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
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.