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Combining genomic data with CRISPR, hiPSC and organoid technologies provides platforms to study the complex genetic architectures of brain disease. These studies could improve genetic diagnosis, drive drug discovery and move the field toward precision medicine.
Efforts to systematically characterize silencers in animal genomes have been limited. Two studies in this issue of Nature Genetics bring silencers into the spotlight, identifying these elements genome wide in human and mouse cells, and providing insights into their function.
Huntington’s disease is a severe progressive neurological disorder caused by a CAG-repeat expansion in the HTT gene. A small molecule shows therapeutic potential by inducing contraction of these expanded CAG repeats in cell and mouse models of the disease.
Recent advances in Hi-C, single-cell imaging and functional genetic studies warrant discussion on the functional relevance of topologically associating domains (TADs) and other classes of chromatin domains.
