Skip to main content
. 2019 Jul 25;20(9):e47592. doi: 10.15252/embr.201847592

Figure EV2. CDK12 kinase activity is essential for optimal G1/S progression.

Figure EV2

  1. 3‐MB‐PP1 does not affect cell cycle progression in WT HCT116 cells. The experiment was performed as shown in Fig 2A. n = 3; representative result is shown.
  2. THZ531 causes G1/S progression defect in WT HCT116 cells arrested by serum starvation. Flow cytometry profiles of control (−THZ531) or 350 nM THZ531(+THZ531)‐treated cells from the experiment outlined in Fig 2A. Red arrow points to the onset of the G1/S progression defect in THZ531‐treated cells. n = 3 replicates; representative result is shown.
  3. CDK12 inhibition delays G1/S progression in thymidine/nocodazole‐arrested AS CDK12 HeLa cells. Flow cytometry profiles of control (−3‐MB‐PP1) or 3‐MB‐PP1 (+3‐MB‐PP1) treated cells from the experiment shown in Fig 2A. Red arrow points to the onset of the G1/S progression defect in 3‐MB‐PP1‐treated cells. n = 3 replicates; representative result is shown.
  4. Experimental outline. AS CDK12 HCT116 cells were arrested by serum starvation for 72 h and released into the serum‐containing medium with (+) or without (−) 3‐MB‐PP1. 3‐MB‐PP1 was washed away and replaced with fresh medium at indicated times after the release, and all samples were subjected to flow cytometry analyses at 15 h after the release.
  5. G1/S progression delay can be rescued by removal of CDK12 inhibitor at early G1 phase. Flow cytometry profiles of propidium iodide‐labeled cells from the experiment depicted in Fig EV2D. CTRL = control samples without the 3‐MB‐PP1. n = 3 replicates; representative result is shown.