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. 2020 Apr 22;12(4):1028. doi: 10.3390/cancers12041028

Figure 5.

Figure 5

The presence of telomerase leads to a reorganization of telomeric chromatin, decrease DDR and replication stress. (a,c,e) Fluorescent microscope images of a single plane of focus of representative ALT, and telomerase+ human brain tumor cells, stained by immunofluorescence (green) combined with Q-FISH (magenta). Antibody against replication stress marker (a, RPA70), DNA damage marker (c, γH2AX), and chromatin methylation marks (e, H3K9me3) were used and counterstaining with DAPI. Insets, dashed frames and arrows show co-localization of immunofluorescence and Q-FISH spots. Scale bar: 5 µm. (b,d,f) Immunofluorescence quantification expressed as the number of foci per nucleus that colocalized with telomeres (n = 25–60 nuclei) for the corresponding samples in (a,c,e); * p < 0.05, *** p < 0.001 between the indicated groups. (g) Fluorescent microscope images of representative ALT and telomerase+ zebrafish brain tumor cells, stained by immunofluorescence (green) combined with Q-FISH (magenta). Antibody against a replication stress marker (RPA70), were used and counterstained with DAPI. Scale bar: 5 µm. (h) Immunofluorescence quantification expressed as the number of foci that colocalized with telomeres per nucleus (n = 25–60 nuclei) for the corresponding samples in (g); * p < 0.05, *** p < 0.001 between the indicated groups.