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. Author manuscript; available in PMC: 2011 Apr 16.
Published in final edited form as: Cell. 2010 Apr 1;141(2):243–254. doi: 10.1016/j.cell.2010.03.012

Figure 2. Deletion of 53BP1 reverses sensitivity of Brca1Δ11/Δ11 cells to PARPi and camptothecin.

Figure 2

(A) Analysis of genomic instability in metaphases from B cells treated with 0, 10 nM and 1μM PARP inhibitor. Charts show the number of radial chromosomes, chromatid breaks and chromosome breaks per 100 metaphases (n=50 metaphases analyzed in each case). Note that genomic instability in Brca1Δ11/Δ11 cells is independent of p53 status and equivalent results were seen in Brca1Δ11/Δ11 p53+/- and Brca1Δ11/Δ11 p53-/- cells. (B) Western blot showing Kap1 phosphorylation in B cells from the indicated genotypes treated with PARP inhibitor or 5Gy ionizing radiation. (C) Analysis of genomic instability in metaphases from B cells treated with 4nM camptothecin (CPT). B cells were cultured overnight with CPT prior to fixation and preparation of metaphase slides.