Radiation-induced chromosome breaks in ataxia-telangiectasia cells remain open.
OBJECTIVE
To determine if broken chromosome-end healing mechanisms through the addition of new telomeric sequences exist in cells having difficulties in rejoining the ends of broken chromosomes.


METHODS
A full-colour painting protocol of all human chromosomes by FISH was combined with a telomeric and centromeric labelling using PNA probes to characterize the rejoining pattern and telomere status of radiation-induced chromosome breaks in ataxia-telangiectasia (A-T) and normal lymphoblastoid cell lines.


RESULTS
It was first established that the cell lines used for chromosome healing analysis were chromosomally stable. FISH analysis provided evidence that the frequency of deleted chromosomes, apparently unrejoined, was much higher in A-T than in normal cells, as expected by the role of ATM in cell-cycle control, as well as in DNA repair. In spite of their high frequency, broken chromosome ends in A-T cells do not seem to act as substrates for telomerase since additional terminal telomere sequences (more than the 92 expected pairs) indicative of chromosome healing were never observed. Broken chromosome ends in A-T cells remained open.


CONCLUSIONS
The disability of cells to rejoin broken chromosome ends does not lead to the healing of DSBs by the acquisition of new telomeric sequences.
Departament Biologia Cel.lular, Fisiologia i Immunologia, Universitat Autònoma de Barcelona, E-08193 Bellaterra, Spain.
M
M
Martín
A
A
Genescà
L
L
Latre
M
M
Ribas
R
R
Miró
J
J
Egozcue
L
L
Tusell
D001260:Ataxia Telangiectasia / Q000235:genetics* / Q000473:pathology*; D002869:Chromosome Aberrations; D002875:Chromosomes / Q000528:radiation effects* / Q000648:ultrastructure; D004249:DNA Damage; D004260:DNA Repair; D005720:Gamma Rays; D006801:Humans; D017404:In Situ Hybridization, Fluorescence; D008677:Metaphase; D008856:Microscopy, Fluorescence; D016615:Telomere / Q000648:ultrastructure