Figure 6.

Unresolved stalled ribosomes cause cell-cycle arrest

(A) Phosphorylation of p38^MAPK and JNK after treatment with anisomycin (ANS) or UVB.

(B) Collided ribosomes at 1, 3, and 6 h after treatment with anisomycin in control or ASCC3-depleted cells.

(C) ASCC3 depletion causes prolonged p38^MAPK phosphorylation in response to anisomycin.

(D and E) p38^MAPK phosphorylation after UVB treatment in (D) or after anisomycin treatment of ASCC3-depleted cells in (E) depends on ZAK.

(F) Cell-cycle distribution in control (C) and ASCC3-depleted cells (A) after treatment with anisomycin. Error bars represent the SD. ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001.

(G) The effect of anisomycin treatment in control and ASCC3-depleted cells on the G2 to M-phase transition measured by trapping the cells in mitosis with nocodazole (Noc).

(H and I) The accumulation of ASCC3-depleted cells in G2 after anisomycin treatment is prevented by pre-exposure to a p38^MAPK inhibitor (p38i) in (H) or depletion of ZAK in (I). ∗∗p < 0.01, ∗∗∗p < 0.001.

(J) ASCC3-depleted cells have a prolonged G1 arrest compared with control cells after anisomycin treatment. Error bars represent the SD. ∗∗p < 0.01.

See also Figure S5.