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• W2090763635 abstract "In a recent review article published in Radiation Research (1), it is suggested that: Based upon the information presented earlier in this section, it is more than likely that any unrejoined chromosome ends formed by chromosome breakage will be capped by a telomere, by telomerase in dividing cells where telomerase can be active or by a proposed telomerase-independent mechanism. We would like to add several more published observations that may refine the above possibility. For example, it has been shown that in recombination-deficient yeast cells only 1% of chromosome breaks induced by HO-endonuclease (which generates a DNA double-strand break within the MA T locus on chromosome 3), exhibited new telomeres (2). Formation of new telomeres, presumably by telomerase, occurred exclusively when telomeric sequences were present proximal to the break site (2). A study of spontaneous and radiation-induced chromosome breakage in mammalian cells suggested a similar possibility, i.e. that arrays of interstitial telomeric sequences represent preferential sites for telomerase-mediated chromosome healing (2). Selectivity in the formation of new telomeres in mammalian cells is further emphasized by the observations that new telomeres formed by telomere capture, or telomere seeding, are usually close to pre-existing telomeres (4, 5). In addition to these results, it has been shown that a yeast chromosome in which one telomere was eliminated by sitespecific chromosome breakage could be propagated for as many as 10 cell cycles without being capped by a new telomere (6). Similarly, Drosophila broken chromosomes (Drosophila has non-canonical telomeres) could be propagated without capping broken ends by addition of new sequences (7). Taken together, these results suggest that (1) capping of chromosome breaks by new telomeres is a rare and highly selective process (developmentally programmed chromosome fragmentation and healing in ciliates may be an exception), and (2) under certain circumstances br ken chromosomes can be propagated without being capped by new acquisition of classical telomeres. These processes include retroposon-mediated repair of chromosome breaks (8, 9), acquisition of telomere function by satellite sequences (10) and heterochromatinization of broken chromosome ends designed to mimic natural telomeres (11)." @default.
• W2090763635 created "2016-06-24" @default.
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• W2090763635 date "1997-09-01" @default.
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• W2090763635 title "Telomere-Mediated Chromosome Healing" @default.
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• W2090763635 doi "https://doi.org/10.2307/3579614" @default.
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