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Abstract：
The chromatin fiber folds into loops, but the mechanisms controlling loop extrusion are still poorly understood. Using super-resolution microscopy, we visualize that loops in intact nuclei are formed by a scaffold of cohesin complexes from which the DNA protrudes. RNA polymerase II decorates the top of the loops and is physically segregated from cohesin. Augmented looping upon increased loading of cohesin on chromosomes causes disruption of Lamin at the nuclear rim and chromatin blending, a homogeneous distribution of chromatin within the nucleus. Altering supercoiling via either transcription or topoisomerase inhibition counteracts chromatin blending, increases chromatin condensation, disrupts loop formation, and leads to altered cohesin distribution and mobility on chromatin. Overall, negative supercoiling generated by transcription is an important regulator of loop formation in vivo.
摘要：
染色质纤维折叠成环，但是控制回路挤压的机制仍然知之甚少。使用超分辨率显微镜，我们可以看到，完整细胞核中的环是由DNA突出的粘蛋白复合物支架形成的。RNA聚合酶II装饰了环的顶部，并与粘附素物理隔离。染色体上粘附素负载增加后的增强循环会导致核边缘和染色质混合处的Lamin破坏，染色质在细胞核内的均匀分布。通过转录或拓扑异构酶抑制改变超螺旋作用抵消染色质混合，增加染色质凝聚，破坏了环路的形成，并导致染色质上的粘附素分布和迁移率改变。总的来说,转录产生的负超螺旋是体内环形成的重要调节因子。
