CHROMOSOME HEALING, TELOMERE CAPTURE AND MECHANISMS OF RADIATION-INDUCED CHROMOSOME BREAKAGE

Citation
P. Slijepcevic et Pe. Bryant, CHROMOSOME HEALING, TELOMERE CAPTURE AND MECHANISMS OF RADIATION-INDUCED CHROMOSOME BREAKAGE, International journal of radiation biology, 73(1), 1998, pp. 1-13
Citations number
72
Categorie Soggetti
Radiology,Nuclear Medicine & Medical Imaging","Biology Miscellaneous
ISSN journal
09553002
Volume
73
Issue
1
Year of publication
1998
Pages
1 - 13
Database
ISI
SICI code
0955-3002(1998)73:1<1:CHTCAM>2.0.ZU;2-C
Abstract
Background: It is generally assumed that radiation-induced chromosome breaks are the result of a cell's inability to rejoin DNA double-stran d breaks (dsb), but the exact mechanisms underlying the failure to rej oin some dsb and the conversion of these lesions into chromosome break s are poorly understood at present. II has been speculated that the co nversion of dsb into chromosome breaks, following exposure of mammalia n cells to ionizing radiation, may be mediated by the enzyme telomeras e. Telomerase is a reverse transcriptase that has two distinct functio ns, to replicate pre-existing chromosome ends (telomeres) and to heal broken chromosomes by de novo addition of telomeric sequences directly on to non-telomeric DNA. Alternatively, dsb may be converted into chr omosome breaks by a telomerase-independent mechanism termed telomere c apture. Purpose: To review telomere biology and to examine the signifi cance of chromosome healing and telomere capture mechanisms for radiat ion cytogenetics. Conclusions: The currently available literature sugg ests that telomere capture may be a more frequent mechanism for stabil ization of broken chromosomes in mammalian cells than telomerase-media ted chromosome healing. However, a definitive conclusion must await im provements in the resolution of molecular cytogenetic techniques to a degree which allows telomerase products to be clearly distinguishable from subtelomeric cryptic translocations indicative of telomere captur e.