Fig. 2.

BAZ1A and BAZ1B accumulate independently to sites of DNA damage and recruit SMARCA5. a Accumulation of endogenous SMARCA5, BAZ1A, and BAZ1B at sites of laser micro-irradiation in parental HeLa cells. The genetic background is indicated on top of the panels. Regions of DNA damage are identified by the presence of γ-H2AX (histone variant H2A.X phosphorylated on S139), and are labeled with cyan arrowheads. Images are representative of at least five individual irradiated cells. Scale bar, 10 μm. b Accumulation of endogenous BAZ1A and BAZ1B at sites of laser micro-irradiation in genome edited BAZ1A-KO and BAZ1B-KO cells. Scale bar, 10 μm. c Accumulation of endogenous SMARCA5 at sites of DNA damage in cells subjected to UVC irradiation through a 5 μm porous membrane⁴⁷. Each square panel is composed of two rectangular representative images showing 6–10 nuclei. The genetic background is indicated on top of the panels. Cyan arrowheads indicate sites of damage identified by the presence of γ-H2AX (top), with concomitant increased SMARCA5 signal (bottom). In contrast, red arrowheads indicate sites of damage without appreciable corresponding SMARCA5 signal. Scale bar, 20 μm. d Recruitment of SMARCA5 as quantified from six independent experiments is shown as histograms of the mean value ± s.e.m and normalized to recruitment in parental cells; the total number of nuclei examined for each case is reported on the figure. The values from individual experiments are shown with black dots. P-values (P < 0.01) were calculated using a two-tailed Mann–Whitney test; n.s. not significant (P > 0.05)