The XRCC2 human repair gene influences recombinational rearrangements leading to chromatid breaks

Citation
H. Mozdarani et al., The XRCC2 human repair gene influences recombinational rearrangements leading to chromatid breaks, INT J RAD B, 77(8), 2001, pp. 859-865
Citations number
40
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Experimental Biology
Journal title
INTERNATIONAL JOURNAL OF RADIATION BIOLOGY
ISSN journal
0955-3002 → ACNP
Volume
77
Issue
8
Year of publication
2001
Pages
859 - 865
Database
ISI
SICI code
0955-3002(200108)77:8<859:TXHRGI>2.0.ZU;2-L
Abstract
Purpose: To test the possible involvement of the XRCC2 gene in the control of intra-versus interchromatid rearrangements leading to chromatid breaks i n G(2) cells by studying the Colour-switch ratio (CSR) in harlequin-stained Chinese hamster irs1 cells. Materials and methods: The V79-1 mutant cell lines irs1 (XRCC2 mutation) an d irs2 (XRCC8 mutation), two WT V79 lines and GT621-1 (irs1 transfected wit h the XPLC2 gene) were labelled with BrdU through two cell cycles, irradiat ed and sampled 1.5 h after exposure. Metaphase spreads were analysed for ch romatid break frequency and frequencies of colour-switch (colour-switch bet ween chromatids at the break point) and non-colour-switch breaks, from Whic h the CSR was calculated. Results: Chromatid breaks were induced linearly with dose in all lines, and frequencies were elevated in irs1 and irs2 mutant Cell lines when Compared with WT lines. An XRCC2 transfected line (GT621-1) showed full radiosensit ivity complementation with respect to frequencies, of chromatid breaks. The CSR was significantly higher in irs1 (13.9%) than in the parental V79-4 (7 .5%) or irs2 (4.9%) cells. GT621-1 cells showed partial, but significant co mplementation with respect to CSR (9.2%). Conclusions: It is concluded that the significantly higher CSR for the irs1 mutant than for the Wild-type parental V79-4 line indicates the involvemen t of the XRCC2 gene product in the control of the rearrangement process lea ding to chromatid breaks.