Topologically associating domains are stable units of replication-timing regulation.
Topologically associating domains are stable units of replication-timing regulation.
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DOI:
10.1038/nature13986
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发表时间:
2014-11-20
期刊:
影响因子:
64.8
通讯作者:
Gilbert, David M.
中科院分区:
文献类型:
--
作者:
Pope, Benjamin D.;Ryba, Tyrone;Dileep, Vishnu;Yue, Feng;Wu, Weisheng;Denas, Olgert;Vera, Daniel L.;Wang, Yanli;Hansen, R. Scott;Canfield, Theresa K.;Thurman, Robert E.;Cheng, Yong;Guelsoy, Guenhan;Dennis, Jonathan H.;Snyder, Michael P.;Stamatoyannopoulos, John A.;Taylor, James;Hardison, Ross C.;Kahveci, Tamer;Ren, Bing;Gilbert, David M.
A study of DNA replication timing in mouse and human cells reveals that replication domains (domains of the genome which replicate at the same time) share a correlation with topologically associating domains; these results reconcile cell-type-specific sub-nuclear compartmentalization with developmentally stable chromosome domains and offer a unified model for large scale chromosome structure and function. The online version of this article (doi:10.1038/nature13986) contains supplementary material, which is available to authorized users. As part of the mouse ENCODE project, David Gilbert and colleagues study the relationship between replication timing and higher order chromatin domains in mouse and human. They find that boundaries of replication domains — domains within the genome which replicate at the same time — share a near one-to-one correlation with topology associated domains. These and other results reconcile cell-type specific sub-nuclear compartmentalization with developmentally stable chromosome domains and offer a unified model for large-scale chromosome structure and function. The online version of this article (doi:10.1038/nature13986) contains supplementary material, which is available to authorized users. Eukaryotic chromosomes replicate in a temporal order known as the replication-timing program. In mammals, replication timing is cell-type-specific with at least half the genome switching replication timing during development, primarily in units of 400–800 kilobases (‘replication domains’), whose positions are preserved in different cell types, conserved between species, and appear to confine long-range effects of chromosome rearrangements. Early and late replication correlate, respectively, with open and closed three-dimensional chromatin compartments identified by high-resolution chromosome conformation capture (Hi-C), and, to a lesser extent, late replication correlates with lamina-associated domains (LADs). Recent Hi-C mapping has unveiled substructure within chromatin compartments called topologically associating domains (TADs) that are largely conserved in their positions between cell types and are similar in size to replication domains. However, TADs can be further sub-stratified into smaller domains, challenging the significance of structures at any particular scale. Moreover, attempts to reconcile TADs and LADs to replication-timing data have not revealed a common, underlying domain structure. Here we localize boundaries of replication domains to the early-replicating border of replication-timing transitions and map their positions in 18 human and 13 mouse cell types. We demonstrate that, collectively, replication domain boundaries share a near one-to-one correlation with TAD boundaries, whereas within a cell type, adjacent TADs that replicate at similar times obscure replication domain boundaries, largely accounting for the previously reported lack of alignment. Moreover, cell-type-specific replication timing of TADs partitions the genome into two large-scale sub-nuclear compartments revealing that replication-timing transitions are indistinguishable from late-replicating regions in chromatin composition and lamina association and accounting for the reduced correlation of replication timing to LADs and heterochromatin. Our results reconcile cell-type-specific sub-nuclear compartmentalization and replication timing with developmentally stable structural domains and offer a unified model for large-scale chromosome structure and function. The online version of this article (doi:10.1038/nature13986) contains supplementary material, which is available to authorized users.
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DOI:
10.1186/1748-7188-9-14
发表时间:
2014
期刊:
Algorithms for molecular biology : AMB
影响因子:
--
作者:
Filippova D;Patro R;Duggal G;Kingsford C
通讯作者:
Kingsford C
影响因子:
16
作者:
McGuffee, Sean R.;Smith, Duncan J.;Whitehouse, Iestyn
通讯作者:
Whitehouse, Iestyn
影响因子:
64.5
作者:
Phillips-Cremins JE;Sauria ME;Sanyal A;Gerasimova TI;Lajoie BR;Bell JS;Ong CT;Hookway TA;Guo C;Sun Y;Bland MJ;Wagstaff W;Dalton S;McDevitt TC;Sen R;Dekker J;Taylor J;Corces VG
通讯作者:
Corces VG
影响因子:
16
作者:
Chandra, Tamir;Kirschner, Kristina;Thuret, Jean-Yves;Pope, Benjamin D.;Ryba, Tyrone;Newman, Scott;Ahmed, Kashif;Samarajiwa, Shamith A.;Salama, Rafik;Carroll, Thomas;Stark, Rory;Janky, Rekin's;Narita, Masako;Xue, Lixiang;Chicas, Agustin;Nunez, Sabrina;Janknecht, Ralf;Hayashi-Takanaka, Yoko;Wilson, Michael D.;Marshall, Aileen;Odom, Duncan T.;Babu, M. Madan;Bazett-Jones, David P.;Tavare, Simon;Edwards, Paul A. W.;Lowe, Scott W.;Kimura, Hiroshi;Gilbert, David M.;Narita, Masashi
通讯作者:
Narita, Masashi
影响因子:
4.3
作者:
Baker A;Audit B;Chen CL;Moindrot B;Leleu A;Guilbaud G;Rappailles A;Vaillant C;Goldar A;Mongelard F;d'Aubenton-Carafa Y;Hyrien O;Thermes C;Arneodo A
通讯作者:
Arneodo A