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. 2019 Feb 4;38(22):4232–4249. doi: 10.1038/s41388-019-0723-8

Fig. 3.

Fig. 3

The G9a-binding defective mutant of cyclin D1 fails to augment H3K9me2. a Confocal microscopy of immunofluorescence for H3K9me2 (red) and nuclear staining with 4′,6-diamidino-2-phenylindole (DAPI; blue) in cyclin D1 wild-type and knockout mouse embryonic fibroblasts (MEFs), and cyclin D1−/− MEFs rescued with MSCV-cyclin D1WT-IRES-GFP, MSCV-cyclin D1C2-IRES-GFP, or vector control. Images demonstrate the reduction in H3K9me2 in cyclin D1−/− cells and rescue with cyclin D1WT. Scale bar, 40 μm with (b) quantitation of mean fluorescence shown as mean ± SEM. c Western blot of cyclin D1−/− MEFs rescued with MSCV-cyclin D1WT-IRES-GFP, MSCV-cyclin D1C2-IRES-GFP, or vector control, with antibodies as indicated