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. 2023 Jun 7;619(7968):184–192. doi: 10.1038/s41586-023-06157-7

Fig. 3. MN bodies exhibit transcription defects and extensive DNA damage.

Fig. 3

a, Defective transcription and H3K27ac in MN bodies. Top, scheme of the experiment (time points are approximate). IF, immunofluorescence imaging. Bottom, representative images of a daughter cell with a MN body from a ruptured micronucleus. Magenta dashed lines indicate a MN body with low RNAP2-Ser5ph and low H3K27ac levels. Scale bars, 5 µm. b, Aggregate data of relative MN body fluorescence intensities (FI) for RNAP2-Ser5ph and H3K27ac as in a (left to right, n = 43 and 41 from 8 experiments). Boxes are median with 95% CI; P values from two-tailed Mann–Whitney test comparing the FI ratio between MN and control PN region in the same cell. c, Decrease in RNAP2-Ser5ph in MN bodies verified by fixed imaging. Cells were fixed approximately 45 h after mitotic shake-off. MN bodies were identified on the basis of the endogenous MDC1 signal. Data points represent relative FI of RNAP2-Ser5ph in MN bodies against control regions (n = 1,447 from 12 experiments). Boxes are median with 95% CI; two-tailed Mann–Whitney test. d, Decrease in H3K27ac in MN bodies (n = 341 from 2 experiments). e, DNA damage in MN bodies. FI measurements of γH2AX intensity (94% of MN bodies were positive, >3 s.d. above the mean of the corresponding nuclear background; n = 195 from 2 experiments). f, 53BP1 accumulation within MN bodies as in e (82% of MN bodies were positive for 53BP1; n = 211, from two experiments). Analyses in df are similar to c.

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