Journal
NUCLEUS
Volume 9, Issue 1, Pages 216-226Publisher
TAYLOR & FRANCIS INC
DOI: 10.1080/19491034.2018.1449498
Keywords
chromatin; differentiation; LAD; lamin A; C; genome conformation; 3D genome
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Funding
- South East Health Norway
- University of Oslo
- Research Council of Norway
- Norwegian Center for Stem Cell Research
- EU Scientia Fellowship FP7-PEOPLE-COFUND [609020]
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The nuclear lamina contributes to the regulation of gene expression and to chromatin organization. Mutations in A-type nuclear lamins cause laminopathies, some of which are associated with a loss of heterochromatin at the nuclear periphery. Until recently however, little if any information has been provided on where and how lamin A interacts with the genome and on how disease-causing lamin A mutations may rearrange genome conformation. Here, we review aspects of nuclear lamin association with the genome. We highlight recent evidence of reorganization of lamin A-chromatin interactions in cellular models of laminopathies, and implications on the 3-dimensional rearrangement of chromatin in these models, including patient cells. We discuss how a hot-spot lipodystrophic lamin A mutation alters chromatin conformation and epigenetic patterns at an anti-adipogenic locus, and conclude with remarks on links between lamin A, Polycomb and the pathophysiology of laminopathies. The recent findings presented here collectively argue towards a deregulation of large-scale and local spatial genome organization by a subset of lamin A mutations causing laminopathies.
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