TABLE 1.
Cell cycle arrest and chromosomal aberrations after cross-linking of wild-type and Ercc1-Xpf mutant cells
Cell type | Treatment | No. of metaphases examined | % in first divisiona | % of metaphases with chromatid aberrationsb | % of metaphases with fusionsc | % of metaphases with chromosome aberrationsd |
---|---|---|---|---|---|---|
Wild-type ES | None | 59 | 0 | 0 | 0 | 0 |
3 μM MMC | 57 | 0 | 2 | 0 | 1 | |
Ercc1−/− ES | None | 64 | 0 | 20 | 0 | 12 |
300 nM MMC | 114 | 46 | 60e | 46e | 50e | |
Wild-type CHO | None | 50 | 6 | 0 | 0 | 0 |
10 μM cisplatin | 47 | 13 | 2 | 13 | 13 | |
Ercc1 mutant CHO | None | 50 | 10 | 0 | 0 | 2 |
1 μM cisplatin | 48 | 100 | 0 | 83 | 62 | |
Xpf mutant CHO | None | 50 | 9 | 4 | 0 | 0 |
1 μM cisplatin | 47 | 100 | 0 | 92 | 49 |
The remainder of the cells had completed a second division in the period following exposure to MMC.
Aberrations restricted to a single chromatid, including gaps, breaks, and radial structures.
Aberrations involving joining of two sister chromatids within a chromosome (ring structure) or different chromosomes (tri- or quadriradials).
Aberrations involving both sister chromatids, including gaps and breaks.
Forty-six percent of these occurred in cells arrested in the first division.