Fig. 3: Cohesin acetylation converts cohesin into a PDS5A-bound state.
From: The cohesin acetylation cycle controls chromatin loop length through a PDS5A brake mechanism
a, Schematic overview of the setup of the haploid genetic screen, comparing control HAP1 cells with ∆HDAC8 HAP1 cells. This genome-wide genetic screen involves the infection of haploid HAP1 cells with a gene-trap virus, leading to a polyclonal collection of knockout cells. Intronic insertion of the gene trap in a sense orientation creates a knockout of the affected gene, while intronic insertion in the antisense orientation does not affect it. If loss of a gene is beneficial for cellular outgrowth, sense insertions will be enriched over time. b, Plot depicting screen results for wild-type and ∆HDAC8 cells. Each dot represents one gene. The percentage of sense integrations in comparison to the total amount of insertions shows the importance of each gene for cell viability. Upward shift in the cloud indicates that loss of PDS5A is beneficial specifically for ∆HDAC8 cells. c, Pulldown experiment on the core cohesin subunit SMC1, revealing an increase in PDS5A binding to cohesin in ∆HDAC8 (∆8) cells. This experiment was performed three times, with similar results.
