Fig. 1: Role of RepID in mitotic exit and G1 entry.

a A model describing the current understanding of molecular interactions among components of the CRL4 and SAC complexes. b, c RepID KO cells delay mitotic exit. b HCT116 RepID WT and KO cells were exposed to nocodazole for 16 h, released into drug-free media, and collected every 3 h, followed by flow cytometry to monitor cell cycle progression. c Percentages of cells from b in G1, G2/M, and subG1 fractions for the experiment shown in b. Error bars in all results represent standard deviation from three independent experiments (*p value < 0.05, **p < 0.01, ***p < 0.001, Student’s t test). d–h RepID KO cells exhibit prolonged metaphase–anaphase transition. d Image montage of a representative single cell expressing APC-degron (mCherry-geminin) and H2B-mTurquiose in HCT116 RepID WT and KO cells after release from CDK1 inhibitor-based synchronization. Images were taken every 5 min. NEB, nuclear envelop break. e Single-cell traces of the intensity of nuclear area in RepID WT and KO cells. The black line illustrates the average trace (left and middle panels). The first drop indicates a reduced area due to chromosome alignment in metaphase and the second drop indicates the segregation of chromosomes via the initiation of anaphase (right panel) (M metaphase, A anaphase). f Single-cell traces of APC-degron in RepID WT and KO cells. Black line illustrates the average trace (left and middle panels). The first drop indicates nuclear envelope breakdown (right panel). The constant APC-degron signal indicates a period prior to anaphase initiation. The second drop indicates anaphase initiation (right panel). g Bar graph indicates time to anaphase from release. h Percentage of anaphase cells in the population after release from nocodazole arrest in HCT116 RepID WT and KO cells.