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. 2019 Jun 17;116(27):13311–13319. doi: 10.1073/pnas.1903847116

Fig. 3.

Fig. 3.

Pak2 is required for de novo H3.3 deposition in senescence cells. (A and B) H3.3 occupancy at the (A) p16INK4a transcription start site (TSS) and (B) IL-6 enhancer region was determined by ChIP-qPCR (n = 3, mean ± SEM, *P < 0.05, **P < 0.01). Values were normalized to input. (C) Experimental scheme for in vivo quench–chase–pulse (QCP)-SNAP labeling of de novo assembly of H3.3 in senescent IMR90 cells overexpressing H3.3-SNAP. (D) Western blotting analysis of lysates from IMR90 cells expressing H3.3-SNAP treated in C. Membranes were probed for the indicated antibodies. α-Tubulin was used as a loading control. (E and F) Pak2 and HIRA depletion compromised the deposition of newly synthesized H3.3 in senescent cells. Pak2 was depleted in H3.3-SNAP-tagged IMR90 cells. After old H3.3-SNAP was blocked using a nonfluorescent blocker, new H3.3-SNAP was labeled with TMR-STAR (the red fluorescent substrate for the SNAP tag) and visualized using fluorescence microscopy (E). The SNAP-TMR signal intensity was quantified and reported as mean ± SEM of 3 experiments (F, **P < 0.01). Depletion of HIRA was used as a control.