranded ends of chromosomes can be distinguished from the potentially catastrophic DNA double-strand breaks, although the chemical composition of broken DNA within the chromosomes does not obviously diVer from normal DNA at the end of the chromosomes. "

    Archives of Toxicology 05/2009; 83(5):405-6. DOI:10.1007/s00204-009-0428-9 · 5.98 Impact Factor
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    Archives of Toxicology 09/2009; 83(11):961-3. DOI:10.1007/s00204-009-0471-6 · 5.98 Impact Factor

  • General, Applied and Systems Toxicology, 09/2011; , ISBN: 9780470744307

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