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Genome Biol. 2015 Aug 7;16:152. doi: 10.1186/s13059-015-0728-8.

Bipartite structure of the inactive mouse X chromosome.

Author information

1
Department of Pathology, University of Washington, Seattle, Washington, USA.
2
Department of Genome Sciences, University of Washington, Seattle, Washington, USA.
3
Institute for Stem Cell and Regenerative Medicine, University of Washington, Seattle, Washington, USA.
4
Division of Hematology, University of Washington, Seattle, Washington, USA.
5
Institute for Stem Cell and Regenerative Medicine, University of Washington, Seattle, Washington, USA. zjduan@uw.edu.
6
Division of Hematology, University of Washington, Seattle, Washington, USA. zjduan@uw.edu.
7
Department of Genome Sciences, University of Washington, Seattle, Washington, USA. william-noble@uw.edu.
8
Department of Computer Science and Engineering, University of Washington, Seattle, Washington, USA. william-noble@uw.edu.
9
Department of Pathology, University of Washington, Seattle, Washington, USA. cdistech@u.washington.edu.
10
Department of Medicine, University of Washington, Seattle, Washington, USA. cdistech@u.washington.edu.

Abstract

BACKGROUND:

In mammals, one of the female X chromosomes and all imprinted genes are expressed exclusively from a single allele in somatic cells. To evaluate structural changes associated with allelic silencing, we have applied a recently developed Hi-C assay that uses DNase I for chromatin fragmentation to mouse F1 hybrid systems.

RESULTS:

We find radically different conformations for the two female mouse X chromosomes. The inactive X has two superdomains of frequent intrachromosomal contacts separated by a boundary region. Comparison with the recently reported two-superdomain structure of the human inactive X shows that the genomic content of the superdomains differs between species, but part of the boundary region is conserved and located near the Dxz4/DXZ4 locus. In mouse, the boundary region also contains a minisatellite, Ds-TR, and both Dxz4 and Ds-TR appear to be anchored to the nucleolus. Genes that escape X inactivation do not cluster but are located near the periphery of the 3D structure, as are regions enriched in CTCF or RNA polymerase. Fewer short-range intrachromosomal contacts are detected for the inactive alleles of genes subject to X inactivation compared with the active alleles and with genes that escape X inactivation. This pattern is also evident for imprinted genes, in which more chromatin contacts are detected for the expressed allele.

CONCLUSIONS:

By applying a novel Hi-C method to map allelic chromatin contacts, we discover a specific bipartite organization of the mouse inactive X chromosome that probably plays an important role in maintenance of gene silencing.

PMID:
26248554
PMCID:
PMC4539712
DOI:
10.1186/s13059-015-0728-8
[Indexed for MEDLINE]
Free PMC Article
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