Cohesin-mediated sister chromatid cohesion is essential for chromosome 
segregation and post-replicative DNA repair. In addition, evidence from model 
organisms and from human genetics suggests that cohesin is involved in the 
control of gene expression. This non-canonical role has recently been 
rationalized by the findings that mammalian cohesin complexes are recruited to a 
subset of DNase I hypersensitive sites and to conserved noncoding sequences by 
the DNA-binding protein CTCF. CTCF functions at insulators (which control 
interactions between enhancers and promoters) and at boundary elements (which 
demarcate regions of distinct chromatin structure), and cohesin contributes to 
its enhancer-blocking activity. The underlying mechanisms remain unknown, and 
the full spectrum of cohesin functions remains to be determined. Here we show 
that cohesin forms the topological and mechanistic basis for cell-type-specific 
long-range chromosomal interactions in cis at the developmentally regulated 
cytokine locus IFNG. Hence, the ability of cohesin to constrain chromosome 
topology is used not only for the purpose of sister chromatid cohesion, but also 
to dynamically define the spatial conformation of specific loci. This new aspect 
of cohesin function is probably important for normal development and disease.