STAG1 has been identified as a hardwired genetic dependency of cancer cells harbouring mutations in the cohesin subunit and emerging major tumor suppressor STAG2 holds the promise for the development of selective therapeutics.
E3 ubiquitin ligase Bre1-induced H2B monoubiquitination is epigenetically important for recruiting replication factor Mcm10 and cohesion establishment factors Ctf4, Ctf18 and Eco1 to early replication origins to establish sister chromatid cohesion.
Absolute quantification of cohesin, CTCF, NIPBL, WAPL and sororin in HeLa cells implies that some genomic cohesin and CTCF enrichment sites are unoccupied at any one time.
The interface formed where Smc3p and Mcd1p bind each other regulates cohesin DNA binding and cohesion by a mechanism independently from its putative role as a DNA exit gate.
A histone modification that alters the nucleosome structure occurs in mitosis and promotes chromosome packaging and the timely removal of condensin I and cohesion, to achieve chromosome segregation.
A critical second step in DNA tethering by cohesin occurs after its stable binding to DNA, and this second step is modulated by the Smc3 ATPase active site in Saccharomyces cerevisiae.
In G1 cells, Scc2 loads and maintains cohesin on chromosomes by counteracting a Wapl-independent releasing activity, which is neutralized in S phase by CDK1.
By specifically antagonizing binding of complexes carrying COH-3/4 kleisins, WAPL-1 regulates chromosome structure and cohesion throughout meiotic prophase.
Systematic analyses of DNA replication machinery components in human cells reveal a requirement of MCM-dependent de novo loading or mobilization of cohesin at replication forks in establishing sister-chromatid cohesion.
Cohesin-regulated 3D genome conformation controls activity of transcription factor Escargot in intestinal stem cells, prevents premature differentiation into enterocytes and maintains intestinal homeostasis.
