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. 2010 Nov 30;124(1):68–81. doi: 10.1242/jcs.071340

Fig. 4.

Fig. 4.

DNA-SCARS do not depend on selected DNA repair or signaling proteins. (A) HCA2 cells were infected at PD25 with a lentivirus expressing GSE22, then stained at PD35 for p53 (blue) and PML (red) (upper-left panel) or 53BP1 (red) and PML (green) (upper-right panel). HCA2 cells were infected at PD35 with a retrovirus expressing E7, then stained at PD50 for E7 (blue) and PML (red) (middle-left panel) or 53BP1 (red) and PML (green) (middle-right panel). HCA2 cells were infected at PD40 with a lentivirus expressing SV40LT, then stained at PD55 for SV40LT (blue) and PML (red) (lower-left panel) or for 53BP1 (red) and PML (green) (lower-right panel). (B) Early-passage primary human fibroblasts deficient for ATM, ATR, NBS1, BLM or Artemis were irradiated with 8 Gy. At the indicated intervals thereafter, they were fixed and stained for 53BP1 and PML. Cell populations were scored for the percentage of cells harboring three or more 53BP1 foci, most of which (>75%) colocalized with PML NBs. (C) HCA2 cells at PD25 were infected with retroviruses expressing eGFP (control, left panel), iE1 (middle panel) or PML-RAR (right panel). At PD29, the infected cells were stained for PML. (D) HCA2 cells expressing eGFP, iE1 or PMLRAR (PD30) were irradiated with 0.5 or 10 Gy. At the indicated intervals thereafter, they were stained for 53BP1 foci. Populations were scored for the percentage of cells having three or more 53BP1 foci.