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. Author manuscript; available in PMC: 2013 Dec 6.
Published in final edited form as: Cell. 2013 May 30;153(6):1266–1280. doi: 10.1016/j.cell.2013.05.023

Figure 4. PTIP is required for NHEJ of dysfunctional telomeres.

Figure 4

(A) WT and PTIP−/− MEFs were infected with a retrovirus expressing either an empty vector or shRNA against TRF2 (shTRF2), and phosphorylated KAP1 (pKAP1) levels were measured by flow cytometry. (B) γ-H2AX (green) in telomere-dysfunction induced foci (TIF) generated in shTRF2-infected WT cells. PNA probe is shown in red, and images are merged on top of DAPI (blue). Scale bar represents 10 μm. (C) Representative images of a metaphase spread from WT and PTIP−/− MEFs infected with shTRF2. Telomere fusions are visualized by a telomeric PNA probe (red) and DAPI (blue). Arrows point to representative telomeric fusions. (D) Quantitation of telomeric fusion frequencies. At least 1800 chromosomes from each genotype were analyzed. Mean value derived from 3 independent experiments. **: p<0.01 (two-tailed unpaired t-test). (E) Distribution of telomeric fusions per metaphase in WT and PTIP−/− MEFs. At least 30 cells were examined in each of 3 independent experiments. p(chi-squared)<1×10−5.