The absence of TDP2 increases etoposide-induced genome instability in mammalian cells.

<p>A. Micronuclei (MN, left) and nucleoplasmic bridges (NB, right) in binucleated (following cytochalasin B-mediated cell cycle arrest) <i>Tdp2^+/+</i> and <i>Tdp2^Δ1–3</i> transformed MEFs following acute treatment (30 min) with indicated dose of etoposide. See insets for representative images. Histogram bars represent the average ± s.e.m. of n≥600 cells coming from three independent experiments. Statistical significance by Mann-Whitney test. B. Primary MEFs in the absence of cytochalasin B treatment (n≥1500). Other details as in “A”. C. Break-type (left) and exchange-type (right) chromosomal aberrations in transformed <i>Tdp2^+/+</i> and <i>Tdp2^Δ1–3</i> MEFs following acute treatment (30 min) with indicated dose of etoposide. See insets for a representative image. Plots show the number of breaks/exchanges per 100 chromosomes from individual metaphase spreads (n = 100) obtained in at least two independent experiments. Average ± s.e.m. and statistical significance by Mann-Whitney test is also indicated. D. Metaphase spreads from primary MEFs (n = 50). Caffeine was added 4 h after etoposide treatment. Other details as in “C”.