Fig. 5: cPRC1 complexes do not regulate stable PIC binding nor contribute centrally to Polycomb repression.
a, A cartoon illustrating the composition of ncPRC1 and cPRC1 complexes. b, Cartoon representation of the degron cell line in which cPRC1 complexes can be depleted and TFIID dynamics measured by examining TAF11 by SPT imaging (left). Western blot analysis illustrating depletion of cPRC1 complexes within 2 h of dTAG-13 treatment (right). BRG1 was used as a loading control. The western blot was performed once. c, Dot plots illustrating the bound fraction (left) and stable binding time (right) for HaloTag-fused TAF11 (HT-TAF11) in untreated or cPRC1-depleted (dTAG-13-treated) conditions. Individually colour-coded dots represent values for individual biological replicates (n = 4) and are connected with grey lines, error bars represent s.d. and horizontal lines show the mean value. P values represent one-sided paired t-tests. P = 0.020877 (fraction bound); and P = 0.846956 (stable binding time). A minimum of approximately 100 cells for bound fraction analysis and approximately 20 cells for stable binding time measurements were measured per biological replicate (indicated as colour-coded dots). d, As in b except PCGF2 was tagged with bromoTAG (bTAG). Western blot analysis demonstrates PCGF2-bTAG degradation after 2 h of AGB1 treatment. This experiment was performed once. e, smRNA-FISH analysis of transcript-per-cell distributions for untreated cells, cells with PCGF2-bTAG depleted (AGB1-treated), and cells with RING1B-AID depleted (IAA-treated). Depletions were performed for 4 h and at least 400 cells were measured for each gene in each condition. Source numerical data and unprocessed blots are available in Source data.
