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. 2019 Jan 21;20(3):e46821. doi: 10.15252/embr.201846821

Figure 5. Cells lacking KMT2C are HR‐deficient.

Figure 5

  1. Immunofluorescence of γH2AX foci (left) and quantitation (right) in control (Scr) and KMT2C‐knockdown (KMT2C/KD1 and KD2) HTB9 cells. BRCA1 knockdown (BRCA1/KD) is used as control. The y‐axis indicates added percentage of cells with 1–5 and > 5 foci for each cell type. Scale bars indicate 5 μm. All comparisons have been performed against Scr control cells. Values in the bargraph represent mean ± SEM from three experiments. Student's t‐test was used. * designates P‐value < 0.05, and ** designates P‐value < 0.01.
  2. Frequency of RAD51 foci in cisplatin‐treated HTB9 control (Scr) and KMT2C‐knockdown (KD1) cells. The y‐axis indicates added percentage of cells with 1–3 and 3 foci. Scale bars indicate 10 μm. Values in the bargraph represent mean ± SEM from three experiments. Student's t‐test was used. * designates P‐value < 0.05, and ** designates P‐value < 0.01.
  3. Sister chromatid exchange (SCE) assay with cisplatin‐treated HTB9 control (Scr) and KMT2C‐knockdown (KD1) cells. Red arrowheads indicate sister chromatid exchange events. Results were obtained from 15 metaphases per group. Mann–Whitney U‐test was used.
  4. DNA fiber assay on control (Scr) and KMT2C‐knockdown (KD1) HTB9 cells. BRCA1‐knockdown cells are used as controls. Experiments performed with or without hydroxyurea (HU) treatment under the conditions indicated in the schematic. Examples of DNA fibers from HTB9/KD1 cells are shown. The length of minimum 100 fibers from each condition was measured. Values in the plot are means ± SEM. Mann–Whitney U‐test was used. ** designates P‐value < 0.01.