Volume 17 Issue 12, December 2016

Physically bridging an enhancer to a β-globin gene increased transcription and explained how enhancers could function over long distances.

Selective autophagy that is dependent on the ER translocon component SEC62 mediates ER recovery following protein stress.

Edith Heard describes how the discovery of lamina-associated domains changed her thinking about the mechanisms of X-chromosome inactivation and gene regulation.

Super-enhancers interact with human nucleoporins at the nuclear pore complex to regulate cell type-specific genes.

The activity of the plant photoreceptor cryptochrome 2 is regulated by a newly characterized interacting protein that prevents cryptochrome 2 homodimerization.

Job Dekker asserts that cases in which data from microscopy- and 3C-based methods appear discordant about genome organization will provide opportunities to improve our models of chromatin folding.

The three-dimensional (3D) organization of eukaryote chromosomes regulates genome function and nuclear processes such as DNA replication, transcription and DNA-damage repair. Experimental and computational methodologies for 3D genome analysis have been rapidly expanding, with a focus on high-throughput chromatin conformation capture techniques and on data analysis.

Mechanistic insights are emerging into how long non-coding RNAs (lncRNAs) regulate gene expression by coordinating regulatory proteins, localizing to genomic loci and shaping nuclear organization. Interestingly, lncRNAs can perform functions that cannot be carried out by DNA elements or proteins alone, such as amplifying regulatory signals in the nucleus.

Mutations in non-coding parts of the genome can cause disease. Technological advances are providing unprecedented detail on genome organization and folding, and have revealed that enhancer–target gene coupling is spatially restricted, as it occurs within topologically associated domains (TADs), and that disrupting such organization can lead to disease-associated gene dysregulation.

Steroid hormone receptors are well known to regulate various aspects of animal physiology by acting as transcriptional regulators in the nucleus. However, it is now evident that these receptors can also be targeted to extranuclear locations (such as the plasma membrane), where they instigate rapid signals that contribute to steroid-mediated cellular responses.

The establishment of various coexisting actin networks supports a plethora of cellular processes and functions. How actin incorporation into these different networks is regulated to balance their growth and maintain homeostasis has remained elusive. Here, the authors propose that the internetwork competition for a limited pool of actin monomers underlies the homeostatic control of actin cytoskeleton organization.