Mo. Sikpi et al., DEFECTIVE MODULATION OF DOUBLE-STRAND BREAK REPAIR IN ATAXIA-TELANGIECTASIA CELLS BY GAMMA-RADIATION, Radiation research, 150(6), 1998, pp. 627-635
Citations number
47
Categorie Soggetti
Biology Miscellaneous","Radiology,Nuclear Medicine & Medical Imaging
Ataxia telangiectasia (AT) cells are defective in responding to damage
induced by ionizing radiation. To study the modulation of double-stra
nd break (DSB) repair by ionizing radiation and a defect in such modul
ation in AT cells, we compared processing of linearized shuttle vector
pZ189 (linear DNA) by unirradiated or gamma-irradiated normal and AT
lymphoblast hosts. The linear DNA processed in unirradiated AT and nor
mal host cells yielded similar mutation frequencies in the supF-tRNA t
arget gene. Irradiation of normal but not AT host cells decreased plas
mid mutation frequency 2-fold if transfection occurred immediately. Ho
wever, if transfection occurred 2 h after host cell irradiation, mutat
ion frequencies increased 2-fold above those in unirradiated controls
in both normal and AT hosts. DSB rejoining capability, based on the ra
tio of the number of progeny arising from equal amounts of linear DNA
and supercoiled, undamaged pZ189, was 25- to 50-fold higher in normal
than in AT hosts when both were unirradiated. Irradiation decreased DS
B rejoining capability 2- to 5-fold in normal hosts but did not alter
that of AT hosts. These findings demonstrate that AT cells normally re
join DSBs as accurately as normal cells but do so less often, and that
AT cells are defective in modulation of DSB rejoining by ionizing rad
iation, (C) 1998 by Radiation Research Society.