Extended Data Fig. 8: Depletion of CEP192 in RPE-1 cells recapitulates the synthetic lethal mitotic phenotypes observed in high-TRIM37 expressing cells.
From: Targeting TRIM37-driven centrosome dysfunction in 17q23-amplified breast cancer
Related to Fig. 3. a, Immunoblot showing the CEP192 levels in indicated control and CEP192-depleted PLK4AS TP53−/− RPE-1 cells. α-Tubulin, loading control. For gel source data, see Supplementary Fig. 1. b, Quantification of mitotic centrosomal CEP192 signal in the same cells as described in a. n = 3 biological replicates, each comprising >30 cells. P values, unpaired two-tailed t-test. Mean ± s.e.m. c, Representative images of centrosomal CEP192 in the same cells as described in a. Scale bars, 5 μm. d, Quantification of the percentage of 3MB-PP1 (3MB)-treated PLK4AS TP53−/− RPE-1 cells with acentrosomal mitotic CEP192 PCM foci. n = 3 biological replicates, each comprising >30 cells. P values, unpaired two-tailed t-test. Mean ± s.e.m. e, Representative time-lapse images of mitotic progression in DMSO- or 3MB-PP1 (3MB)-treated control and CEP192-depleted PLK4AS TP53−/− RPE-1 cells. Cells are labelled with H2B-iRFP and tagRFP-tubulin. n = 3 biological replicates.
