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Cohesin-based chromatin interactions enable regulated gene expression within preexisting architectural compartments.
TLDR
These findings indicate that cohesin-mediated long-range interactions facilitate discrete gene expression states within preexisting chromosomal compartments, suggesting an important role for cohesIn in genome organization.
A role for cohesin in T cell receptor rearrangement and thymocyte differentiation
TLDR
A cell-division-independent role for cohesin in Tcra locus rearrangement is firmly established and a comprehensive account of the mechanisms by which cohes in enables cellular differentiation in a well-characterized mammalian system is provided.
Metazoan Scc4 Homologs Link Sister Chromatid Cohesion to Cell and Axon Migration Guidance
TLDR
The data show that sister chromatid cohesion in metazoans involves the formation of a complex similar to the Scc2-Scc4 interaction in the budding yeast, consistent with increased selection pressure to conserve additional essential functions, such as regulation of cell and axon migration during development.
Spatial enhancer clustering and regulation of enhancer-proximal genes by cohesin.
TLDR
A model for cohesin-dependent gene regulation is proposed in which spatial clustering of enhancer elements acts as a unified mechanism for both enhancer-promoter "connections" and "insulation" in mouse thymocytes.
Nuclear genetic regulation of the human mitochondrial transcriptome
TLDR
Using whole-genome genetic data, 64 nuclear loci associated with expression levels of 14 genes encoded in the mitochondrial genome are identified, including missense variants within genes involved in mitochondrial function, implicating genetic mechanisms that act in trans across the two genomes.
Cohesin and chromatin organisation.
Intellectual disability-associated factor Zbtb11 cooperates with NRF-2/GABP to control mitochondrial function
TLDR
It is shown that Zbtb11 plays essential roles in maintaining the homeostasis of mitochondrial function, and improves the understanding of the transcriptional mechanisms of nuclear control over mitochondria, and may help to understand the aetiology of ZBTb11-associated intellectual disability.
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