Early G2/M checkpoint failure as a molecular mechanism underlying etoposide-induced chromosomal aberrations
J. Clin. Invest. Shinichiro Nakada, et al. 116:80 doi:10.1172/JCI25716 [
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Figure 3FISH analysis for chromosome 11. (
A) Representative image of metaphase ATM-deficient fibroblasts hybridized with the CH11C probe (green) and MLL probes (green and red overlap). Chromosomes were stained by DAPI. The arrows indicate overlapping MLL signals. (
B) Representative image of metaphase ATM-deficient fibroblasts hybridized with probes for whole chromosome 11 (red) and MLL (green and red overlap). (
C) Flow diagram of the cell fractionation procedure. (
D) Etoposide-treated postmitotic G1 phase ATM-deficient fibroblasts with 1 (upper panel) and 3 (lower panel) centromeric 11q23 signals. (
E) Proportion of metaphase and postmitotic G1 phase cells with gain (red) and loss (blue) of CH11C (left) or centromeric 11q23 (right) probe signals.
n > 250 for each. *Odds ratio (OR) for etoposide treatment. **
P = 0.77 and
†P < 0.0001, differences in OR between postmitotic G1 and metaphase cells when cells were hybridized with CH11C and centromeric 11q23 probes, respectively (
P for interaction term of cell cycle phase × treatment by a logistic regression model). (
F) Micronuclei containing centromeric 11q23 signals (arrows). Cells were hybridized with centromeric 11q23 probes. Original magnification of FISH images, ×600.
