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    Intestinal stem cells protect their genome by selective segregation of template DNA strands.

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    Authors
    Potten, Christopher S
    Owen, Gary
    Booth, Dawn
    Affiliation
    Epithelial Biology Department, Paterson Institute for Cancer Research, Christie Hospital NHS Trust, Wilmslow Road, Manchester M20 4BX, UK. potten@epistem.co.uk
    Issue Date
    2002-06-01
    
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    Abstract
    The stem cells in the crypts of the small intestinal mucosa divide about a thousand times during the lifespan of a laboratory mouse, and yet they show little evidence of any decline in proliferative potential and rarely develop carcinogenic mutations, suggesting that their genome is extremely well protected. Protection against DNA-replication-induced errors can be achieved by the selective sorting of old (template) and new DNA strands with all template strands retained in the stem cell line. The template strands in the stem cells can be labelled during development or during tissue regeneration using tritiated thymidine ((3)HTdR). Labelling newly synthesised strands with a different marker (bromodeoxyuridine, BrdUrd) allows segregation of the two markers to be studied. Template strand label is retained ((3)HTdR), whereas label in the newly synthesised strands (BrdUrd) is lost following the second division of the stem cell. Random errors may occur in the template strands owing to environmental elements. These are protected against by the altruistic cell suicide (apoptosis) of the cells incurring such errors. A final level of protection for the tissue compensates for excessive deletion of stem cells via the apoptosis pathway. This is achieved by a hierarchical age structure in the stem cell compartment, with some cells being able to efficiently repair DNA damage and hence being more radioresistant. The presence of these protective mechanisms ensures that the small intestine rarely develops cancer and that stem cells can sustain the extensive cell proliferation needed during life.
    Citation
    Intestinal stem cells protect their genome by selective segregation of template DNA strands. 2002, 115 (Pt 11):2381-8 J. Cell. Sci.
    Journal
    Journal of Cell Science
    URI
    http://hdl.handle.net/10541/84316
    PubMed ID
    12006622
    Type
    Article
    Language
    en
    ISSN
    0021-9533
    Collections
    All Paterson Institute for Cancer Research

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