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. 2020 Jun 5;16(6):e1008799. doi: 10.1371/journal.pgen.1008799

Fig 3. Telomeres uncapping, telomere replication defect and fragile telomeres induced by BRM depletion.

Fig 3

(A) Metaphase telomere FISH detection of telomere loss and fusion or multiple telomeres signals at ends of chromosomes. Control or BRM-depleted VA13 cells were treated with nocodazole for 6 h, and subjected to FISH. (B) Q-FISH assay to determine telomere length of control and BRM-depleted VA13 cells. Number of telomeres analyzed (n) is indicated in figures, red bar indicated the average length of telomeres. (C) Quantification of (A). The percentage of chromosomes with one or more telomere-free ends was calculated. Data represent the mean ± SEM of three independent experiments, ***P < 0.001, ****P < 0.0001. (D) Quantification of (A). The percentage of chromosomes with fusion was calculated. Data represent the mean ± SEM of three independent experiments, **P < 0.001. (E) Quantification of (A). The percentage of fragile telomeres was calculated. Data represent the mean ± SEM of three independent experiments, **P < 0.001. (F) IF-FISH detection of PCNA foci in control and BRM-depleted VA13 cells. (G) Quantification of (F). Data represent the mean ± SEM of three independent experiments (n ≥ 100 cells), *P < 0.05, **P < 0.01. (H) IF-FISH detection of RPA1 foci in control and BRM-depleted VA13 cells. (I) Quantification of (H). Data represent the mean ± SEM of three independent experiments (n ≥ 100 cells), **P < 0.01, ***P < 0.001.